…and this is a 
There in the foaming welter of email constantly flooding my in-box was an actual, real, good, sincere question from someone who didn't understand how chromosome numbers could change over time — and he also asked with enough detail that I could actually see where his thinking was going awry. This is great! How could I not take time to answer?
So here's the question:
How did life evolve from one (I suspect) chromosome to... 64 in horses, or whatever organism you want to pick. How is it possible for a sexually reproducing population of organisms to change chromosome numbers over time?
Firstly: there would have to be some benefit to the replication probability of the organisms which carry the chromosomes. I don't see how this would work. How is having more chromosomes of any extra benefit to an organism's replicative success? Yes, perhaps if those chromosomes were full of useful information... but the chances of that happening are non existent and fly in the face of 'small adaptations over time'.
Secondly, the extra chromosomes need to come from somewhere. I'm not sure about this, but I believe chromosome number are not determined by genes, are they? There isn't a set of genes which determines the number of chromosomes an organism has. So the number is fixed, determined by the sexually reproducing parents. Which leads me to believe that if the number does change, and by chance the organism is still alive and capable of sexual reproduction, that the number will start swinging back and forward, by 1 or 2, every generation, and never stabilising. The chances of this happening are also very very slim.
Let's clear up a few irrelevant misconceptions first. Life probably started with no chromosomes — early replicators would have been grab bags of metabolites, proteins, and RNA that would have simply sloppily split in two, with no real sorting. DNA and chromosomes evolved as accounting and archiving tools: they were a way to guarantee that each daughter cell in a division reliably received a copy of every gene. Also, most living things now just have one 'chromosome', a loop of DNA, and perhaps a small cloud of DNA fragments. So to keep this simple we're going to ignore all that, and consider only us diploid eukaryotes, where the question of chromosome numbers becomes a real issue.
Normally, I'd be scribbling madly on a whiteboard, so we'll have to make do with some scribbles on the computer screen. Here, for instance, is a typical cartoon chromosome. It's a string of DNA, and scattered along it we have sequences for genes, that I've labeled "A", "B", "C", "D", and "E". I've also drawn a circular blob in the middle: that's important. It's not a gene, it's a structure called the centromere, which gets all wrapped up in proteins to form a kinetochore. It's a sort of anchor point; when the cell needs to move chromosomes around, as it does during cell division, it hitches motor proteins to the kinetochore and using drag lines called spindle fibers, tows it to a new destination.
I mentioned that this was a diploid organism — that just means that every chromosome comes in pairs. This cell would have a similar chromosome to the one that has the ABCDE genes on it; here I've draw it as containing the same genes, but in slightly different forms: abcde. This matters because during meiosis, when gametes (sperm and egg) are formed, the two chromosomes line up with one another and the cell machinery tows one chromosome to one daughter cell, and the other to the other daughter cell. It's accounting; it makes sure each daughter gets a copy of all of the genes, one A or one a, one B or one b, etc., for instance.
For now, put the fact that there are two copies of each chromosome at the back of your mind and don't worry about it. Let's think about a single chromosome and ask what can happen to it.
Here's something fairly common. An error in copying the DNA can lead to the loss of a piece of DNA. This happens with a low frequency, but it does happen — if we sequenced your DNA, we might well find a few bits missing here and there. We can get situations like this, where a whole gene gets lost.
Don't panic! Remember that we have two copies of every chromosome, so while this one is missing the "D" gene, there's that other chromosome floating around with a "d" gene. This is not necessarily bad for the individual, it just means he doesn't have a spare any more.
Another kind of error that can happen with a low frequency is a duplication, where the machinery of the cell accidentally repeats itself when copying, and you get an extra copy of a piece of a chromosome, like so:
This person has two copies of D on this chromosome now (and remember that other chromosome, with it's d gene — he actually has 3 copies in total now). This is not usually harmful: it gives the individual a little extra redundancy, and that's about it. It can change the total amount of the D gene product in the cell, and if it's a gene for which precise dosage is important, it can have visible effects…but in most cases, this is a neutral change.
You may have noticed that nothing has changed the chromosome numbers yet. Here's a situation that can lead to the formation of a new chromosome: what if there is a duplication of the centromere, rather than a gene?
Remember, I told you that the centromere/kinetochore is where the cell attaches lines and motors to haul the chromosome to the appropriate daughter cell. In this case, two lines are attached; what if one tries to pull one centromere to the left, and the other tries to pull the other centromere to the right? Tug of war!
The end result is that the chromosome is broken into two chromosomes. I think this is a key concept that the questioner is missing: chromosome numbers really aren't significant at all! You don't need to add significant new information to create a new chromosome, and as I'll show you in a moment, a reduction in chromosome numbers does not represent a loss of genetic information. Chromosome are disorganized filing cabinets, nothing more; we can shuffle genes around between them willy-nilly, and the cell mostly doesn't care. A fission event like the one described above basically does nothing but take one pile of genes and split them into two piles.
But there are some important effects. This may not be an entirely neutral situation. Let's bring back that abcde chromosome, and pair it up with our two new chromosomes, AB and CDE.
The accounting is accurate. This cell has two copies of the A gene, an "A" and an "a", just like normal, and the two new chromosomes can still pair up efficiently with the old chromosome in meiosis, just like before. This is a healthy, functioning, normal cell, except for one thing: if it goes through meiosis to make a sperm or egg, it's going to make a larger number of errors. There are three centromeres there, to be split into two daughter cells! Never mind what the Intelligent Design creationists tell you — the cell is really, really stupid, and it will more or less decide by eeny-meeny-miny-moe how to divvy up those chromosomes. If by chance the split is that one daughter gets AB + CDE, and the other gets abcde, both daughters have the full complement of genes and all is well. However, the split could also be that one daughter gets AB and nothing else, while the other gets CDE + abcde … and that's no good. One is missing a whole bunch of genes, and the other has an overdose of a bunch.
The net result is that although this individual is fine and healthy, a significant number of his or her gametes may carry serious chromosomal errors, which means they may have reduced fertility. They aren't sterile, though; some of their gametes will have the full complement of genes, and can similarly produce new healthy individuals who will probably have fertility problems. (Note: the significance of those fertility problems will vary from species to species. Organisms that rely on producing massive numbers of progeny so that a few survive to adulthood would be hit hard by a change that cuts fecundity; species that rely on producing a few progeny that we raise carefully to adulthood, like us, not so much. So you have to have sex 20 times to successfully produce a child instead of 5 times; that won't usually be a handicap.)
So our two chromosome individual will have a reduced fertility as long as he or she is breeding with the normal one chromosome organisms, but those split chromosomes can continue to spread through the population. They are not certain to spread — they're more likely to eventually go extinct — but by chance alone there can be continued propagation of the two chromosome variant. Which leads to another misconception in the question: something doesn't have to provide a benefit to spread through a population! Chance alone can do it. We don't have to argue for a benefit of chromosome fission at all in order for it to happen.
So we can have a population with a low frequency of scattered chromosomal variants, some carrying the rare two chromosome variant and others the more common one chromosome form. What if two individuals carrying the two chromosome variant breed? They can produce offspring that look like this:
How many centromeres are there? Four, not three. This is a situation the cell machinery can handle reliably, and this individual will consistently produce good gametes that accurately carry AB + CDE, nothing more, nothing less, and will have no reduction in fertility. Now we have a potentially interesting situation: individuals with the one chromosome situation have full fertility when breeding with other individuals with one chromosome; individuals with two chromosomes have full fertility when breeding with other individuals with two chromosomes; it's when individuals with two different chromosome arrangements try to breed that fecundity is reduced. This is a situation where speciation is a possibility.
One last thing: what about reducing chromosome numbers? That's easy, too. Here's an organism with an AB chromosome, and a different chromosome with the genes MN on it. They can simply fuse in the region of the centromere.
This happens with a low frequency, too, and has been observed many times (hint: look up Robertsonian fusions on the web.) I think the key issue to understand here is that chromosome number changes are typically going to represent nothing but reorganizations of the genes — the same genes are just being moved around to different filing cabinets. This has some consequences, of course — you increase the chances of losing some important file folders in the process, and making it more difficult to sort out important information — but it's not as drastic as some seem to think, and chromosome numbers can change dramatically with no obvious effect on the phenotype of the organism. These really are "small adaptations over time", or more accurately, "small changes over time", since there is no necessary presumption that these are adaptive at all.
I've discussed fusion events and how they relate to evolution before, and there's an interesting difference in context there, too. My prior article was a response to Casey Luskin, an ignorant creationist who used his misunderstanding of genetics to foolishly assert the existence of a major problem, and that's where we have a conflict: ignorance is not a problem, but stupidly using your ignorance to push invalid ideas is. This question in my mailbox is also ignorant — the fellow really doesn't understand the basics of genetics — but it's self-recognized ignorance that, in a good way, prompts him to ask a sincere question.
If you want to dig a little deeper, there are many ways genetic information can be rearranged on chromosomes, and this has opened the doors to some interesting evolutionary research. I've described how we can map the reshuffling of chunks of genetic information over time, a process called synteny mapping, which allows us to reconstruct ancestral chromosomes. A fish might have 42 chromosomes, and we might have 46, but we can still trace how the ancestral arrangement was scrambled in many different ways to generate the modern arrangements.
Life Science
Comments
Posted by: Milo Johnson | April 21, 2008 10:55 AM
Wow. Thank you for answering a zillion questions in one fell swoop!
Posted by: Wiggy | April 21, 2008 11:00 AM
Thanks PZ! I asked my biology teacher the same question in high school but she couldn't tell me. Not that I was trying to disprove evolution or anything, I was just curious! Ever since then I've always had a mild curiosity about this very question but never got around to digging up the answer. Now (15 odd years later) I finally know!
Posted by: GBruno | April 21, 2008 11:02 AM
Superb!
Posted by: Hairhead | April 21, 2008 11:03 AM
Now THAT was a great answer, PZ! And it disproves the notion that you're an old poopy-head who just wants to make fun of the sincere god-bots. You treat others as they treat you; a respectful and intelligent question gets a response in kind, whereas a threatening, abusive letter filled with cant and deliberate gets either chucked, or held up for contempt.
Just to repeat: great answer -- thorough, thought-provoking, and clear. Why the hell couldn't the National Geographic specials have stuff like you just did, instead of the pretty, but vapid and (mostly) dumbed-down stuff they produce?
Posted by: boomer | April 21, 2008 11:04 AM
I've just started reading Relics of Eden, by Daniel Fairbanks. It describes these kind of things very well for a layman like me, and I have been writing down parts of it that I know will be very good ammunition for my debates with IDers and creationists.
Posted by: dorght | April 21, 2008 11:05 AM
Thank you, I've wonder the same thing for a long time. I'm sure I'll recover to normal or increased levels of "self-recognized ignorance" after I've thought about this awhile.
Posted by: Andy | April 21, 2008 11:05 AM
Thanks for addressing this topic. This has been something I have been wondering about since I learnt some basic genetics at school.
Posted by: alex | April 21, 2008 11:06 AM
hurrah *much applause*
Posted by: Eric | April 21, 2008 11:08 AM
This is one of the questions that I had always wondered about but never taken the time to look up. Thanks for answering it.
Posted by: Glen Davidson | April 21, 2008 11:10 AM
And remember, it actually takes good working replication machinery even to keep chromosome numbers the same over generations.
In cancer cells, aneuploidy, the "wrong number" of chromosomes, is very common. Yet cancer cells are notorious for surviving, and even adapting through darwinian selection. Even many normal cells in our bodies can be aneuploid.
The fact is that it is all too easy to change chromosome numbers, and what is amazing is how meiosis usually manages to keep the right number. Selection has to weed out many changes in chromosome number, while occasionally a change in numbers is either beneficial, or perhaps simply neutral yet able to give rise to a new species. The fusion that gave rise to our chromosome 2 may be an example of the latter.
Glen D
http://tinyurl.com/2kxyc7
Posted by: Kitty | April 21, 2008 11:11 AM
Excellent.
Posted by: firemancarl | April 21, 2008 11:13 AM
Oh SNAP!
Kudos to whomever asked this question, your answer PZ helped me understand how the process works. Thanks again.
Posted by: Spencer | April 21, 2008 11:14 AM
Wow. That was marvelously lucid. Thank you:)
Posted by: Lurker #753 | April 21, 2008 11:22 AM
Some examples: Humans have 1 fewer chromosome than the rest of the great apes - our chromosome #2 is recognisably the fusion of 2 of the ape chromosomes (now called 2A and 2B).
Horses have 64 chromosomes, donkeys have 62 - they can interbreed, and the result is almost always sterile, no idea whether the success rate is lower than normal.
As I understand it, plants do this far more often than animals - including by simply doubling up - i.e. the child plant has 2x the chromosomes (and evolution can then create differentiation, assuming that the plants are fertile (domesticated wheat) or just by slow mutation even if they're not, but helpful humans propagate cuttings (banana).
Posted by: wÒÓ† | April 21, 2008 11:23 AM
(.)(.)
Posted by: PaulH | April 21, 2008 11:24 AM
As a long time lurker, time to stick my head above the parapet and say 'brilliant'. Thanks for a great explanation.
Posted by: lytefoot | April 21, 2008 11:29 AM
Awesome! I hadn't actually wondered about that--I'd assumed arrangements were made. (I guess that makes me a dogmatic believer in evolution, like the creationists are always accusing us of being? Except that I've always known the answers to these questions existed, if I cared to look for them.) Nonetheless, this is a very cool thing to know.
One thing I'm wondering about, though: what's the likelihood that several organisms within a species would have a break in the same place? Is it happening when the cousins get to breeding mostly? Or is that "same place" an oversimplification, where there's various nonsense to either side of the break? Or is there something about certain segments of DNA that make them more likely to sprout an extra centriole? Or is it just a large numbers fallacy--it's going to happen, because there are a huge number of trials?
Posted by: Beowulff | April 21, 2008 11:29 AM
That was refreshing, thanks :)
Posted by: cynthax | April 21, 2008 11:30 AM
That's what I like about this blog! It is at the same time very entertaining and very educational. Creationists have actually done me a favor: I would never have learned so much about biology if it hadn't been for their making claims out of ignorance. Thanks once again, PZ!
Posted by: Chris | April 21, 2008 11:34 AM
Very descriptive, thanks PZ.
Posted by: Patrick Conley | April 21, 2008 11:35 AM
Ah! Written so even a physicist can understand it.
Thanks, unnamed emailer!
Posted by: boomer | April 21, 2008 11:35 AM
I seem to recall reading about a species of fern that has a ridiculously large number of chromosomes, like on the order of 20,000 or so... but I can't seem to find the name of it now. Does anybody know anything about this, or was this a lie I read on wikipedia?
Posted by: Liam | April 21, 2008 11:37 AM
A THEORY IN CRISIS!!!!!!
Posted by: don kane | April 21, 2008 11:37 AM
I believe there are examples of balanced translocations being dominant in populations of Drosophila on some islands. If the translocation break points don't wreck genes, the duplicated translocation can be perfectly viable, an least in the balanced form. I don't have the time to go into the details (they are in many genetics books), but this is a pretty straight forward way that two populations can lose the ability to interbreed.
And I used to think that Hu Chromossome 2 was an ape Robertsonian, but then they had to go find a telomere or centromere in there somewhere...
that was such a nice nice hypothesis until it ran into a little data....
-d
Posted by: Cuttlefish, OM | April 21, 2008 11:38 AM
I once wrote a pair
Of Haikus, related, but
Willing to fuse--please
Don't ask me how one
Limerick now replaces
The Haikus in twos
*****
I once wrote a pair of Haikus
Related, but willing to fuse
Please don't ask me how
One limerick now
Replaces the Haikus in twos
(OT-- http://digitalcuttlefish.blogspot.com/2008/04/i-just-love-xkcd.html )
Posted by: NP | April 21, 2008 11:38 AM
I wish you were my prof, PZ!
Posted by: Will Davies | April 21, 2008 11:40 AM
Yay! Learning!
Posted by: dubiquiabs | April 21, 2008 11:40 AM
One of the arguments more learned creationists have raised is that the great apes have 48 chromosomes, but humans have only 46. How could humans have possibly evolved from the same phylogenetic ancestor as we have? One answer is in a great paper:
Hillier LW, and lots of others.
Generation and annotation of the DNA sequences of human chromosomes 2 and 4.
Nature. 2005 Apr 7;434(7034):724-31.
Apparently, in the course of our evolution, two ancestral primate chromosomes fused to make chromosome 2 in humans, an illustration of the point PZ Myers makes toward the end of his nifty piece. Added beauty is a stretch of telomeric TTAGGG repeats --inside-- the chromosome. So, not only does this find support the idea that we evolved from a common ape ancestor, it also shows just how it must have happened.
Posted by: raven | April 21, 2008 11:45 AM
Chromosomal numbers can vary within the same species. This number is very plastic. Mice colonized Madeira 1000 years ago and the 6 populations all have varying karyotypes. This is fast in evolutionary terms.
Same thing is observed in Tunisian mice. The latter are thought to be undergoing speciation, driven in part by karyotypic differences and lower fitness in hybrids.
Posted by: jck | April 21, 2008 11:45 AM
Your smackdowns of creationists are fun, but stuff like this is priceless for us laypeople. Have you considered putting these in a book?
Posted by: Bouncing Bosons | April 21, 2008 11:46 AM
Ahhh, always a good day when gains new understanding before lunch. Even if it is from the gooier, more icky sciences. =)
Seriously though, very enlightening, many kudos PZ.
Posted by: Carlie | April 21, 2008 11:48 AM
Lovely dip into the refreshing pool of knowledge. Besides helping the general public, stuff like this helps people like me see easier ways to explain things than I can come up with myself. Thanks!
Posted by: brokenSoldier | April 21, 2008 11:49 AM
Rarely do I ever get that deep into biology, precisely because its specifics are not easily explained. Thanks for the detail - I can now say I understand at least one involved concept in biology.
(Though I finally got my brain around the explanation, it took just enough time to confirm that my choice to enter philosophy and anthropology was the correct one...)
Posted by: Tulse | April 21, 2008 11:49 AM
Great post, PZ!
And Cuttlefish, I am always in awe of your mad skilz, but that is astoundingly inventive! Perhaps there are other biological phenomena you could represent in concrete poetry...
Posted by: freehand | April 21, 2008 11:52 AM
Happy, happy, joy, joy.
Every now and then somebody puts real information in front of me, and I unwittingly learn something. Rarely so elegantly presented, however. Thank you. I'll show this to my wife when she gets off work.
Posted by: PeteC | April 21, 2008 11:54 AM
There's an interesting twist on the breakage fusion business pointed out in a nice paper (full text available) -- that since female meiosis is asymmetric (two cell divisions produce only one egg and some polar bodies, so some chromosomes get thrown away) there is competition between chromosomes for getting into the egg. If you have one breakage, or one fusion, you will have an odd number of total centromeres (like PZ drew above). It turns out there is a slight preference for the 'extra' centromere to either go to the egg, or to the first polar body - different ways for different organisms. This is why if you look at mammalian karyotypes, you will see that they are either all-metacentric (centromeres near the middle) like humans, or all-acrocentric (telomeres near one end) like many mice, but never a mixture of both, as would be expected if inheritance were random. That's chromosome evolution put into high gear by a 'selfish' phenomenon.
Posted by: R N B | April 21, 2008 11:54 AM
Excellent. I often wondered about this too. And I've heard the same assertions from idiots thinking that chromosomes make speciation impossible.
One answer that I give is to repeat the line that they often use: "interspecies hybrids are usually sterile". As in the horse donkey example, as in ligers and tigons, as in many others. But there was an important word in there. They are usually sterile. Not always.
Posted by: Jason B | April 21, 2008 11:55 AM
The more you post like this, the more I consider going to Minnesota to finish my bio degree.
Hint: Move to Arkansas. We need the education.
Posted by: Duae Quartunciae | April 21, 2008 11:56 AM
One thing I found of interest when I looked some of this stuff up for a discussion on a Christian webforum I inhabit is the frequency of fusions in humans, right now.
Something like 1 in a 1000 human individuals in the general population have a Robertson translocation, in which different chromosomes are fused into a single larger chromosome. Details are available in Changes to Chromosome Structure (pdf file); fact sheet 7 from the Australian Centre for Genetic Education.
There is probably no real effect for such individuals, until they try to have children, when they are likely to have some difficulty with fertility.
I passed this information on without the depth of education that a biologist would bring to the subject. Posts like this one here are a great help.
Posted by: Mr_P | April 21, 2008 11:58 AM
Wow PZ, that was great!
Posted by: PZ Myers | April 21, 2008 11:58 AM
There are other mechanisms for changing numbers that I didn't discuss: polyploidy and alloploidy, for instance. This post only describes a few of the ways we can get variations. Don Kane also mentioned translocations, which are sneaky ways for a chromosome to gradually scramble itself around, piece by piece.
Posted by: Etha Williams | April 21, 2008 11:59 AM
This is great. I envy your students. None of my biology professors ever explained this question so clearly, and although I've had a general notion of it, I've always still been a bit confused. (Bad me for not doing the research to clear up any confusion, I know.) Now I understand much better. Thanks, PZ!
Posted by: D | April 21, 2008 12:01 PM
I've wondered about this recently, thanks, this is a really good answer
Posted by: ctenotrish | April 21, 2008 12:01 PM
Great great great post - thanks again PZ for a fine post!! An additional point is that depending on the literature source you read, somewhere between 1 in 600 to 1 in 1000 people carry a balanced translocation (the numbers vary depending on the type of study performed). That is, one chunk of a chromosome has switched places with another - no gain or loss of genetic material, but instead the re-shuffling that PZ discussed above. Such people are perfectly normal, and may never be aware that they carry a balanced translocation. Or, they may have a history of infertility or spontaneous abortions, or have a child or children with congenital anomalies. This is why it is standard practice to have chromosome analysis performed as part of a reproductive-issues work up, or if a child is born with anomalies. Chromosome rearrangements in humans (well, all animals with chromosomes) are neither common nor rare.
BTW - Cuttlefish is a poetry ROCK STAR. Love the fusion!
Posted by: KeithB | April 21, 2008 12:04 PM
If it hasn't been done already, this needs to be sent to Wilkins as a "Basics of Science" post.
Posted by: drerio | April 21, 2008 12:04 PM
Great answer. The question asked about selective advantage and your answer (accurately) says that there needn't be a necessary selective advantage to propagate through the population. However, there is a potential selective advantage (and disadvantage) to having material scattered across several chromosomes (for a diploid eukaryote). With only one chromosome, all of your material is in one cabinet, inherited wholesale from parent to child, child to grandchild. You'll necessarily have an exact copy of one of your ancestors chromosomes (leaving aside meiotic recombination), bringing both the good and the bad copies of genes along. Splitting up your genetic material into chromosomes that can be inherited independently means you will get a mixture of the grandparental genes. You won't be an exact genetic copy. This allows increased mixing and matching of genetic material, potentially improving the chances of a beneficial combination of genes.
Of course more chromosomes also means more record keeping. More centromeres and telomeres to handle during duplication and meiosis/mitosis. I think the jury is still out on whether there might be some optimum number of chromosomes (rhinos have 84!).
Interestingly, most avian species have numerous microchromosomes. Up to 25% of the DNA (and 50% of the coding sequence) is not in conventional chromosomes but rather in a pool of smaller chromosomes. In these microchromosomes, recombination and mutation rates are significantly higher than in standard chromosomes, which may have significant impacts on their evolution.
There is interesting research into the origin of these microchromosomes and chromosome number in general. Nakatani Y et al (2007 - Genome Research 17:1254) suggest that microchromosomes may represent an ancestral vertebrate state where fusions have produced the 20-30 large chromosomes found in most vertebrate clades.
Posted by: raven | April 21, 2008 12:08 PM
True. I personally know 2 people who have altered karyotypes, balanced. They were picked up on the basis of a family history of fertility problems and miscarriages. These weren't severe though, one of the ancestral families ended up with 6 kids.
Posted by: Anonymous | April 21, 2008 12:10 PM
Wow, a post from PZ Myers about science, on Scienceblogs of all places!
Posted by: Dustin | April 21, 2008 12:12 PM
Great post, PZ!
But one critical point: perhaps you could have included a little more about what the *evidence* is for what you've just said. I can just hear the creationists saying "But how do YOU know?" I think that one general problem with the way science is often taught is that it is taught in abstraction from the evidence for/context of discovery of the claims being presented to the student. Although you usually do a pretty darn good job of not making that mistake.
Here's something to ponder: how many big bang doubters have you met that could name one single piece of alleged evidence for the big bang? I sure haven't met any.
Not surprisingly, those who are aware of the evidence believe, those who aren't, don't.
Posted by: Nan McIntyre | April 21, 2008 12:19 PM
I wish you were my prof, PZ!
The archive here makes him everybody's prof.
Dig in - it's the best part of the place.
Not least because the prof can really employ multimedia.
I recommend "How to make a vulva". I won't link to it directly because I have no idea whether the comments are worksafe in the land of patriarchal womb-control ;-)
Posted by: Tim Foreman | April 21, 2008 12:22 PM
Thanks PZ, this was a wonderful read.
I'm a long time lurker, occasional commenter.
This kind of stuff is so much cooler than just saying "Goddidit."
Posted by: Tim Mills | April 21, 2008 12:23 PM
Thankyou for this, P-Zed. It's always a treat to learn something from an expert without having to become an expert first.
Honestly, if more people were able to communicate technical concepts like you communicate this one, I doubt we would have nearly as much problems getting people to accept sound science and reject nonsense.
Posted by: Paul Lundgren | April 21, 2008 12:23 PM
It's such a pleasure seeing a pro on top of their game. Well done, sir.
Posted by: Brownian, OM | April 21, 2008 12:27 PM
That was a beautifully concise explanation! Well done.
I'm given to sentimentality on occasion, and PZ's mini-lecture brought me back to the class on genetics and heredity I took way back in 2001. The instructor was Dr. Mike Harrington here at the U of A, and he shared PZ's talent for clarity as well as a sense of humour. (Plus, he wrote some of the best exams I've ever had the pleasure of taking--yes, you read that correctly: a well-written exam can be a pleasure for a prepared student.)
Man, I loved that class. Now I feel like quitting my job and going back to school.
Posted by: benny | April 21, 2008 12:31 PM
Wow... that's all I can say. That was an amazing explanation. Good job!
Posted by: Ignorant Atheist | April 21, 2008 12:31 PM
I wish I were smart enough to understand all this stuff, but I read a few paragraphs and my brain does a short circuit. Bzzzt. But even not understanding what you are saying, I realize you have an infinitely better argument for evo than the creos.
Posted by: Ignorant Atheist | April 21, 2008 12:34 PM
Weird, my post deleted all my spacing between sentences.
Posted by: Kenneth Oberlander | April 21, 2008 12:34 PM
Cuttlefish, this is honestly your best yet!
I bow in awe.
Posted by: jeff | April 21, 2008 12:35 PM
Great post, great thread.
Regarding the reduction of chromosome numbers in Humans vis a vis the great apes, some work by Simon et al. several decades ago uncovered some circumstantial yet intriguing evidence that the process was specifically influenced by the mother. I don't have the text handy, but one section I recall rather clearly said something to the effect "Mama, don't take my Chromosome away."
Posted by: Nan McIntyre | April 21, 2008 12:36 PM
Sorry, the link to the listing of articles is stripped from my bad html.
This is it:
http://pharyngula.org/articles.html
Posted by: Nick | April 21, 2008 12:40 PM
There is plenty of evidence for this. Take some of the human genetic illnesses. Some of these involve extra chromosomes, and yet they are people who function, albeit in these cases with varying degrees of handicap.
It's clear that some mutations like this aren't noticed because the effects aren't extreme. If they lead to an advantage, you would get the growth of organisms with extra chromosomes.
Nick
Posted by: Ignorant Atheist | April 21, 2008 12:44 PM
@Raven:
karyotypes:
AAAAAAAAAAAAAAhhhhhhhhhhhhhh!
lol.
Posted by: Charles | April 21, 2008 12:56 PM
Boomer, I did a quick google search and found indications that the species is Ophioglossum reticulatum, which apparently has 630 pairs (1260, a bit less than your recollection of 20000, but still ridiculous consider that animals seem mostly to be in the double digits). Note, this is after about 5 seconds of looking by a nonbiologist, so it's possible that I've missed something. The website I found is http://www.vivo.colostate.edu/hbooks/genetics/medgen/basics/minmax_chromos.html
Posted by: shrimplate | April 21, 2008 12:59 PM
Thanks, PZ. I enjoy reading such explanations. That's one reason why I visit this site regularly.
Posted by: Greg Gyetko | April 21, 2008 12:59 PM
Nice post! This will make a fantastic addition to the things I send to brash, ignorant creationists. I can't wait until the creationists read it. I'm sure their response will looks something like this ...
PZ Myers has admitted that, on the subject of evolution: "Chance alone can do it."
Posted by: bigjohn756 | April 21, 2008 1:12 PM
Lucid lesson! I really wasn't interested in this subject, but, I started reading and I was hooked on learning more.
Posted by: Dave | April 21, 2008 1:13 PM
Nothing original in my comment, I just want to chime-in and say how fantastic and accessible that explanation was. I just got a biology lesson from a professor for free (complete with whiteboard illustrations)! If people really do learn something new every day, this will probably be the most interesting thing I'll learn this week (now that the John Adams miniseries is concluded). Thanks PZ!
Posted by: ildi | April 21, 2008 1:14 PM
OK, I'm officially in love with Cuttlefish! Haiku to limerick? Let me catch my breath....
Posted by: Vic | April 21, 2008 1:24 PM
(OP Kudos)
What an excellent post. Thanks PZ.
(snark)
Where are Nisbet and Mooney? This is a frame they should really see.
(Comment Kudos)
Cuttlefish, that was brilliant, and inspiring seeing as my timestamp math says you did it in less than an hour.
Posted by: Vazrick | April 21, 2008 1:29 PM
This is very illuminating indeed ... However: What about species that have holocentric chromosomes (i.e., no centromeres?). Many insects, for example, are notoriously variable in chromosome numbers, and often with no correlation to their phylogenetic history. And they have holocentric (or holokinetic) chromosomes.
Posted by: 938MeV | April 21, 2008 1:35 PM
There is one part of this explanation that I don't understand.
When there is a single chromosome with two centromeres, the chromosome is split when one part (AB) is pulled in the opposite direction of the other (CDE). However this would produce one cell with the chromosomes (AB) and (abcde) and another with (CDE) and (abcde). I imagine these cells wouldn't do that well, but even worse in the case of gametes we would have 4 cells with (AB), (abcde), (abcde) and (CDE).
So how do we go from a cell splitting a single chromosome into two different cells, to the state with a cell containing (AB) (CDE) and (abcde).
Thanks PZ
Posted by: dave | April 21, 2008 1:36 PM
Very interesting, neutral mutations propagating, then a benefit for reproduction of two chromosome offspring which could lead to speciation. Great stuff, keep on posting science stuff I learn so much from reading your posts.
Posted by: Russell | April 21, 2008 1:39 PM
Good biology lesson! Here's a followup question: How does the cell pair homologous chromosomes during meiosis? Are centromeres unique (tagged, somehow) to the chromosome pair?
Posted by: DrA | April 21, 2008 1:40 PM
The whole idea of chromosome number goes much deeper. Basically prokaryotes and the vast majority of eukaryotes are haploid. If they reproduce sexually, the zygote is the only diploid stage. Only animals and the sporophyte generation of plants are routinely diploid (dikaryon in basidiomycetes). What's the advantage of being diploid? It allows you to be heterozygous for one thing, and meiosis allows for recombination of parental genotypes. So ultimately this leads to your point, more chromosomes allows for more gene combinations, more variation upon which selection can act. With the exception of the rattlesnake ferns, which have some very high chromosome numbers (paleopolyploids?), there must be some optimal range (1 to 4 dozen) of chromosome number to accomplish this efficiently.
Posted by: bobz | April 21, 2008 1:41 PM
What I find fascinating is the implication that divergence of species would occur most readily when an individual with a chromosome split or fusion becomes a member of a small isolated (in-breeding) group. The likelihood of such a mutation gaining any traction in a large population would be quite small. So island populations in particular would be prone to divergence.
Posted by: MikeM | April 21, 2008 1:43 PM
I've often wondered why we don't have just one chromosome, and your explanation even offers an inkling why that would be unlikely.
Thanks for your patience.
And now I'm waiting for the inevitable question: "But have you OBSERVED this?".
I want to see some of your post-Expelled hate-mails, too. Hopefully, from someone who had never heard of you before this weekend. The more basic errors these emails contain, the better.
Posted by: Pantrog | April 21, 2008 1:43 PM
Case Luskin recently returned (in typically obtuse manner) to the subject of the fused ape chromosomes 2A&2B.
Intelligent Design 101: Casey Luskin on Human Chromosomal Fusion
He argues that the similarities are caused by common design, but of course he doesn't mention the degenerate centromere and vestigal telomeres (i.e. evidence of dysteleology), and he also doesn't manage to mention the potential biological importance of looking at the genes surrounding the fusion point (PGML/FOXD/CBWD) for changes that may have led to the origins of modern human abilities.
But he has this silly scenario which he explores at the end of the podcast. To paraphrase - imagine, a population of future humans derived from modern H. sapiens. These future humans ("the double fuser people" or DFP) have inherited a new chromosome fusion which is fixed in the population (i.e. reached 100% frequency, they now have 44 chromosomes - 22 pairs).
Modern H. sapiens are extinct, all their knowledge is unavailable and DFP humans are starting again from scratch. The DFP humans compare themselves with surviving chimps. These future DFP humans would think they had a common ancestor with chimps, but with 2 chromosomes fusions in between.
However, Luskin argues that this inference would be logically invalid, as the second hypothetical fusion event took place in modern H. sapiens, and has:
Is Luskin being intentionally dense? In his scenario either of the fusion events could have taken place at almost any arbitrary generation in the history of the population - between the last common ancestor with the outgroup (chimps in this case) and long enough before the karyotype is tested to fix the variant across the population.
In his own scenario, if 'the double fuser people' humans got hold of a modern human karyotype and thought "perhaps we share a common ancestor with this organism, except for a single chromosome fusion event", they would be completely correct.
Posted by: ColinB | April 21, 2008 1:46 PM
I second the comment at #30 about a book - why not, at the very least, put a collection of your 'science' posts together, similar in vein to Science Blogging Anthology - or at least have your own chapter in the next edition? Are you listening, Coturnix? :-)
Posted by: DarkSyde | April 21, 2008 1:46 PM
That was really, really good.
Posted by: Darby | April 21, 2008 1:52 PM
Great. I already throw more details at the freshman than they want, and you give me a few more to rattle around and spill out.
On the question of big chromosome numbers, here's an info page - don't know how authoritative it is, but I'm betting moreso than Wikipedia:
http://arbl.cvmbs.colostate.edu/hbooks/genetics/medgen/basics/minmax_chromos.html
Posted by: drew | April 21, 2008 1:59 PM
@ #71
A little hard to explain without the use of pictures but here goes.
The chromosome during mitosis will be two pieces of almost identical, tightly coiled, double stranded DNA, held together at the centromere. The spindle fibers attach to one piece of DNA and at the proper time pull the two apart. With two centromeres if both spindles grabbed the same piece of DNA there would be no break. If however they each attach to opposite strands the break will occur.
So in this case we have chromosome ABCDE (with two centromeres) copying for mitosis. So there are two identical pieces of DNA held together at the centromeres. We'll call one ABCDE and the other A'B'C'D'E'. If the spindle attaches on the ABCDE strand at one centromere and the A'B'C'D'E' strand at the other, when separated (and broke) one resulting daughter cell will end up with AB and C'D'E' while the other one ends up with A'B' and CDE resulting in no net imbalance of information.
I hope that I didn't confuse you more.
Posted by: SC | April 21, 2008 2:02 PM
I particularly like the "SNAP!" and "FUSE!" bits. I imagine your students do, too.
Posted by: Drew | April 21, 2008 2:03 PM
PZ gave a great explanation but he could've made it even greater if he drew the replicating chromosomes as X's rather than lines
Posted by: HenryH | April 21, 2008 2:04 PM
Cool stuff PZ! I'd been wondering about this for years. Many thanks.
Posted by: (((Billy))) | April 21, 2008 2:06 PM
Thank you. If I had had science teachers with your interpretive abilities, maybe I would have studied a hard science rather than history (though I love history).
My understanding is that even though chromosomes can snap or fuse, the information encoded upon them remains (relatively) unchanged? Does this mean that the position of the gene on the chromosome does not really matter? Cool.
Posted by: Don Kane | April 21, 2008 2:16 PM
To #59:
"Mama, don't take my Chromosome away."
One of the common causes of Down's is improper segregation of Ch 21 in females.
The idea is that because female meiocytes (look that word up!) are formed in the early months of gestation, they are about 20 years old when there is the first possibility of them being used (should be used?), and as late as 45 or even 50 years old.
Women in their 20s have about a 1/3000 chance of a Down's kid; in their 40s it's more like 1/50. Those old chromosomes git suck....
Interesting to think about how old you really are. In my case, the maternal set of chromosomes for my early divisions, I remember them well, was some time in 1927....
Posted by: NoniMausa | April 21, 2008 2:18 PM
My big grin for the day, thanks PZ.
So I take it this means that organisms which become isolated in contained environments will speciate more quickly than those in large mixing populations? (because the oddballs' offspring are contained together).
I do know that colour and coat and size variations jump up like dandelions as soon as an animal is taken into domestication. Look at hamsters , only kept as pets since the 1930s.
Noni
Posted by: 938MeV | April 21, 2008 2:19 PM
@#81
Thanks for the explanation drew, but I'm still a little confused. It seems to me that you are saying both homologous chromosomes would have to have the double centromere for this to occur, which would then make sense. However, I don't think that's what PZ said. He seems to have your A'B'C'D'E' notated as abcde, and his abcde remains intact and single centromered throughout the process. Is this correct?
Posted by: LARA | April 21, 2008 2:26 PM
Not only are cells really, really stupid, they are rather egotistical as well and don't like sharing their ice cream cones.
Really, I thought your microtome-sharp wit was only reserved for the bible types and spared us flakey folks who occaisionally entertain the possibility that cells might be smarter than just bags of goo. I really wonder if that silly notion fits in the same category with Creationism. Okay maybe it fits in the same big fat "wrong" category, but still.
I enjoyed your very lucid writing anyway, even if it was for me a bit of a bullet with butterfly wings, metaphoricaly speaking.
Posted by: Ted Powell | April 21, 2008 2:27 PM
#5 boomer
I just finished it yesterday--it's good all the way through!http://www.cbc.ca/news/viewpoint/vp_savory/20080311.html is an article on science vs. creationism, featuring Fairbanks.
http://www.cbc.ca/technology/technology-blog/2008/03/your_interview_daniel_fairbank.html is a page for comments on the article, though there don't seem to be any there yet.
http://search.barnesandnoble.com/Relics-of-Eden/Daniel-J-Fairbanks/e/9781591025641 is the Barnes&Noble page for the book.
Chapter 1 of the book explains the fusion of chromosomes 2A and 2B to form human chromosome 2. In includes a full-page DNA sequence showing the fusion site--two partial telomeres joined, with a flip--all the surrounding telomeres, and a bit more for context.
Appendices 1 and 2 are heavy-duty stuff, "The Story of NANOG and Its Pseudogenes" and "The Nine Inversions", the latter being a detailed discussion of the nine places where portions of the human or chimpanzee genome (in chromosomes 1, 4, 5, 9, 12, 15, 16, 17, and 18) are inverted relative to their common ancestors.
I particularly enjoyed Appendix 3, From Darwin to the Human Genome : A Brief History. It's about the people, and what they did.
There's a nice description of "Rosalind Franklin, a physicist with a superb talent for x-ray diffraction."
Posted by: Dan Freiberg | April 21, 2008 2:28 PM
Thank you for the explanation.
I learned in high school and college (1950s and 60s) that I had 48 chromosomes. I find out now that apparently I've lost two of them. Does that happen to everyone when they get old?
Dan Freiberg
Posted by: Dahan | April 21, 2008 2:29 PM
Thanks PZ. It's been a while since my freshman biology class. For us non-scientist loving scientists, it's nice to get a refresher now and then. As I was reading through, I kept thinking "Oh yeah! That's right. I totally forgot about that."
Keep up the good work.
Posted by: miller | April 21, 2008 2:33 PM
I don't always read your science posts, but for whatever reason I read this one. I'm not sure what it is, but you've obviously done something right!
Posted by: Mark | April 21, 2008 2:34 PM
I was under the impression that a driving theory that the numbers could change by the HERV ?
http://www.ncbi.nlm.nih.gov/pubmed/7831772
Todays APOD has a rather nice family photo of phage family
http://antwrp.gsfc.nasa.gov/apod/ap080421.html
I wonder if the secret lies with mitochondrial DNA?
http://sci.odu.edu/biology/directory/greenwood.shtml
anyway, good post
Posted by: Scott de B. | April 21, 2008 2:38 PM
And the subject of a lovely essay by Stephen Jay Gould in Bully for Brontosaurus which, by coincidence, I was reading yesterday.
Posted by: Falyne | April 21, 2008 2:47 PM
*applause*
Posted by: Spaulding | April 21, 2008 2:48 PM
Very nice, accessable descriptions, PZ. The paragraph about ignorance was a fitting coda in light of Luskin and the other recent rant. It's been said before, but ignorance is not usually a failing or an insult. Everyone is ignorant about a huge number of things, but the way one reacts to ignorance is the important part. When you recognize the limits of your knowledge in an area of importance or personal interest, and that ignorance leads to an honest search for more information, then ignorance becomes a motivator of personal and cultural improvement.
The problem comes when ignorance is coupled with arrogance, as "willful ignorance" - when a person insists that their own unfounded opinions are of greater worth than the evidence, which of course will be selectively ignored and fallaciously opposed in order to maintain an unaltered opinion.
Posted by: drew | April 21, 2008 2:53 PM
#88
Not quite.
I think your problem is that you're forgeting the DNA duplicates before all of this starts.
So we're dealing with a diploid organism here so there is 1 pair chromosomes. This pair will have roughly same genes but different alleles (most likely), i.e. similar but not identical. So one we'll call (as PZ does) ABCDE, and the other we'll call abcde. ABCDE mutates into a chromosome with two centromeres. When they ready for mitosis they'll make copies of them selves we'll denote by the prime('). So going into the cycle the cell will have ABCDE with its copy A'B'C'D'E' joined at the two centromeres, and abcde joined with its copy a'b'c'd'e' at its only centromere. So lowercase will look like an X, while uppercase will look like an X with two crosses. Now there are spindles that attach to the centromeres, the other end stretches to the edge of the cells, one pulls right one pulls left separating the two strands to opposite sides of the cell just before the cells split.
When the cell divides the two daughter cells will each get a copy of abcde, that are identical to each other, they'll separate with no problem. The only problem will come when trying to separate the one with two centromeres.
For the purpose of visualization perhaps think in colors, Let's make ABCDE red and A'B'C'D'E' blue. The left side of the cell attaches to the red strand at centromere 1 and the blue strand at centromere 2, and likewise the right strand attaches to blue at c1 and red at c2. At the proper phase the threads will start to pull and it's going to create a lot of mechanical stress on the DNA molecules, and they'll break. So each daughter will get part blue and part red.
So you'll end up with two daughter cells each containing one small chromosome AB, another small chromosome CDE, and a large (original size) chromosome abcde.
I hope I'm helping but I may be confusing you more.
Posted by: Ted Powell | April 21, 2008 2:54 PM
PZ: Great article! Have you decided what you're going to present at the Denver AG?
Posted by: Jim Thomerson | April 21, 2008 2:59 PM
And the smallest chromosome number is one, in males of a species of Australian ant. Nicely done presentation.
Posted by: Scooty Puff, Jr. | April 21, 2008 3:01 PM
Neat! I never knew that. See kids, you can learn things by reading the Internets.
So if I'm understanding you correctly, since changes in chromosomal numbers is a factor that can lead to speciation, speciation itself is a consequence of both accident and divergence from other populations due to adaptation. Am I crazy, or do I actually have that right?
Posted by: Spaulding | April 21, 2008 3:07 PM
Also, I've seen complaints from some creationists that science textbooks, etc. use too many illustrations and not enough photos. Given the power of modern microscope technology, I'd say that's a useful criticism. How about adding in some photos of chromosomes or metaphase to help illustrate what you're talking about? There are many beautiful examples.
Posted by: Mark | April 21, 2008 3:11 PM
PZ, could you add more detail about how the chromosomes line up, and how daughter cells normally end up with a complete set of them rather than one getting two chromosome 1s and the other getting two chromosome 2s? Then, why does the situation in 7chrom.jpg make that not work?
Posted by: Magnifico | April 21, 2008 3:12 PM
Now THIS is what the internet is for. For me anyway. Thanks!
Posted by: Ichthyic | April 21, 2008 3:13 PM
speciation itself is a consequence of both accident and divergence from other populations due to adaptation.
Essentially, that's the gist of it, yes.
Chromosomal duplication is just one avenue of generating new diversity of genetic material (there are many others), which of course ends up producing new phenotypes selection can act on.
Then it becomes even more complicated, as selection doesn't always have a strong effect on the direction traits can take within a given population.
often, just drift can shape which phenotypes we see in a population as well.
It entirely depends on what kinds of selection pressures a given population is under, and it's relative size and level of isolation.
In some populations, selection pressure on some traits is so low that they "drift", and so much of the variation in phenotypes we see is just the result of what we call neutral theory:
http://en.wikipedia.org/wiki/Neutral_theory_of_molecular_evolution
If you have a grasp of the fact that there are many sources of potential variation (like chromosomal duplication, point mutations, horizontal gene transfer, etc.), and that selection can be highly variable as a mechanism for effecting the observed phenotypes within a given population, you have a pretty good grasp of the modern theory of evolution.
Posted by: 938MeV | April 21, 2008 3:14 PM
@#88
You are correct, I did make a notational error, thanks for clearing that up, yet I still think something isn't quite right here. It's my understanding that this type of duplication error (that is doubling of the centromere) would only happen in, well, duplication. So you don't have a cell that just starts out with a chromosome containing two centromeres, you start out with a cell with both homologous chromosomes having one centromere each. Then, when mitosis begins ABCDE (with its single centromere) has some replication error and produces A'B'C'D'E' (with two centromeres). This leads to the problem I described above.
Thanks for taking the time to explain this, I hope we're nearly done. :)
Posted by: Ichthyic | April 21, 2008 3:20 PM
Chromosomal duplication is just one avenue of generating new diversity of genetic material (there are many others), which of course ends up producing new phenotypes selection can act on.
I should modify that as well to include that the "of course" part is a gross oversimplification of how genes interact with the environment itself, whether we are talking during development, or even before. One things we have certainly learned over the last 30 years (and PZ will certainly stress) is the rather large role environment can play on development. We know from mapping the human genome (and other things) that there isn't a one-to-one correspondence between gene and phenotype like I learned when I was young. Hence, the entire evo-devo field.
Epigenetics also rather complicates the whole issue.
http://www.pbs.org/wgbh/nova/sciencenow/3411/02.html
all that said, what you said was essentially correct.
It's just that in actuality, there is a lot going on behind what appears as such a simple statement.
:)
Posted by: Ichthyic | April 21, 2008 3:27 PM
Posted by: Scooty Puff, Jr.
...oh, and one more thing to remember...
"Scooty Puff, Jr. suuuuccckkkksss!"
Fry recommends the Scooty Puff, Sr.: The Doombringer.
Posted by: Craig Helfgott | April 21, 2008 3:32 PM
I seem to recall learning in high school Bio that there are some organisms (plants? insects? I can't remember) with an interesting pattern of chromosomal inheritance -- they alternate generations with N chromosomes with generations with 2N chromosomes.
Could you maybe talk about that?
Posted by: Nic Nicholson | April 21, 2008 3:33 PM
PZ, thanks once again for your extraordinary public service. Your efforts are appreciated by many!
Posted by: Brownian, OM | April 21, 2008 3:39 PM
Yeah, well, the bible ain't got no photos or illustrations 't'all, and them creos ain't questionin' it none.
Posted by: caynazzo | April 21, 2008 3:44 PM
Now I'm no expert, but PZ's post is a produced-for-mass-consumption (though eloquent) explanation of a few fundamentals in cell biology. And this is what creationists manage to befuddle so completely and consistently. It is hard to come away thinking anything other than they criticize what they are stridently unwilling to understand. And why with them it is more effective to ridicule than to reason.
Posted by: MartinSGill | April 21, 2008 3:51 PM
This is a great article. I'm here for the education in the science and the belly laughs as you destroy the creationist loonies.
Keep it up.
Posted by: thalarctos | April 21, 2008 4:04 PM
I think that's true sometimes, Spaulding, but it's also true that photorealistic illustrations can include too much unnecessary detail which distracts from the main pedagogical purpose of the illustration. It depends on what you're trying to communicate, in what context, and to what audience. Schematics, properly used, can reduce an illustration to its essentials, and remove the distraction of unnecessary detail.
I don't know what the creationists you mention are complaining about, but given all the anti-science and anti-education I've read from them, I'd venture to guess they perceive the use of a carefully-crafted schematic drawing emphasizing teaching points as more "biased" than a photo full of noise.
Some of the criticisms of the Expelled cell video are a case in point--there is simply too much going on for non-specialists to watch and extract the salient features the illustrators want to concentrate on in real time. So the XVIVO illustrators pick and choose particular features from photorealistic images to include, and others to leave out.
(The fact that the Expelled video included the same set of features the XVIVO video did, and excluded the same set of features the XVIVO video did--well, at the very least, it looks like plagiarism, although establishng the facts of the matter may have to await a court case, if there is one. But it gets back to the fact that photorealistic images can contain too much information, if the pedagogical point trying to be made risks getting lost in the noise of realistic detail, and that illustrators can select features for emphasis, which may serve the teaching better than the undifferentiated detail can serve it.)
Posted by: mod | April 21, 2008 4:06 PM
More praise over here, that was a wonderful explanation - I vote for more uses of the virtual whiteboard.
I also second the vote for a book. This reminded me of reading "The Extended Phenotype" only in a tone as if PZ was writing it and I realized I would buy a book of that in a second.
Thanks PZ!
Posted by: frog | April 21, 2008 4:06 PM
#109:
You're mostly talking about haploid vs. diploid generations - they're not generations in the general sense, but a reproductive pattern most obvious in plants like ferns, where you have child independent organisms that reproduce asexually alternating with sexual generations.
But really, every multicellular organism does this. Humans have a haploid state as well, the egg and sperm. The haploid has simply been reduced, like in flowering plants. I don't know of any multi-cellular organism without meiosis.
What's stranger is that some organism do gender determination by chromosome number - the common pattern is that males get N, and females get 2N. The males are unfertilized eggs, so they are more closely related to their mothers than the females, leading to all kinds of breeding complexities in social insects.
Posted by: DH | April 21, 2008 4:16 PM
@#106:
Just wondering if this is a meiosis mitosis ambiguity. If we are talking about changes that are getting passed on to offspring, we are most likely talking about meiosis. Quick and dirty meiosis: the DNA gets duplicated (error produces two centromeres in ABCDE), homologous pairs divide, the break occurs, and you should have gotten 2 haploid cells with duplicated DNA, which then go on to divide up that duplicated DNA. But, with the two centromeres, you get 3 "chromosomes" once the break occurs in the first division. Since you can't divide 3 evenly 2 ways, you have a couple possibilities. You can have the AB/CDE and abcde in the daughter cells, or AB/abcde and CDE, or CDE/abcde and AB. Both of the second cases will probably mean the kid won't survive. The first case however, would give rise to a change in chromosome number with no ill effects as you still have all the genes, and in the right amounts. The only thing is that the child would have both AB and CDE pairing with an ABCDE chromosome from the other parent. That COULD get by and survive in a population. Eventually, you might get one of these heterozygous individuals (AB/CDE for one, and the whole ABCDE for the other) mating with another heterozygous individual, in which case some of their children (1/4) would have 2 fragments matching up with 2 fragments, and thus would have increased their chromosome number.
Hope that helped.
Posted by: Paul Flocken | April 21, 2008 4:21 PM
PZ Myers said: This question in my mailbox is also ignorant -- the fellow really doesn't understand the basics of genetics -- but it's self-recognized ignorance that, in a good way, prompts him to ask a sincere question.
And prompts you to write a sincere answer. The most excellent kind of framing indeed! What the 'good-framing-agitators' (frame botherers?) keep missing is that the agitprop of the creationists is never a sincere search for knowledge and there is no frame capable of piercing that. When someone has a legitimate, sincere question, the good scientists like PZ can produce the most composed, the most collected, the most AMICABLE of responses.
The fire-breathing is reserved for the willful and wanton ignorance peddlers.
Posted by: DH | April 21, 2008 4:22 PM
Wow, I really should proof read my posts better. In my 3 examples, the 2nd two cases can lead to some pretty interesting outcomes (increase and decrease in gene dose), but I focused on the first since it is the simplest.
Posted by: LP | April 21, 2008 4:23 PM
Awesome.
Posted by: llanitedave | April 21, 2008 4:27 PM
I'm 113 posts in, and not a single creationist troll has opted to chime in. Why is that? Could it be that when the science lessons begin the creationists hit the road?
Posted by: Randy Mountcastle | April 21, 2008 4:28 PM
PZ,
That was a wonderful explaination of how the number of chromosones may change. Thank you. I am a Christian and wanted you to know we don't all hate you! Thanks again.
-Randy
Posted by: Beowulff | April 21, 2008 4:33 PM
I can't say how nice it is to see a thread where people just exchange information instead of butting heads. Too bad it's bed time here, I'd love to see more, but it'll have to wait for tomorrow. Just wanted to say "Thanks" and "Keep it up" to the commenters as well :)
Posted by: drew | April 21, 2008 4:36 PM
938MeV
Not necessarily. That's one way it could happen, another way could be if the centromere existed in the middle of a transpable element and was reinserted into the chromosome. But I think you're right in that a replication error is probably the most likely event. Also remember that the spliting of the double centromered chromosome doesn't necessarily have to happen on the same mitotic event as the replication error.
There is another error you're making with regard to the DNA replication itself, and I should note that with the way I explained it I could carry partial responsibility. I used ABCDE and A'B'C'D'E' for ease of notation and being able to explain it to you, but you're not going to have original and copy. The original chromosome is divided equally between the daughters, so in my two copies ABCDE and A'B'C'D'E' both contain half new material and half original material.
Also of note, I'm explaining it here as it would pertain to mitotic cell division, this is going to be partly different in the case of meiotic division which gives rise to sex cells where it would almost certainly exert a greater effect on progeny. And in that case The daughter cells of which there are (eventually) 4 would each contain 1 chromosome instead of 1 pair. Biology is a little messy and can be difficult to explain sometimes.
Posted by: Dark Matter | April 21, 2008 4:37 PM
We covered this a little in my intro to human evolution class, but not in any detail at all, so it's nice to have the extra information. It's very clear and succinct. Thank you!
Posted by: Galapagos | April 21, 2008 4:42 PM
whoa, you should do updates like this more often.
Posted by: 938MeV | April 21, 2008 4:46 PM
@#117
I see what you are saying, but the issue I have is right after the "DNA gets duplicated (error produces two centromeres in ABCDE)." Let's let * stand for a centromere
We start out with:
(AB*CDE and ab*cde)
DNA replication with error producing centomere doubling:
((AB*CDE, AB**CDE) and (ab*cde, ab*cde))
Now concentrating on just AB**CDE, the cetromeres attach to the spindle, randomly both centromeres may pull the chromosome in the same direction leaving us with an unbroken AB**CDE in one cell (scenario A):
cell 1 cell 2
(AB*CDE) (AB**CDE)
Or (and here is the crux of the problem), the centromeres may pull in different directions, causing the break in AB**CDE to form AB*/*CDE giving us (scenario B):
cell 1 cell 2
(AB*CDE, AB*) (*CDE)
or
(AB*CDE, *CDE) (AB*)
My point is if, as PZ presents it, it is the action of the centromeres being pulled in the different directions that causes the actual break in the chromosome, then we can't get (scenario C) where we end up with:
cell 1 cell 2
(AB*CDE) (AB* *CDE)
because this is the scenario where both centromeres are pulled in the same direction, and thus the chromosome doesn't snap. Yet, scenario C is where the rest of the explanation that PZ offers goes on from.
Do you see my confusion?
This is probably all just an artifact of the explanation PZ gave was simplified for mass consumption, but I do want to understand and I certainly don't want to be caught with my pants down when some creationist tells me that increase in chromosome # prevents speciation.
Posted by: omar ali | April 21, 2008 4:55 PM
some commentators here express mild embarassment at taking a biologist's word for some aspect of biology. Its great that they want to know more, but I think there is nothing to be ashamed of if someone accepts evolution "on faith" (faith in the scientific community, in this case). All the sciences are now at a point that the details become too complicated for most non-specialists, but that does not prevent us from believing that "superconductivity is a quantum phenomenon on a classical scale" or any other startling and (in its details) extemely complicated physical phenomenon. PZs explanation was great, but I just wanted to point out that evolution is only controversial because some religious nuts find it hard to swallow. Otherwise, it is mainstream science and laymen should feel reasonably comfortable with taking it "on faith", just as they take other scienctific facts "on faith"....its great that so many want to know the details, but there is no special reason why THESE details should be on everyone's fingertips, just as there is no particular reason why the mathematical treatment of the wave function should be on every person's fingertips..
Posted by: sailor | April 21, 2008 5:09 PM
Thanks PZ,
Interesting, the creationists are rather scarce in the comments section of a post like this.
Posted by: Ron Sullivan | April 21, 2008 5:12 PM
Now that's what I call a productive question. It evoked a fascinating, clear explanation, a number of interesting digressions and refinements, links to lots or related information, and a hilarious conceptual tour de force from the beloved and respected Cuttlefish.
Made my day!
Posted by: Duke York | April 21, 2008 5:27 PM
Excellent! Thanks, PZ!
Posted by: DH | April 21, 2008 5:40 PM
@#127:
Ah, now I've figured out where the problem in communication is. The duplicated AB*CDE NORMALLY forms an X shaped pair (the two left arms being ABCDE and the two right being A'B'C'D'E'). The crossing point of the X is the SHARED centromere. If the centromere was doubled, the resultant tetrad would look like two X's stacked on top of each other (TWO crossing points). You would not have one set of arms on the tetrad having one centromere, and the other set with two, with the tetrad only crossing at one point, and a free centromere hanging off on one of the loose arms.
Hope it makes more sense now.
Posted by: Richard Wolford | April 21, 2008 5:44 PM
This post kicks ass. At times like this, I almost wish I went into biology instead of comp sci...almost...
Posted by: Moses | April 21, 2008 5:50 PM
I don't believe this was a creationist. You gave yourself away: no "Comic Sans" font.
:p
Posted by: David Harmon | April 21, 2008 6:11 PM
Pretty nice article! I've thought for a while that in some sense Downs folks (trisomy 21 et misc) were like a "first draft" of a potential subspecies.
Posted by: Neil B. | April 21, 2008 6:12 PM
Another good and related question is, how does DNA evolve "vertically"? IOW, I get about ACTG sequences being changed and selected, but how does DNA evolve to be longer (roughly but not dependably correlated with "advancement") with time as well of course as adapted at the same time?
Posted by: craig | April 21, 2008 6:14 PM
AHA! You said "mechanisms!" And as we all know, you can't have a mechanism without a mechanic!
Sorry. There was too much smart in this thread and I was feeling left out. Had to inject some stupid.
Posted by: 938MeV | April 21, 2008 6:22 PM
@#132
That makes sense, as long as both ABCDE and A'B'C'D'E' _both_ have double centromeres, (for this illustration let's have AB*C*DE): Sorry about the .s instead of spaces, but the posting software has mangled my beautiful ascii art.
A....A'
.B..B'
..**
.C..C'
..**
.D..D'
E....E'
Otherwise, why wouldn't you have the dangling centromere? If we start out with a AB*CDE and have a replication error to make A'B'*C'*D'E' wouldn't it be:
A....A'
.B..B'
..**
.C..C'
.D...*
E.....D
.......E
Don't we need two double centromeres chromosomes to line up, in order to make the double X as above?
And if we have a dangling centromere my objection above stands. But to not have a dangling centromere, we need to have a cell _start_ with a chromosome with double centromeres, before replication. And how would that happen?
Thanks for sticking with this and explaining the a few of the details.
Posted by: Brownian, OM | April 21, 2008 6:24 PM
From PZ's post:
Posted by: Maureen Lycaon | April 21, 2008 6:39 PM
He who knows not, and knows that he knows not, is a student. Teach him.
He who knows not, and knows not that he knows not, is a fool. Shun him.
That, I think, sums up the difference between this questioner and a creationist. My thanks to both the questioner and PZ for one of the best posts I've ever read on Pharyngula; like many others commenting here, I learned a lot from it.
Posted by: RBH | April 21, 2008 6:41 PM
llanite Dave noted
Sure. And it demonstrates that it's not about the science for them. 'Course, we all knew that.Posted by: Monado, FCD | April 21, 2008 7:03 PM
PZ, that was simple enough even for me. Can you label it as one of the "Basics" posts everyone was going to do last year?
Firemancarl [#12], "Kudos to whomever asked this question" is not quite right. "Kudos to her" is right. But when you replace "him" or "her" with a clause, the whole clause is the object of "to" but within the clause, "Wh..." is the subject of "asked" so it's "Who": "Kudos to whoever asked this question."
Then, you just have to remember that "kudos" is a Greek singular meaning "glory" and you're home free.
Posted by: DH | April 21, 2008 7:10 PM
@#138:
Do be honest, I don't know exactly why you can't have a dangling centromere. There are some vague notions floating around in my brain, and I seem to remember being told why it wouldn't happen. But I do not have my good reference material handy (in another country in fact) and couldn't find anything good in a brief perusal of the net. So I will not insert a quite likely wrong answer into this conversation and will hope someone else knows.
Posted by: reuben | April 21, 2008 7:16 PM
This post is the perfect example of how I got hooked on this site years ago. Thanks PZ!
Posted by: Arnosium Upinarum | April 21, 2008 7:17 PM
I'm with Milo. Beautiful!
Thanks again PZ...
This makes me wonder though: here is a perfect example of a relative ignoramus (me) learning new details (and very clearly!!!) from an expert (in this case, PZ).
What I want to know is why - W-H-Y - some folks, who are every bit as ignorant as I am in biology, can't seem to digest this abundantly clear and crisp example of what biologists in fact know? WHY can't they even TASTE, let alone SWALLOW DOWN this material, just to see if it MAKES ANY SENSE?
Never mind. I already know the answer to those rhetorical questions. It's because these details don't reinforce the Big Idea that some god-thang is behind it all, WHATEVER the detailed mechanisms involved.
Isn't it funny? How many times have we been accosted by ID'ers chastising us for having what they characterize as "closed minds"?
But there's something else. WHY should I be so easily willing to defer to an expert in the science in order to update my knowledge? And WHY are the religiously-inclined so unwilling to accept the very same evidence?
The difference must be in the psychological foundation between these...and it must be due to whatever cultural forces cultivate it from early childhood. Mighty powerful stuff. It's been said before, but the systematic RESTRICTION of a child's natural curiosity - whatever the culture - is tantamount to a kind of child abuse. In life-long effect, it's every bit as outrageous as the worst physical abuse imaginable.
Posted by: Monado, FCD | April 21, 2008 7:22 PM
Spaulding [#102],
There's one exception to creationists complaining when drawings are used instead of photos: Dembski's Flagellum.
Posted by: Sastra | April 21, 2008 7:30 PM
I thought this a very clear explanation -- and I'm curious about whether the person who asked the original question also thinks so. Are they satisfied now, or do they still have issues? For all I know, they've already shown up in Comments.
Posted by: drew | April 21, 2008 7:39 PM
938MeV,
Now I think I get where you're coming from, and you're right. It could happen that way. Probably immediately nothing goes wrong...Because only one strand has the second centromere sequence it probably wouldn't form up the joint and it would hang off like your little ascii thing suggests. That's not really a problem. Don't forget that the proteins involved in all this probably wouldn't form it up properly because they depend on the context of having both sides in the pocket...it's all about conformation. In other words, since the coresponding "leg" doesn't have the centromere sequence, the one that does will probably just super coil up like the rest of the DNA with probably a few extra proteins bound to it unstably because they can't form up the proper conformation without their "match"
That means that the problem wouldn't establish itself until the next generation (be it next set of replications in mitosis or next individual in meiosis). Which means that replication would start up with the double centromere sequence being present from the start.
Posted by: molliebatmit | April 21, 2008 8:38 PM
Mark, #103:
When the chromosomes are duplicated, they are linked together by a complex of proteins called the cohesin complex. I like to visualize this as a rubber band binding the two sister chromatids into a single pile.
There are structures called spindle set up at opposite ends of the cell. Each centrosome has a complex called a kinetochore, which attaches to a fiber that's connected to only one spindle pole. When pairs of sister chromatids are attached to opposite spindle poles, the cohesin complex is dissolved (the rubber band is cut), and the sister chromatids are pulled to opposite sides of the cell.
There's a more technical (and probably better) explanation here in Molecular Cell Biology, 4th ed. Figure 13-18 is particularly useful.
Posted by: Vic | April 21, 2008 8:38 PM
Noting how many recent commenters have said how polite and troll-free this post is, as it was driven by an honest question, I wonder - PZ, did the original questioner ever respond to your answer here? What did s/he have to say about it?
Posted by: The Wholly None | April 21, 2008 8:47 PM
Excellent! Takes me back 50 years when I learned my science from reading Isaac Asimov. A clear explanation in a conversational tone plus a simple schematic, and all with humor. PZ, when you retire from teaching university students, could you write a few science texts for teenagers (and those adults who function as adolescents when it comes to science)? You could really do science education a great service and this blog proves that you have the verbal flow for it. What a pleasure that was to read!
Posted by: Ichthyic | April 21, 2008 9:18 PM
hey, some dude (who has probably escaped his dungeon cell, and hasn't figured out that the next step is an IP ban), just to make you happy...
Fuck You!
You're a world-class asshole who is even beyond being called a demented fuckwit.
congratulations.
Posted by: Spaulding | April 21, 2008 9:29 PM
#114 thalarctos , et. al.:
I absolutely agree that a diagram can often be more didactically useful than a photo. However, there are numerous situations where the photos are both beautiful and useful. Illustrating ion channels in a college textbook might be done with illustrations, but talking about extinct species, microorganisms, etc., can be compellingly done with photos of fossils and specimens, rather than drawings. Yeah, obviously the images are already there for people who want to do a Google search, and nobody is demanding photos of The Fossil of Jesus; but if using more photos makes some people slightly less hostile towards science, and gives everyone beautiful textbooks, I don't see a downside.
Except of course, for heavier, more expensive books. But that's not an issue on the internet!
Posted by: Crudely Wrott | April 21, 2008 9:34 PM
And the nitwit some dude had to show up just after a comment mentioning Asimov, who taught me at least as much as any three of my favorite teachers! I was reliving a chapter from "Only a Trillion." I think it was titled "The Abnormality of Being Normal. Now comes an exception to the rule. Dammit, boy!
Dude, your timing is crude
But you'll not spoil my mood!
You're not only rude
But potential squid food!
Now to the forgetting and ignoring. No forgiving this fool . . .
Posted by: Some Dude | April 21, 2008 9:38 PM
Hey, Ichthyic:
FUCK OFF, LOSER
Posted by: Some Dude | April 21, 2008 9:40 PM
Hey, Ichthyic:
FUCK OFF, LOSER
Posted by: Crudely Wrott | April 21, 2008 9:41 PM
It would be remiss of me to not say, "Thank you, thank you very much" to PZ, the masked questioner and (nearly) all of the above commenters. This has been a true delight; enlightening, entertaining and educational. Who could want for more?
Posted by: Laser Potato | April 21, 2008 9:43 PM
Well...uh...erm...HERRING AND GRUEL AND PORRIDGE AND MILK!
Posted by: Ichthyic | April 21, 2008 9:45 PM
Well...uh...erm...HERRING AND GRUEL AND PORRIDGE AND MILK!
...and lions and tigers and bears?
Posted by: bek | April 21, 2008 9:51 PM
PZ, can you get in your way-back machine and travel to 1998 to teach my genetics class? Because then it might actually have made sense.
*Waits patiently for brain to flood with tasty info from the past*
Posted by: genesgalore | April 21, 2008 10:47 PM
i doubt very seriuosly that genes control the number of chromosomes, they may precipitate a change in chromosome number but that would be causal.
Posted by: wazza | April 21, 2008 10:55 PM
One cool application of this stuff: Making beer
See, hops that are diploid produce enormous numbers of seeds, which are exceptionally bitter, and making beer from these plants produces bitter beer. But for lager, you need a smoother taste. Unfortunately, it's hard to get the seeds out.
Luckily, science has the answer! By treating diploid plants with chemicals, you can produce tetraploid plants, which behave in exactly the same way as diploid plants. Bummer. But if you breed them with diploid plants... you get triploid plants, and they produce hardly any seeds at all!
Yay for science/beer/beery science/sciency beer!
Posted by: Benjamin | April 21, 2008 10:58 PM
Hi, I thought I ought to comment as I was the one who asked the original question.
Yes, this post answers my query and I enjoyed reading it very much. Thank you PZ Myers.
My ignorance stems from the fact that I am a (very young) philosopher, and pretty much trust the sciences to get it right without getting involved much. I write almost exclusively on natural selection, so perhaps my ignorance of genetics is a bit shameful. I see that a few people have recommended the book "Relics of Eden" which I intend to pick up now.
Thanks again.
Posted by: Ichthyic | April 21, 2008 11:00 PM
Science Beer...
Brilliant!
Posted by: Crudely Wrott | April 21, 2008 11:13 PM
Ah, Benjamin! See what you have done! Single handedly* you have sent a soft breeze of accord to gently smooth the normally raised hackles that are a familiar feature of this blog! You have caused a hush to fall upon the loud voices and brought back, if only fleetingly, a sense of wonder that unites us in our joy of learning. And all it took was an honest question and humble implication that you would really, really like to have an honest answer. Wow, Ben. Way cool. Go well and return often.
*Ok, PZ helped some.
(Now back to our regularly scheduled free for all.)
E Pluribus Unum
Posted by: Richard Simons | April 21, 2008 11:44 PM
Polyploidy was mentioned in a comment by PZ. This happens when cell division is normal except the cell does not physically divide in two, resulting in a cell with twice the normal number of chromosomes. This is quite frequent in plants but much less so in animals. Lurker mentioned bananas. These are interesting in that in a normal diploid (having a pair of each chromosome) the chromosomes doubled to make a tetraploid. This then crossed with the original to give plants with three sets of chromosomes, the cultivated bananas. At meiosis (the cell division that gives rise to the egg cells and pollen) when the number of chromosomes is halved, the three sets causes great confusion resulting in very few viable egg cells and pollen grains. This is part of the reason why you never find a seed in a banana. It also causes major headaches for people trying to breed disease resistence into bananas.
Posted by: alison | April 22, 2008 12:37 AM
Truly a wonderful post & the comments thread is the icing on the cake.
@ 116: no multicellular organisms without meiosis - what about things like rotifers with their amictic eggs? I remember seeing a headline in our local paper a year or few ago, for an article on rotifers: No sex for millions of years! (It was unfortunately juxtaposed with a photo of the researcher profiled in the story...)
Posted by: kj | April 22, 2008 1:53 AM
That was the best, most lucid
geneticsscience post I've ever seen. Bravo!Posted by: Fedor | April 22, 2008 2:25 AM
Thanks! Although having studied biology myself, molecular genetics is not my speciality (fossils are), so I am not always certain about all the issues. At least now I won't be embarassed by a creationist stumping me with this! :-)
Posted by: pcarini | April 22, 2008 3:02 AM
Here's a thought:
PZ and Cuttlefish team up for a book. Biology made accessible for us lay-folk, interspersed with Cuttlefish's poetry.
You're welcome.
Posted by: embertine | April 22, 2008 4:24 AM
Brilliant, PZ! Very very clear, even to a non-scientist like myself. Also, I feel even more smug about the fact that I Googled Robertonian fusions only yesterday. Bwah.
Posted by: Dave Wisker | April 22, 2008 5:11 AM
Re: chromsomes with two centroemeres being pulled apart.
In most cases, one of the two centromeres is inactivated--or so it seems. Recent work seems to suggest that in reality, centromeres are not equally efficient at assembling the kinetochore, which is that part of the centromere where the spindle attaches. In essence, one centromere gets the job done before the other can interfere.
Posted by: Some Dude | April 22, 2008 5:26 AM
...the sock puppet love fest continues...
Posted by: Mrs Tilton | April 22, 2008 6:10 AM
PZ,
brilliant stuff, thanks! Have you considered taking up teaching? I think you might be good at it.
This question in my mailbox is also ignorant -- the fellow really doesn't understand the basics of genetics -- but it's self-recognized ignorance that, in a good way, prompts him to ask a sincere question.
Slate magazine's "Explainer" column routinely thanks not only the experts who answer questions, but the questioners as well. An excellent practice, to my mind, so: thanks, dude, for giving PZ a chance to increase not only your knowledge but mine as well.
Finally, Cuttlefish @25: I've always loved your stuff, but this one has me gasping like a landed rockcod, gobsmacked by sheer technical brilliance.
Posted by: wazza | April 22, 2008 7:01 AM
Some Dude, we don't need updates on your love life
however, for anyone who wants to know about mine, I had a date tonight, and it went extremely well.
Posted by: Selcaby | April 22, 2008 8:18 AM
Thanks both to PZ and to the person who asked the original question. This was something I wanted to know too but wouldn't have dared ask.
Posted by: Flywheel | April 22, 2008 10:13 AM
Very enlightening. It reminded me of Przewalski's horses, which have a different number of chromosmes than domesticated horses. http://nationalzoo.si.edu/animals/asiatrail/fact-phorse.cfm
Posted by: Mark | April 22, 2008 10:28 AM
Re 103, 149,
That makes sense for mitosis; after DNA replication, the two sides just remain associated. I was asking about how homologous chromosomes are associated with each other in meiosis. The only thing I can think of is that all the chromosomes are opened up, so individual nucleotides on one chromosome can stick to complementary nucleotides on another. After that, I could see the process you described working, but still want to know what prevents both chromosomes from attaching to fibers connected to the same spindle.
Posted by: Pat Silver | April 22, 2008 11:19 AM
Thank you,PZ. I always enjoy your science posts, you are truly an excellent teacher.
Posted by: Spaulding | April 22, 2008 11:19 AM
Benjamin, everyone's ignorant about lots of things. There's NOTHING shameful about honestly seeking more information! Good question, educational response. Everyone wins.
Posted by: David Marjanović, OM | April 22, 2008 1:37 PM
25: :-o
:-o
:-o
:-o
:-o
[someone please close my jaws, I'm drying out]
73:
No, the crossing-over is what connects the pairs, and crossing-over can only happen between very similar chromosomes, i.e., those of the same pair. Crossing-over involves DNA strands partly separating and joining up with those of the other chromosome, see comment 178.
85:
Precisely.
(Unless there happens to be an enhancer or silencer close by.)
91:
No, you simply forgot to unlearn everything you were taught that long ago. :-) At that time, it hadn't been noticed yet that the X and Y chromosomes are a pair. So it was thought that everyone had two X and two Y chromosomes, and that the missing ones had simply been overlooked so far (which was plausible at that time). Also, something tells me nobody had yet looked at what karyotype women have. :-)
101:
Behind "and", add "/or".
136:
By gene duplications, and by the proliferation of junk. Which is why it's not even roughly correlated to anything interesting except cell size.
161:
You don't need to doubt. It's already known that chromosome number is not controlled at all except by how well meiosis and fertilization work.
167:
Yes, the bdelloid rotifers don't do meiosis. They get away with it by being tetraploid (which lets them repair their DNA easily) and by somehow having got rid of transposable elements.
Posted by: John Phillips, FCD | April 22, 2008 3:54 PM
To add to the love fest, deservedly so by the way, PZ, excellent article.
And Cuttlefish, WOW, just WOW, I am humbled. How do you do it?
Posted by: Tom Marking | April 22, 2008 4:39 PM
"Here's something fairly common. An error in copying the DNA can lead to the loss of a piece of DNA. This happens with a low frequency, but it does happen -- if we sequenced your DNA, we might well find a few bits missing here and there. We can get situations like this, where a whole gene gets lost.
Don't panic! Remember that we have two copies of every chromosome, so while this one is missing the "D" gene, there's that other chromosome floating around with a "d" gene. This is not necessarily bad for the individual, it just means he doesn't have a spare any more."
http://en.wikipedia.org/wiki/Cri_du_Chat
Just the loss of a small portion of band 15 of chromosome of the short arm of chromosome 5 can have devastating effects so it really depends on what genetic material is missing.
"Cri du chat syndrome is due to a partial deletion of the short arm of chromosome number 5. Approximately 80% of cases results from a sporadic de novo deletion, while about 10-15% are due to unequal segregation of a parental balanced translocation where the 5p monosomy is often accompanied by a trisomic portion of the genome. The phenotypes in these individuals may be more severe than in those with isolated monosomy of 5p because of this additional trisomic portion of the genome. Most cases involve terminal deletions with 30-60% loss of 5p material. Fewer than 10% of cases have other rare cytogenetic aberrations (eg, interstitial deletions, mosaicisms, rings and de novo translocations). The deleted chromosome 5 is paternal in origin in about 80% of the cases.
Loss of a small region in band 5p15.2 (cri du chat critical region) correlates with all the clinical features of the syndrome with the exception of the catlike cry, which maps to band 5p15.3 (catlike critical region). The results suggest that 2 noncontiguous critical regions contain genes involved in this condition's etiology. Two genes, Semaphorine F (SEMA5A) and [delta catenin] (CTNND2), which have been mapped to the critical regions are potentially involved in cerebral development and its deletion may be associated in CdCS patients. Also the deletion of the telomerase reverse transcriptase (hTERT) gene localized in 5p15.33 should contribute to the phenotypic changes in CdCS.
Posted by: Tom Marking | April 22, 2008 4:54 PM
"and chromosome numbers can change dramatically with no obvious effect on the phenotype of the organism."
I think that also depends on exactly what genetic information is being reorganized. For example, Down syndrome (trisomy 21)
http://en.wikipedia.org/wiki/Down_syndrome
involves the duplication of the entire 21st chromosome (so there are 3 copies of chromosome 21 instead of 2) certainly has severe phenotypic effects. The same is true for the following genetic diseases which are all trisomies (addition of a 3rd chromosome):
Edwards syndrome (trisomy 18)
http://en.wikipedia.org/wiki/Edwards_syndrome
Patau syndrome (trisomy 13)
http://en.wikipedia.org/wiki/Patau_syndrome
On the other hand, some trisomies involving the sexual chromosomes (X and Y) can be relatively benign:
XXX syndrome
http://en.wikipedia.org/wiki/XXX_syndrome
Klinefelter's syndrome (XXY)
http://en.wikipedia.org/wiki/Klinefelter_syndrome
XYY syndrome
http://en.wikipedia.org/wiki/XYY_syndrome
So the statement that chromosome numbers can change without any obvious effects is too sweeping. There are many cases where even the addition of a single chromosome has devastating effects.
Posted by: Longtime Lurker | April 22, 2008 4:55 PM
Best post EVER, even though PZ obviously has a diploid-centric view of the universe... Now, plants, plants are just kinky, chromosomally speaking.
Cuttlefish, all other poets must bow down before you in awe. Truly, you performed a feat that will be studied by future generations of comp-lit types.
Posted by: DH | April 23, 2008 2:32 AM
#184:
The relatively benign nature of trisomies in sex chromosomes (or even a monosomy: XO) is due the tiny size of the Y chromosome and the inactivation of all but one X chromosomes (http://en.wikipedia.org/wiki/Barr_body). Notice that there is no clinical conditions corresponding to trisomy 1 for instance, that kid wouldn't even make it to being born.
Posted by: (((Billy))) | April 23, 2008 2:17 PM
My understanding is that even though chromosomes can snap or fuse, the information encoded upon them remains [...] unchanged? Does this mean that the position of the gene on the chromosome does not really matter?
Precisely.
(Unless there happens to be an enhancer or silencer close by.)
Okay. I thought I understand. What the hell is an enhancer or a silencer and how could they affect the effectiveness of the gene as it relates to chromosomal position? Does this mean that the proximity of a gene to another set of instructions can either turn the gene off or, conversely, turn the gene on? And, following the same idea, if a snap pulls a gene away from a silencer, that gene can become active again? Do I have that right? (Keep in mind, I'm a liberal arts major (and a practicing historian)).
Posted by: James McGrath | April 25, 2008 1:29 PM
Thanks for this helpfully clear explanation. I've long wondered about this, and whether chromosomal fusion would involve an "evolutionary leap" in terms of the resulting organism's characteristics. Thank you for taking the time to explain this subject in a way that those who are not biologists/geneticists can understand!
Posted by: ck1 | April 25, 2008 9:59 PM
What a lovely explanation. Clear as a bell.
thank you.
Posted by: Kee Chung | April 26, 2008 1:22 AM
Thanks for the explanation. However, what selective advantages could fusion of chromosomes provide since humans have a fused chromosome 2? Or does this boil down to chance events?
(Disclaimer: I'm not a creationist, but just wanted to ask this in case my creationist friends pressure me for an explanation)
Posted by: Nigel D | April 26, 2008 2:37 PM
Thanks very much, PZ. I would have had to do much background research to answer that question. Your explanation was lucid, thorough and very readable.
Posted by: Dave Fafarman | April 26, 2008 10:54 PM
Thanks, PZ, for the crystal-clear and fascinating explanation (I'd long wondered about this). I should come here more often.
Posted by: Frank B | April 26, 2008 11:11 PM
Thanks PZ for a great lesson in genetics. A lot of other people are willing to share their knowledge too. Keep it up.
Posted by: Stacey | April 30, 2008 2:24 PM
Relatedly, a pretty good and very relevant review just came out about this in the Journal of Cellular Biochemistry: Centromeres in cell division, evolution, nuclear organization and disease
Posted by: Karl Lembke | May 1, 2008 12:31 AM
So when are you going to add a category called "Basics"?
Posted by: John Farrell | May 1, 2008 12:49 PM
A fantastic post, which I need to print out and save. If I understand it correctly (at first pass), then, re: the Chromosome 2 discovery in Hiller et al, is that what must have happened is one of the original chromosomes of our common ancestor with chimps lost a telomere during replication and that prompted its binding/fusing with its neighbor, correct?
Posted by: Calilasseia | June 5, 2008 8:01 PM
I've just found this (late as usual to the best parties - sigh) ...
My first thought after digesting this was as follows ... if there are any animators among the regular posters here on PZ's blog, turn this article into a quality animation pro bono and mail him the result. Because it deserves it. Don't forget to embed appropriate copyright notices in case Dembski tries to rip it off though!
If I had decent artistic skills, I'd be tempted to do this myself. Trouble is, any effort I came up with would look as if Salvador Dali cut loose with Adobe ImageReady whilst smoking weapons-grade hallucinogens ...
Posted by: frank | August 11, 2008 10:50 PM
A fantastic post indeed
Posted by: nana | August 15, 2008 3:57 PM
How can chromosome numbers change?
great explanation
Posted by: franco | August 20, 2008 9:56 AM
chromosome numbers can change
Posted by: PH Tran | April 3, 2009 5:21 AM
I wasn't the one asking the question, but I am one that has serious doubts. So yes, this is how chromosome numbers could increase.
I still believe we have no evidence of this process actually happening.
Suppose this theory were in fact true and the main mechanism for increasing chromosome numbers. With thousands and thousands of mammal species living today, we'd then expect to find "same" species among mammals with different number of chromosomes.
Well, we found some. Problem is, if these are a result of chromosome change, it is known to be fusion, not fission or polyploidy.
So honestly, if you ask me, this is a theory that is nice in theory only, but without proof of it to have happened with evolution of mammal species.
Call me ignorant or stupid. At least I don't believe everyhing I been told without real physical proof!
Posted by: clinteas | April 3, 2009 5:26 AM
LOL
Ok,I call you ignorant and stupid !
Posted by: Kel | April 3, 2009 5:47 AM
Well PH Tran, what do you propose instead that can account for the different numbers of chromosomes that we observe in different species? Keep in mind that evolution has been demonstrated beyond all reasonable doubt, so keep common ancestry in mind in any answer you give.
Posted by: clinteas | April 3, 2009 5:59 AM
Regardless of the drive-by trolls commenting on year-old threads(Potato,Tran??),I like to go back in time and read through them nevertheless,brings back memories LOL.
Posted by: dan | September 5, 2009 7:23 PM
wow! thanks for this explanation ... i've womdered how this could happen for years!
Posted by: NotTires | September 10, 2009 7:30 PM
To further help answer your original questioner's question:
"there would have to be some benefit to the replication probability of the organisms which carry the chromosomes."
First, No, and Second, Yes!
1) There wouldn't have to be a benefit as long as there was no harm. If it is harmless enough, then chance will make some changes permanent and widespread even without a direct benefit (genetic drift). However, the cost of chromosomal errors is big enough that this probably isn't the answer.
2) Yes! There can be a benefit to having more chromosomes. While this can be taken to an extreme where it probably no longer helps (I once studied a plant with 110 chromosomes!), for reasonable numbers, there ARE two advantages.
All genes on the same chromosome are linked in some degree -- they must be inherited together most of the time. Imagine if a really good mutation or a really bad one appears. With few chromosomes, that bad mutation will drag down all the good genes it is linked to on the chromosome (or the reverse). The more chromosomes, the better chance that each allele (gene variant) gets to 'speak for itself' instead of being linked to a really good or really bad mutation. Extra chromosomes make selection more efficient because it can select against bad mutations and for good ones without as many being linked to them 'caught in the crossfire'.
The other advantage is that more chromosomes provide more genetic variability amongst the offspring without any mutation or other stuff. The more chromosomes, the more combinations of alleles are possible in the offspring, since fewer are linked together. (in the example above, it is hard to get De or dE.) Having more chromosomes means the same genetic diversity from a parent can be arranged in more combinations in its gametes (sperm & eggs) and more variation means a better chance of having an offspring match the selective conditions it is about to face. With only one pair, ABCDE and abcde are the only frequent options because those genes are physically linked on the chromosome and cannot be mixed and matched in offspring easily. With humans we can get 2^23rd different possible groupings of Mom's copy vs. dad's copy of my genes into my offspring from my 23 chromosomes.
Now, this can be taken to absurdity, since I'm pretty sure there would be a penalty past a certain number of chromosomes, and I've been casual with the terminology, but here is one way in which it is _better_ to have a few more chromosomes that might explain part of why so many species have lots.
Posted by: drj11.wordpress.com
|
July 15, 2010 5:01 AM
Have you read Kinetochore reproduction in animal evolution: Cell biological explanation of karyotypic fission theory? It suggests that (for mammals and insects) a mitotic checkpoint that is sensitive to spindle attachment tension will generally ensure that a daughter cell will get a balanced set of chromosomes. There may be no reason to suspect that gametes will have anything but a full set of genes, even when chromosomes have been split.
Excellent article, by the way.
Posted by: crazdave
|
August 17, 2011 1:36 PM
I find it hard to believe Francis Collins is ignorant in the aspect of genetics, yet look at the conclusion he has come to. Makes one think... I do believe in evolution on some scale, it just makes sense and we have proof, yet there seems to be a boundary that species cannot jump past and I do not think that random mutations here and there in history can drastically change much anything. Perhaps for a little bit or in a small isolated part of the world but nothing on the scale of an entire planet. Also, many many scientists have agreed that life is so complex that pure chance cannot fully explain it. The human eye is a vastly complex organ and yet we cannot even replicate it with the technology we have today, let alone the human brain. Ignorance is defined as a lack of information, which basically defines science. Such as how quantum mechanics and the theory of relativity contradict each other, yet both are true in their own way, which leads one to believe there is a flaw with one or both. In biology we surely do not understand how everything works exactly, but we keep looking and learning. Many people in history that are wrong have called others ignorant and the tables ended up being turned on them. This was a good read though you explained this very well, I'm 15 by the way.
Posted by: Heather Clemenceau
|
September 11, 2011 7:08 PM
I haven't read all the comments here but I've always wondered - why ACTG - Why are there 4 base pairs?
Posted by: lundahl.hans
|
November 3, 2011 11:29 AM
I hate to see that your posts on desecrating hosts are still there.
Before leaving your blog, let me just notify you that I have quoted this post (did I already state that in comments earlier?) and that my answer is to be found on this blog post on my Creation(ism) versus Evolution(ism) blog.
The short of it is, if a centromere is reduplicated in one generation, it cannot split into two viable chromosomes with one centromere each, since each such half would be lacking a telomere. The sad fact about your diagram is that you left out telomeres in the drawing. They may be inconsequential when it comes to cross-over studies and such, but not to this question.
Posted by: Amphiox, OM
|
November 3, 2011 2:26 PM
The objection in @210 is like trying to argue that because the lift-to-weight ratio of bumblebee wings is too small, it must be impossible for bumblebees to fly.
But of course bumblebees do fly.
The centromere splitting mechanism PZ describes here is not theory, it is a repeatedly observed fact.
And it is also a repeatedly observed fact that offspring with such split chromosomes ARE VIABLE, and the telomere problem is, one way or another, solved in a single generation.
There are human beings walking around today with abnormal chromosome numbers produced by centromere duplication and splitting, fully healthy, with healthy parents who do not have the chromosome abnormality, and with healthy children inheriting the chromosome abnormality. This of course means that we know exactly in which generation the chromosome split occurred.
(Some of these people do have fertility problems, and are often identified when they present to fertility clinics for treatment.)
The same processes, of course, have also been repeatedly observed in experimental lab organisms.
If I had to hypothesize as to a mechanism, I would guess that the telomerase enzyme, which is active embryologically, is capable of adding a new telomere to the freshly broken end. Of perhaps the split chromosomes get telomeres via recombination.
It doesn't have to happen every time, and it could easily be that the majority of the time, cells that split chromosomes fail to solve the telomere problem and apoptose (and we'll never observe them at all).
Also, the lack of telomeres may not even be a problem for several generations. Research in cancer indicates that the Hayflick limit (which telomeres protect against) actually may not be a problem at all for normal cells undergoing number numbers of duplication rounds in normal organisms, and it only becomes a problem for cells that are forced to divide an abnormally high number of times, like cancer cells, or cells maintained artificially in culture. If the region immediately at the frayed chromosome end is a non-coding region, then it could be shortened over quite a large number of divisions, spanning several generations, before critical genetic information is lost (since it is only a few nucleotides that get lost per division). This of course gives ample time for a telomere to be obtained, perhaps by recombination, at a different time.
But, just like the flying bumblebee, we actually observe such chromosome splitting happening and surviving and reproducing in real time, so in the end it doesn't matter precisely what mechanism is responsible for solving the telomere issue in the longterm, we know that it is easily solved and not a problem at all for the question of chromosome splitting.
Posted by: lundahl.hans
|
November 4, 2011 12:09 PM
The centromere splitting is observed fact, says #211, but where is it observed, please?
There are human beings walking around today with abnormal chromosome numbers produced by centromere duplication and splitting, fully healthy, with healthy parents who do not have the chromosome abnormality, and with healthy children inheriting the chromosome abnormality. This of course means that we know exactly in which generation the chromosome split occurred.
Source, please?
Posted by: Nerd of Redhead, OM
|
November 4, 2011 4:10 PM
What's the matter creobot, don't know how to find scientific evidence? After all, the only thing that refutes science is more science. You need to present said science, not your religious presuppositions, which refute nothing.Check some of the references in the thread above, they may contain the information you think refutes something...
Posted by: Ichthyic
|
November 4, 2011 5:31 PM
Source, please?
read any of these papers; they will either detail the mechanisms involved themselves, or link to other papers that do in their bibliographies.
http://scholar.google.co.nz/scholar?q=polyploidy+in+humans&hl=en&as_sdt=0&as_vis=1&oi=scholart
Posted by: Amphiox, OM
|
November 4, 2011 6:20 PM
The key thing about all the examples given (Tom Marking @184) is that there is an abnormal gene copy number. The abnormal chromosome number is actually incidental to this. The problems are caused by the altered number of genes, because copy number is one of the things that regulate gene expression, for some genes. (There is also the effects of differential imprinting in cases of chromosome deletions).
But in the scenarios described by PZ, when one large chromosome breaks into two, the chromosome number goes up by one, by the number of gene copies does not change. (Or, alternately, if two chromosomes fuse end to end, the chromosome number drops by one).
And that is usually a neutral change.
Posted by: Amphiox, OM
|
November 4, 2011 6:45 PM
Oh look, the creo troll is engaging in cargo cult citation requesting!
Here's one:
http://www.genetics.org/content/159/3/1179.short
Posted by: Amphiox, OM
|
November 4, 2011 6:47 PM
Here's two more:
http://humrep.oxfordjournals.org/content/21/6/1484.full
http://www.ncbi.nlm.nih.gov/pubmed/7116675?dopt=Abstract
Posted by: Amphiox, OM
|
November 4, 2011 6:49 PM
Here's two more:
http://www.nature.com/jhg/journal/v36/n1/abs/jhg19918a.html
http://www.ncbi.nlm.nih.gov/pubmed/1183067?dopt=Abstract
Posted by: Amphiox, OM
|
November 4, 2011 6:53 PM
Here's another:
http://humrep.oxfordjournals.org/content/19/6/1345.full
This one is ludicrously common, 1 in 1000 in normal humans (with normal fertility), although it is even more common in males with fertility problems, so it does appear to sometimes reduce fertility.
Posted by: Amphiox, OM
|
November 4, 2011 6:56 PM
Here's yet another:
http://pages.cs.brandeis.edu/~jlittman/MedCases/Med%20Cases/translocation.htm
A pregnant mother with a fetus diagnosed with a chromosome abnormality, on further investigation found to have herself a different but related chromosome abnormality that was the precursor of the baby's.
And note at the end, the baby was born normal.
Posted by: Amphiox, OM
|
November 4, 2011 7:04 PM
And here's yet another, not in a human, but in a mule. The supposed stereotypical example of infertility due to chromosomal mismatch.
http://news.bbc.co.uk/2/hi/science/nature/2290491.stm
The most amazing example I ever heard of was in a popular TV science program, with a mother with no less than SIX extra chromosomes due to various chromosome breakages and fusions, with a healthy daughter.
Sadly, I can`t find any written citation to this, so we`ll have to leave it as apocryphal for the time being.
Posted by: Amphiox, OM
|
November 4, 2011 7:06 PM
(I tried to put all those links in the same post, but I got a `placed in moderation` error. Too many links triggered a spam filter of some sort, I guess. And PZ did say that due to his sheer volume of spam, moderation is where posts go to die, so I reposted them separately).
Posted by: lundahl.hans
|
November 5, 2011 6:13 AM
@ #214 - irrelevant to my question, since it was about or rather against scenario of centromere split. By the way, polyploid embryos in mammals are aborted by immune system of mother.
@ #216 - I quote:
Whenever paired chromosomes have different numbers of centromeres, the inherent asymmetry of female meiosis and the polarity of the meiotic spindle dictate that the partner with the greater number of centromeres will attach preferentially to the pole that is most efficient at capturing centromeres. This mechanism explains how chromosomal variants become fixed in populations, as well as why closely related species often appear to have evolved by directional adjustment of the karyotype toward or away from a particular chromosome form.
Too dense for me, I am not a specialist, but I did catch words like "This mechanism explains how chromosomal variants become fixed in populations" and wonder if the statement in #211 is true, how come there is no fixed chromosome variant with karyotype 2n=48 with those split chromosomes in split pairs?
@#217 first link: did not find chromosomal split, was I brushing through it too quickly or was it not there?
Posted by: lundahl.hans
|
November 5, 2011 6:27 AM
@#217 second link: no mention of chromosomal centromere split in that abstract
@#218 first link: dito
@#218 second link: dito
@#219: was about Robertsonian translocation, not about Robertsonian split (have I been misled by splits being called translocations? I find that somewhat improbable!)
@#220: was about translocation - thus not split! - as already apparent from URL
@#221: involves no split, only chromosomal mismatch
So you claimed above that chromosomal splits are walking around, I challenged you to give a source, you give a series of links none of which is a source for your claim, like trying to impress by the mere number of your links.
What is the inverse of creo troll? Infid troll? If there is such a word, you are close to earning the title by such a procedure!
Posted by: lundahl.hans
|
November 5, 2011 6:39 AM
I checked: this diagram shows that Robertsonian translocation does not increase chromsome numbers.
Maybe infid troll is a bit harsh, you were just not on par with getting the precise question.
Unfortunately, since you did make a precise statement and I asked you to back up precisely that one.
As to the TV program, in case you did not misremember, I would like to know if perhaps reporters might have misunderstood things like splits, which you cannot answer of course. But I would also like to know if it was recently, or before 1999 or between 1999 and early 2000-s or after 2003.
Because in 1999 a talkorigins article had declared this precise question a mystery (yes, I do link to it on my blog post, unless I happen to misremember) and the several parts of my blog post were first written - at least one of them - before 2003.
Meaning that after 2003 or even more so after 2005, a misunderstanding of mechanisms in favour of chromosome splits occurring, would have been in the interest of evolutionists.
There, does that earn me a tin foil hat for conspiracy theorizing?
Posted by: lundahl.hans
|
November 5, 2011 6:55 AM
Oh, by the way, I was linking to wrong diagram in #225, it showed a balanced translocation.
A Robertsonian one is one that involves sth close to fusion, hence making chromosomes fewer:
People with Robertsonian translocations have only 45 chromosomes in each of their cells, yet all essential genetic material is present, and they appear normal. Their children, however, may either be normal and carry the fusion chromosome (depending which chromosome is represented in the gamete), or they may inherit a missing or extra long arm of an acrocentric chromosome. Genetic counseling and genetic testing is offered to families that may be carriers of chromosomal translocations.
The problem I mainly posed and PZ tried to answer above was getting chromosomes more numerous, especially chromosome pairs more numerous.
Have I made a point?
I may add, if you try to engineer - any of you, not just Amphiox OM or P Z Myers - beings with an extra chromosome pair, that does not count. Classic Evolution theory in the supposed past millions of years of existing mammals is not about genetic engineering.
Posted by: Nerd of Redhead, OM
|
November 5, 2011 7:14 AM
NOPE. You cited nothing.Posted by: Amphiox, OM
|
November 5, 2011 9:40 AM
Most mammals.
There is a tetraploid rat.
And plenty of polyploid plants.
Posted by: Amphiox, OM
|
November 5, 2011 9:45 AM
OF COURSE IT COUNTS. If engineered to simulate natural processes, it counts.
The say it does not count is to say that the entire scientific methodology is invalid.
Only the intellectually dishonest would claim that it would not count.
Posted by: Amphiox, OM
|
November 5, 2011 9:53 AM
Robertsonian translocation is a chromosome fusion, which reduces chromosome number.
Since you make a big deal about this, I presume you accept the fact that such fusions do occur, then, and are viable?
And since you accept this, then presumably you also must accept the basic premise of the OP, that chromosome numbers can change through evolutionary mechanisms?
Because I hope you understand that if fusions occur, then splits MUST also occur.
If not, chromosome numbers would not be stable, and after only a short number of generations, all species would all have only ONE big chromosome.
Posted by: Amphiox, OM
|
November 5, 2011 10:35 AM
From #216;
Fission = chromosome SPLIT.
From #217;
Fragile sites are places where chromosomes can split.
Supernumerary markers are indicators of increased chromosome numbers.
And here's an example of a straight up centromere duplication.
http://onlinelibrary.wiley.com/doi/10.1002/pd.1970110713/abstract.
Here's another example of a chromosome fission.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1690759/
Only a very bad one.
Posted by: Amphiox, OM
|
November 5, 2011 10:52 AM
Oh, and another thing, the mechanism of a Robertsonian translocation starts with a chromosome FISSION event (without a centromere duplication) near the centromere, followed by fusion events that produce one translocated chromosome with a fused centromere and one without any centromere, that gets lost in later cell divisions.
In other words, if the fission occurs without a centromere duplication, you end up with a Robertsonian translocation. But if a centromere duplication occurs first, then the same mechanism that produces Robertsonian translocations will produce the scenario PZ describes.
It's all the same and closely related mechanisms. If one exists, the other must also.
Indeed, the mere presence of acrocentric chromosomes is strong evidence that the mechanism of chromosome splitting described by PZ exists and occurs frequently.
Posted by: Amphiox, OM
|
November 5, 2011 10:57 AM
And here's a case of a healthy adult woman with a split chromosome 11.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2693553/
If the telomere problem described by our creobot was actually real, this woman should have died as an embryo.
Posted by: Amphiox, OM
|
November 5, 2011 11:02 AM
And here's an article discussing telomerase adding new telomeres to freshly broken chromosome ends.
http://www.ncbi.nlm.nih.gov/pubmed/8967898
As well as an article discussing how telomeres can be maintained by recombination.
http://www.ncbi.nlm.nih.gov/pubmed/11101843
Posted by: Amphiox, OM
|
November 5, 2011 11:07 AM
I just love it when creobots try to challenge the literature.
They expose the sheer ignorance, dishonesty, and intellectual bankruptcy of their positions so easily.
And I not infrequently end up learning interesting new things when I do the research to refute them.
I guess this is why the smartest and most dishonest of the creobots never try.
Posted by: Amphiox, OM
|
November 5, 2011 11:20 AM
Here's another related example:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2742575/
This occurs in a human brain tumor, and is very interesting medically, because this particular genetic change is a positive prognostic factor and predicts improved survival (relatively).
A nonbalanced translocation occurs between chromosomes 1 and 19. One arm of 1 and another arm of 19 break off and fuse together. The fusion product is usually lost (possibly because it doesn't have a centromere, but sometimes it is retained for a while, which would suggest that it must have had some way of saving itself in mitosis), leaving the abnormality we can see as a co-deletion of one arm of 1 and one arm of 19.
This is believed to be one of the early, transformative events for this kind of tumor.
Crucially, the breakages should have left both 1 and 19 without a telomere on one end. Which, per our creobot's objection, should have rendered the cell unable to divide.
And yet this thing is a tumor cell. Not only is it fully able to divide, it divides TOO well. It's immortal and capable of dividing INDEFINITELY.
(Actually this is dirt common in cancer cells. Many of them have a multitude of chromosome abnormalities, duplications, fissions, translocations, deletions. You name it, there's a cancer cell line out there that has it. ALL of them are immortal cell lines that clearly have no problem overcoming the telomere problem supposedly associated with chromosome breakages).
(I wonder if our creobot will turn out to be so ignorant as to try to pipe up with the objection that these are not viable mutations, as if that was even relevant to the point....)
Posted by: lundahl.hans
|
November 5, 2011 1:36 PM
@#231
First link is about centromere reduplication without any word indicating any subsequent fission. It is about a real time example.
A real time example as you claimed to exist, but not about viable fission, only about what is considered theoretically a preparation for fission, the centromere reduplication. So, not what you claimed.
Second link is about a fission - but between species, not individuals, so depending on Evolutionist analysis of fact, not on fact, also Hymenoptera (Virgin Wings in Greek - meaning, I presume, bees and ants) are not mammals.
Since neither human nor real time, not what you claimed either.
I do accept polyploidy in plants, but they are outside the mammal system, so there are no plant fœti in plant mother individuals to be accepted or aborted by such. So plant polyploidy being viable does not explain any possibility of mammal polyploidy being viable.
I also accept fusion, and if you had actually read my article, you would have known that I put down the mouse having chromosome numbers ranging from 2n=22 to 2n=40 to precisely - fusion: from an original 40 downward.
Sure the rats go in tetraploid varieties? A source precisely for that?
Posted by: lundahl.hans
|
November 5, 2011 1:51 PM
Oh, and another thing, the mechanism of a Robertsonian translocation starts with a chromosome FISSION event (without a centromere duplication) near the centromere, followed by fusion events that produce one translocated chromosome with a fused centromere and one without any centromere, that gets lost in later cell divisions.
In the case of translocation, I take it that the fission followed by a fusion ends up fusing in such a way that telomeres are there all along the way, right?
In other words, if the fission occurs without a centromere duplication, you end up with a Robertsonian translocation. But if a centromere duplication occurs first, then the same mechanism that produces Robertsonian translocations will produce the scenario PZ describes.
Precisely not, since the problem in his scenario is where telomeres come from.
From article with healthy woman, centric fission chromosome 11, repeated miscarriages, I quote:
Centric fission results when a metacentric or submetacentric chromosome splits at the centromere, giving rise to two stable telocentric products, isochromosomes, or ring chromosomes.
When first writing my article, I did not know telocentric chromosomes (extreme of acrocentric) even existed.
A centromere reduplication, then splitting in one of two centromeres, that can happen, but only one of the splits will be a "full chromosome" (not full as in full information of original chromosome, but full in form, as in two telomeres, one centromere between them and two arms between centro and each telo), the other one will be only be telocentric - i e have gene loci on a string between two telomeres (one original telomere, one half of one centromere) and no centromere between them. Geometry.
A centromere reduplication with split between the two will probably not lead to anything viable at all, telomeres will be lacking.
First link in #234 has this quote:
In this article we discuss the consequences of telomere loss and the possible mechanisms that the enzyme telomerase employs to form telomeres de novo on broken chromosome ends.
"Possible" does not state that actual examples have been found, still less that they are relevant or what the source for it is.
Posted by: lundahl.hans
|
November 5, 2011 1:55 PM
Second link 234:
Some immortalized human cell lines and some tumours maintain their telomeres in the absence of any detectable telomerase activity by a mechanism referred to as alternative lengthening of telomeres (ALT).
That is beside the point I raised, about two telomeres and two centromeres plus split (1 c = 2 t) being unable to produce twice (2 t + 1 c).
Posted by: lundahl.hans
|
November 5, 2011 1:57 PM
And #236 is not at all about fission, but about fusion.
So, who has made a point in a very bad way?
Posted by: Nerd of Redhead, OM
|
November 5, 2011 3:28 PM
Not one citation to the peer reviewed scientific literature lundahl. Ergo, you have nothing but bullshit. Your inane opinion is worthless, and you have been found lying. So, what do you hope to gain by further embarrassment to yourself? You need real science, not your opinion, to change our minds...
Posted by: Amphiox, OM
|
November 5, 2011 3:56 PM
Again this is the bumblebee scenario. We know that it happens. It happening is FACT, not theory. And since it happens it means either that your telomere objection is fundamentally wrong and not a problem, or it is a problem that is easily solved by some mechanism we don't yet know of.
And as I have already pointed, and you have consistently ignored, and gave you citations for, we have at least two good hypotheses as to the mechanism.
The fusion "saves" the chromosomes form needing to get new telomeres, as the two frayed telomere-less ends are the ends that fuse together (ie they're not the end of the chromosome anymore after the fusion).
The ONLY reason people are interested in trying to figure out "possible" mechanisms is because we ALREADY KNOW THAT IT HAPPENS. We have OBSERVED IT HAPPENING.
We look at that reality and think "hey, wait a minute, what about the telomeres? Shouldn't the telomere problem make this impossible?"
But, you see, it is the bumblebee issue again. It SEEMS impossible that bumblebees should be able to fly, but THEY DO FLY. And that means that there MUST be some other, as yet known mechanism, by which bumblebees are able to fly. And since we actually observe chromosomes splitting at their centromeres, and surviving, despite the telomere problem, that means there either there is something going on to fix the telomere problem, or the telomere issue isn't as show-stopping a problem as we think it is.
You mistakenly assume that @236 was intended to be a direct response to you in any way at all, as opposed to an interesting related observation to point out for others to note and comment on if they wish.
Posted by: Ichthyic
|
November 5, 2011 3:57 PM
Lundahl is correct about mammalian polyploidy (at last check, there are no examples in the field).
as to:
Sure the rats go in tetraploid varieties? A source precisely for that?
There indeed WAS a paper published in 1999 on Tympanoctomys barrerae claiming to have found tetraploidy.
but:
http://www.sciencedirect.com/science/article/pii/S0888754305000029
and, FWIW, that paper also elucidates the current hypothesis about why polyploidy is rare in mammals.
but then, I'm confused about what his point actually IS?
Posted by: Amphiox, OM
|
November 5, 2011 4:27 PM
Then you should rewrite your article, seeing as this little factoid (which was well known long before you wrote your article, and should have been available to you to find out with only the most cursory of literature searches) completely invalidates your objection to the big picture - that evolutionary processes cannot result in increases in chromosome number.
Understand that centromere =/= telomere. Even a telocentric chromosome has telomeres on both ends. So this example of a healthy adult woman with 47 chromosomes instead of 46, due to chromosome 11 splitting into two telocentric hemi-chromosomes, must have included some way around the telomere "problem" you describe, or else, she would never have survived as an embryo.
The original chromosome 11 was:
telomere-11p-centromere-11q-telomere (p and q are how we name chromosome arms).
But in this woman, the chromosome split and she has:
telomere-11p-centromere
centromere-11q-telomere
And neither of these arms would have had the second telomere at the moment of centric fission.
However, this conformation was VIABLE. It became a healthy embryo, and grew into a HEALTHY adult.
So either these two chromosome halves somehow got their second telomeres, all in that one generation, or the absense of the telomere did not prevent the individual to growing up into a healthy adult.
In other words, your telomere "problem" is NOT a problem. It will be interesting to figure out exactly HOW the problem is solved, but we already know for a fact that it IS solved.
Actually, neither of the splits will start out as "full" chromosomes. Both of them will be telomere-chromosome arm-centromere-empty end with no telomere at the start.
But that's irrelevant, as we have already observed that, one way or another, it is possible for this telomere-chromosome arm-centromere-empty end chromosome to be viable. It either gets a telomere somehow, or it doesn't need that second telomere to be viable. And when you're describing the situation in an educational setting for laypeople, and/or students, as PZ is doing, you can justifiably ignore the telomeres entirely, as their presence has no relevant impact on the mechanism as presented.
Posted by: Amphiox, OM
|
November 5, 2011 4:30 PM
Fascinating. Thanks Ichthyic.
It was here on Pharyngula that I was first informed about the tetraploid rat. Fitting that it'd be here on Pharyngula that I'd find out it has been disproven.
Posted by: Amphiox, OM
|
November 5, 2011 4:34 PM
In most cases, it probably doesn't. In most cases, such a split will probably immediately trigger apoptosis of the unfortunately affected cell.
But it only has to happen in a tiny minority of cases to be a viable evolutionary mechanism. Indeed, if it happened too often, it would be a bad thing, and natural selection would act to limit such occurrences, such as via apoptosis.
Posted by: Amphiox, OM
|
November 5, 2011 4:42 PM
Note that centromeres in most eukaryotes consist of tandemly repeating sequences. In other words most centromere are already duplicated sequences. And that is part of the reason why a straight centromere split produces two "half" centromeres that can still function as full centromeres.
Or, to put it another way, in PZ's description in the OP, the centromere duplication event has actually already happened in most eukaryotic chromosomes.
Posted by: Amphiox, OM
|
November 5, 2011 4:47 PM
Note also that chromosome geometry is, like chromosome number, probably mostly incidental.
A centromeric split will always produce either a telocentric chromosome or at best an acrocentric chromosome.
But it only takes a small recombination mutation to turn a telocentric chromosome into an acrocentric chromosome.
And it only takes a translocation (Robertsonian or non-Robertsonian) event to turn a telocentric chromosome into a metacentric or submetacentric chromosome.
So it's entirely possible for a chromosome number addition to start with new telocentric chromosomes, and then have these telocentric chromosomes gradually evolve into other morphologies.
Posted by: Owlmirror
|
November 6, 2011 1:54 AM
Hm.
Clicking on the "Cited by" for that paper in Google Scholar brought up some more research:
Molecular cytogenetics and allotetraploidy in the red vizcacha rat, Tympanoctomys barrerae
[And here's one for Ichthyic:
Natural triploidy in Leporinus cf. elongatus bearing sex chromosomes]
Ah. Most recent paper sides with the naysayers:
The genome diversity and karyotype evolution of mammals
Disclaimer: Not an expert.
Posted by: Ichthyic
|
November 6, 2011 3:00 AM
yeah, the paper I cited covers it.
Posted by: lundahl.hans
|
November 6, 2011 7:47 AM
@#244, re this:
But that's irrelevant, as we have already observed that, one way or another, it is possible for this telomere-chromosome arm-centromere-empty end chromosome to be viable. It either gets a telomere somehow, or it doesn't need that second telomere to be viable.
That is being doctrinaire.
I asked you to cite any current proof that this actually happens, you have not, and while not doing so, you have still used ten to twenty links trying.
I asked you about tetraploid rats, someone else provided a link you are wrong.
So, sorry, but the words of Nerd of Redhead are really worthy to be directed at you.
Let us cover it again:
A centromere and a telomere do not have the same position, but very similar make up, or so I have been told. In other words, a telomere can join another telomere to form a centromere, and a centromere can split into two telomeres.
Telomeres are needed, and there is nothing to prove they could be supplied by "telomere lengthening" onto telomere lacking stumps.
A break between two centromeres, when centromere reduplication has taken place, is not viable, and so much for the Myers' scenario. A break in one of them forming two telomeres is. But whichever of them breaks into two, it will not lead to forming two mesocentric or two acrocentric chromosomes, that is a geometric impossibility.
If telomeres are written T, centromeres C, a centromere broken into two telomeres CT, and the actuel genome is written with underscores, the process can go like this:
Generation 1:
T1_C_T2 > reduplication in sex cell
Generation 2 one of the two chromosomes has:
T1_C1_C2_T2 > stable split
Generation 3 one of the two chromosomes is either one of two possibilities:
T1_C1_CT (meso- or acrocentric) + CT_T2 (telocentric)
OR
T1_CT (telocentric) + CT_C2_T2 (meso- or acrocentric).
Now, the woman in one link had a stable split in chromosome pair 11, and she had miscarriage after miscarriage.
Unlikely to be any generation 4 or more where this leads to one extra pair, one of which is anyway telocentric.
But saying "we know splits occurred in evolutionary history of species X" is begging the question rather than bumble bee scenario - except that true believers in evolution will of course call that knowledge and call it a bumble bee scenario.
Posted by: Nerd of Redhead, OM
|
November 6, 2011 8:08 AM
Still no evidence presented by you lundahl. Evidence is citations to the peer reviewed scientific literature. You are mentally masturbating.
Posted by: Nerd of Redhead, OM
|
November 6, 2011 8:34 AM
And lundahl, if you have a true scientific point, present it to the world. Manuscript submission information for
Science
Nature
Posted by: lundahl.hans
|
November 6, 2011 10:06 AM
You forget that logic is evidence against illogical things - among other things illogical scenarios.
The scenario by P Z Myers above (for which he did not present any reference from peer reviewed publications) is as illogical as steps:
1
T1_C1_C2_T2
2
T1_C1_? + ?_C2_T2
with ?=telomere from nothing.
For my part I referred to every link given by the other user name.
As for being published in Science or Nature, my essay is already published on my blog and I have already given anyone, including these publications the right to republish.
My essay is on this (short) link: http://o-x.fr/hspi and my conditions for re-use are on this one: http://shrt.st/ujx - feel free to forward to either or both of them./HGL
Posted by: Owlmirror
|
November 6, 2011 11:35 AM
He was presenting textbook genetics. Textbooks are compiled from peer-reviewed results.
I don't think you know what illogical means. Obviously, if something exists, it is not illogical.
Telomeres are not "from nothing". They are from amino acids.
In order to be published, you have to convince experts in the field you are writing on -- peers -- that you know what you're writing about.
You don't seem to have done that step.
Posted by: Owlmirror
|
November 6, 2011 11:39 AM
And you don't have to publish in Science or Nature. You could try submitting to PLoS Genetics, for example.
But you still have to convince experts that you know what you're writing about.
Posted by: Nerd of Redhead, OM
|
November 6, 2011 11:43 AM
Typical excuse of cranks who know they are not scientific. Until you publish it in the peer reviewed literature, you will be seen as nothing but a crank. Why are you afraid to do so??? Perhaps you know it wouldn't get published due to real scientific deficiencies in your inane ideas?Posted by: lundahl.hans
|
November 6, 2011 1:47 PM
What about them not daring to publish due to real deficiency in the Myers' idea.
It is supposed to be from textbooks, but no one mentioned which textbook.
Besides, textbooks have been known to be wrong on an occasion or two, even if a textbook wrong ojn every item would - so far - hardly come into print.
How come the owner of this blog did not allow automatic publishing of my answer to Owlmirror on http://o-x.fr/h114 post?
Posted by: Ichthyic
|
November 6, 2011 2:32 PM
You forget that logic is evidence against illogical things - among other things illogical scenarios.
*headdesk*
ah, I get it now...
you're a demented fuckwit.
here I thought you might have something of interest to offer regarding polyploidy, mechanisms of chromosomal breakage and recombination, or evolution.
but I can see I wasted my time.
Posted by: Amphiox, OM
|
November 6, 2011 2:52 PM
You fail to realize that if this is true, it completely invalidates your entire objection, because it allows for a freshly split centromere to act as a telomere, meaning there is no need for adding the new telomere in the first place.
Your initial chromosome is:
T-arm-C-arm-T.
After the split you have:
T-arm-C(half)
and
C(half)-arm-T.
And because C(half) can act as a telomere (if what you claim above is true), then both the new chromosomes have a functional telomere on either end, and your objection is completely wrong.
Unlikely to be any generation 4 or more where this leads to one extra pair, one of which is anyway telocentric.
Unlikely is why we don't see a large number of humans running around with 47 chromosomes instead of 46. But unlikely doesn't mean impossible.
This woman's fertility problems are irrelevant to your objection. Your claim is that, thanks to the telomere problem, the gamete that produced her would have been inviable. If your objection is a real one, then this woman could never have been born.
But she was born.
Ergo, your supposedly logical objection is proven false.
Posted by: Amphiox, OM
|
November 6, 2011 2:57 PM
Perhaps in a single step. But that is irrelevant.
Perhaps all new chromosomes start out as telocentric. Perhaps no newly added chromosomes start out as acrocentric or mesocentric. (This is not the reality, of course, there are plenty of mechanisms that can add a new meso or acrocentric chromosome, such as whole chromosome duplications).
But as we have already seen, a telocentric chromosome can TURN INTO a acrocentric or mesocentric chromosome later by a variety of mechanisms.
In addition to the fusion mechanisms already described, there is also the well known phenomenon of neo-centromere formation, wherein a new centromere forms from a mutation somewhere in the middle of the chromosome, and the old centromere at the end is turned off. This would turn a telocentric chromosome into a mesocentric chromosome.
Posted by: Amphiox, OM
|
November 6, 2011 3:03 PM
IF your contention that a centromere can act as a telomere, there is no need to produce a telomere from "nothing".
After a few rounds of cell division, T1_C1_? will have the _? lost, producing T1_C1. So long as the _? is short and non-coding (which in PZ's scenario it is), then T1_C1 is stable, because, per your own claim, C1 can act as a telomere. The same thing can happen to ?_C2_T2.
Thank your for conceding the entire argument using simple logic alone.
Posted by: Amphiox, OM
|
November 6, 2011 3:06 PM
Is your blog peer-reviewed?
Ha ha. Real funny. Do you even read the scientific literature? Or know real scientists? They LOVE nothing more than to tear down each other's ideas. 95% of ALL papers begin with "such and such scientist proposed hypothesis X in paper [citation]. However, there is a problem with hypothesis X, and here we demonstrate an experimental result that shows that hypothesis X is wrong".
He who resorts to conspiracy theory automatically lose the argument.
Thank you for conceding the debate. You can go away now.
Posted by: Amphiox, OM
|
November 6, 2011 3:13 PM
The telomerase enzyme is a special reverse transcriptase (enzymes that take an RNA template and produce DNA from it), that has both a protein and an RNA component. The RNA component contains the complementary sequence for the telomerase.
It works by binding to any frayed end of a DNA chain with an overhang (DNA polymerase leaves an overhang of 3 base pairs, which shortens the DNA by 3 on the next round of division), and then using its own RNA as a template to produce new DNA with the telomere sequence.
Telomeres come from the RNA template that is part of the telomerase enzyme. And that template is encoded in the DNA of the telomerase gene.
Posted by: Amphiox, OM
|
November 6, 2011 3:22 PM
Only if there is noncentromeric sequence between C1 and C2 after the duplication. (And most commonly duplications occur in tandem, without intervening sequence).
What you actually most commonly end up is:
T1-C1C2-T2. And after the split you get
T1-C1 and C2-T2. And given that most centromeres are repeat tandem sequences, C1 is actually CCCC, so C1 can split by itself already.
And as I already explained, even if you have T1-C1-C2-T2 splitting into T1-C1-? and ?-C2-T2, all that will happen without a telomere is that the -? region will get progressive shorter with subsequent divisions. If there is important coding information in that area, then this will result in gene loss which may or may not be viable. If there isn't coding information in the -? (which is often quite short), you'll eventually end up with T1-C1 and C2-T2.
And IF what you claim about centromeres and telomeres being the same, then the above is stable, and your telomere "problem" automatically goes away.
Posted by: Amphiox, OM
|
November 6, 2011 3:32 PM
No, that is applying simple, basic logic.
It is funny how you try to base your entire argument on logic without attempting the cite the literature, but you even fail to use logic properly, at all.
Yes I have. The plain fact that the woman in the citation I gave you is alive is ABSOLUTE PROOF that it happens.
Your inability or deliberately dishonest refusal to recognize a clear proof buzzing like a bumblebee in your face is not my problem.
I repeat, the woman in the citation IS ALIVE. She is a LIVING EXAMPLE of an event that turned one mesocentric chromosome into two telocentric chromosomes.
Your objection was that because of the telomere problem, such a chromosome fission is NON-VIALBE AT THE CELL LEVEL. NOT the organism level. NOT the next generation reproduction level. AT THE CELL LEVEL.
But that woman proves your objection wrong. Her BEING ALIVE is ABSOLUTE PROOF that your telomere "problem" WAS SOLVED. It is an EXACT demonstration of the mechanism proposed by PZ. PZ didn't mention telomeres in his explanation because he knows, from examples like this, that the telomere "problem" ISN'T a problem. We may not know exactly how it is solved, but we know, because this woman is alive, that it WAS SOLVED.
Buzz buzz.
Posted by: Amphiox, OM
|
November 6, 2011 4:08 PM
Our creo troll who loves to babble about centromeres and telomeres also apparently doesn't even understand how telomeres work.
There's nothing special about telomeres at all. They are just an inert, non-coding tandemly repeated sequence.
Because DNA polymerase cannot completely sequence an entire straight DNA chain, and will always leave a single stranded overhang of 3 base pairs, with each mitotic division the straight chain DNA gets shortened by 3 base pairs. This will have ABSOLUTELY NO EFFECT unless those 3 base pairs are critical coding ones.
Now of course if the cell wants to continue dividing, for, say, forming an embryo (or a tumor), it's progeny will lose 3 base pairs with every division. Sooner or later, it's going to end up losing important genetic information.
How soon is soon?
There are something like a trillion cells in a human body. A single cell, exponentially dividing in 2, will hit 1 quadrillion cells in 50 divisions. Now embryology is a little more complicated that simply exponentially dividing (some cell lineages are halted from further division at various points, and others are killed off), and we have to add in cell turnover over an individual's lifetime. So let's be conservative and go up a factor of 3, and say at least some of the cells in the adult will have to go through 150 divisions in an adult lifetime. So without a working telomere, you will end up losing 450 base pairs from the telomere-less end of your chromosome over an average adult lifetime. There are over 3 billion base pairs in the haploid human genome, over 23 chromosomes, which gives us an average of 130 million base pairs per chromosome. Just how much damage would losing 450 base pairs do?
Since there are many noncoding stretches in our DNA well longer than 450 base pairs, the loss of a telomere could easily DO NOTHING in terms of genetic information loss, for several generations.
(And this is why the old telomere hypothesis of aging is now known to be false. Cells do NOT go senescent primarily because their telomeres run out. There's enough telomere length there to last several human lifetimes.)
Of course, eventually, no matter what, this slow loss of base pairs is bound to result in loss of genetic information. So how do you fix it?
Simple. You just add some extra non-coding DNA to the end of your chromosome. This DNA becomes "sacrificial" DNA for the next cycle of cell division, so IT get lost, instead of potentially important stuff.
And that's what telomerase does. It adds a little chunk of DNA (6 base pairs long) to the end of the newly duplicated. And the repeated activity of telomerase results in the telomere being a continuous tandem repeat of those 6 base pairs. But the actual sequence of the telomere is irrelevant. Any non-coding sequence will work.
So what happens if you lose the telomere by some genetic mutation?
So long as the telomere-less end has a stretch of non-coding DNA, nothing much will happen at all. The non-coding DNA already present will function perfectly fine as a telomere, and a few mitotic divisions later, the telomerase enzyme will recognize the 3 base-pair overhang caused by the DNA polymerase, and lengthen the chain by adding the 6 base pair telomere sequence to it. And now you'll end up with a "proper" telomere.
Now we all know that modern cells in "advanced" organisms, have proof-reading mechanisms. One of these detects the absence of telomeres, and will often trigger apoptosis in a cell that has such a defect. It probably evolved as a protective mechanism against cancer, and perhaps also to increase fertility.
But these defensive mechanisms aren't perfect. Some cells with telomere loss from chromosome fission are not pegged for apoptosis, and so a steady rate of chromosomal number abnormalities will enter the population.
Individuals with these kinds of balanced chromosome number abnormalities, as already discussed, usually have fertility problems, so the frequencies of the abnormality will remain low in the population. But, crucially, thanks to genetic drift, that frequency will not always be driven to zero by natural selection.
And that is all it takes for chromosome number to evolve and change over evolutionary time.
Posted by: Amphiox, OM
|
November 6, 2011 4:19 PM
This of course, is not actually true (hence why I always qualified my prior arguments with "if it is true").
It is true only in the sense that both are made of DNA and both are tandem repeat sequences.
The telomere is a single tandem repeat sequence that is specific for each species, determined by the RNA part of the telomerase enzyme that each species has.
Centromeres in most eukyaryotes, including mammals, are sequentially variable tandem repeat sequences, and are a different between different chromosomes.
Centromeres in some eukaryotes, like yeast, are a specific sequence of about 150 base pairs.
The statement above is clearly something our creo-bot pulled out of his ass (note the lack of citation) to try to explain away the example given of the viable chromosome 11 split, because the dishonest liar KNOWS that it shoots his objection to pieces by the mere act of existing.
The fact that it turns out to be such a spectacular logical own-goal is just another amusing demonstration of his idiocy.
Posted by: Amphiox, OM
|
November 6, 2011 4:25 PM
Here's another citation:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC16892/
Note the section on de novo telomeres.
Posted by: Amphiox, OM
|
November 6, 2011 4:32 PM
Here's another citation, in yeast, where the acquisition of a new telomere after chromosome fission of dicentric (ie duplicated centromeres) chromosomes is directly observed.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1202252/
And here's another one:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC400796/
Posted by: Amphiox, OM
|
November 6, 2011 5:59 PM
Here's ANOTHER citation, showing several human cases, some by pure centric fission, and some by peri-centric duplication. It also describes yet another mechanism for getting around the telomere "problem", formation of a ring chromosome.
http://www.ncbi.nlm.nih.gov/pubmed/15712016
Posted by: Amphiox, OM
|
November 6, 2011 6:10 PM
And here's another:
http://www.nature.com/hdy/journal/v81/n5/full/6884210a.html
Which contains this:
Demonstrating one mechanism by which telocentric chromosomes can change to another morphology as a later step.
Posted by: txpiper
|
November 6, 2011 9:01 PM
amphiox,
"Of course, eventually, no matter what, this slow loss of base pairs is bound to result in loss of genetic information. So how do you fix it?
Simple. You just add some extra non-coding DNA to the end of your chromosome."
Well, the solution might be simple. But how would you propose that such a buffer 'evolved'?
"Now we all know that modern cells in "advanced" organisms, have proof-reading mechanisms."
Are there 'primitive' self-replicating organisms that don't?
"One of these detects the absence of telomeres, and will often trigger apoptosis in a cell that has such a defect."
Yeah, noticing that something is missing is one of those activities that does not look like a chemical reaction.
Posted by: https://me.yahoo.com/a/_4KIfrwRxNWU8qEsAFrxolQ6Tw--#4599c
|
November 6, 2011 10:01 PM
I notice that your intelligence is missing, and I do some via a (rather complex chain of) chemical reaction.
Posted by: txpiper
|
November 6, 2011 11:16 PM
4599c,
"I do some via a (rather complex chain of) chemical reaction."
Well, not just chemical though. It is electrical as well.
But this is sortof what I was getting at. Enzymes are just complex molecules. But they recognize that something is wrong, and correct the situation.
Compare them with yourself, the beneficiary of 100 billion neurons and 100 trillion synapses. A mind, that in your mind, is the result of natural selection acting on DNA replication errors.
Which is more noble? The lowly functional enzyme, or oblivious you?
Posted by: Nerd of Redhead, OM
|
November 6, 2011 11:18 PM
Yawn, still no citations from txpiper. All opinion, no evidence. Liar and bullshitter confirmed once again. Only more science refutes science. And Txpiper doesn't do science, he does religion.
Posted by: lundahl.hans
|
November 6, 2011 11:25 PM
Oh, I have conceded the point, have I?
No, since:
T1_C_T2
can at utmost give:
T1_CT + CT_T2 (two telocentric)
and starting with reduplication in middle:
T1_C1_C2_T2
either:
T1_C1_CT + CT_T2
or:
T1_CT + CT_C2_T2
and either way at least one is telocentric.
As you said yourself, the one given by P Z Myers:
T1_C1_? + ?_C2_T2
would soon enough be:
T1_CT1 + CT2_T2
again two telocentric.
Now, if only ever mesocentric or acrocentric chromsomes added up to at most 48 and anything over 48 is telocentric, then we might be talking. But we do see chromosome numbers above 48 in mammals that are not limited to telocentric chromosomes.
Except that the woman who had a stable split in chromosome 11 - one of them as usual and one split into acrocentric and telocentric and she had miscarriage after miscarriage. Obviously her mother cannot have had that stable split before her or she would have been one of the miscarriages rather than having them.
There is a reason why mankind has not developed a variety with split chromosome 11 in both chromsomes of the pair.
Someone added: "if my claim is true" - it was given by a Danish brewer and evolutionist, or by someone seconding him, so it is not mine. It seems to make sense that telomerase and centromerase is same substance.
Posted by: lundahl.hans
|
November 6, 2011 11:34 PM
@#268 saying:
The telomere is a single tandem repeat sequence that is specific for each species, determined by the RNA part of the telomerase enzyme that each species has.
Centromeres in most eukyaryotes, including mammals, are sequentially variable tandem repeat sequences, and are a different between different chromosomes.
Centromeres in some eukaryotes, like yeast, are a specific sequence of about 150 base pairs.
Do check up statement, will you!
If you are right, then possibilities I conceded to near-Myers' scenarios are even gone with the wind.
The stable split would then of course have been producing miscarriages because a split centromere is not two telomeres but two pseudotelomeres that do not work as they should.
Thank you for ruining even further the case for increasing chromosomes.
@ someone asking about polyploidy, that does not work in placental mammals.
Immediate miscarriage.
Even trisomy in one of the bigger chromsomes (1, 2, 3), unless only mosaical (i e not all cells) triggers miscarriage and thus gives no viable syndrome carriers. So much more triploidy, i e trisomy in all pairs, or tetraploidy, tetrasomy in all pairs.
That is why I was wary about the supposed tetraploid rat.
But thank you again, it was not me who pulled "centromere=telomere" out of my ass, but an evolutionist who pulled it out of his. Thank you so much for ruining his case.
Posted by: lundahl.hans
|
November 6, 2011 11:44 PM
Oh, just read #264:
It works by binding to any frayed end of a DNA chain with an overhang (DNA polymerase leaves an overhang of 3 base pairs, which shortens the DNA by 3 on the next round of division), and then using its own RNA as a template to produce new DNA with the telomere sequence.
As in:
T1_C1_? + ?_C2_T
getting added new telomeres:
T1_C1_NT + NT_C2_T2?
That would indeed get to fixing the problem. That is why I ask you to provide a source for new telomeres appearing (observed in real time).
Meanwhile, as someone (you?) asked if my blog was peer reviewed, in a sense yes, insofar as I am an amateur and it is read thus reviewed by amateurs.
If you had been reading it and commenting it, it would have been not peer reviewed, but superior reviewed.
At University I did not do biology or anything, but mainly Latin and Greek.
Posted by: lundahl.hans
|
November 6, 2011 11:49 PM
#261:
Whole chromosome duplication is trisomy, and extremely unlikely to get dominant, as especially tetrasomy is not evening matters out but worsening them.
In addition to the fusion mechanisms already described, there is also the well known phenomenon of neo-centromere formation, wherein a new centromere forms from a mutation somewhere in the middle of the chromosome, and the old centromere at the end is turned off. This would turn a telocentric chromosome into a mesocentric chromosome.
If it is well known, no doubt there is a source for it too.
Posted by: https://me.yahoo.com/a/PSPW0GU_zfVn3qhjy1tC0lwbbxJLm3O14w--#c1afa
|
November 6, 2011 11:55 PM
It shows. Your ignorance of biology is appalling.Posted by: https://me.yahoo.com/a/_4KIfrwRxNWU8qEsAFrxolQ6Tw--#4599c
|
November 7, 2011 3:53 AM
Not a criterion of what is true. And there's nothing noble about having your head stuck up the ass of a myth, oblivious to evidence and logic, or being so grossly dishonest as you have demonstrated here over and over.
Posted by: lundahl.hans
|
November 7, 2011 5:27 AM
@#282 - who asked "which is more noble?"
Ah, got it: Txpiper in #275!
He continued: "the lowly enzyme or the oblivious you?"
OK.
A kind of argument, and not quite honest of #282 to him to make it misunderstood by omission after so many posts.
Will go back and read Txpiper's posts and see what he has to say.
Posted by: lundahl.hans
|
November 7, 2011 5:44 AM
Amphiox in #269 linked to:
"Kinetochore reproduction in animal evolution: Cell biological explanation of karyotypic fission theory"
Theory, not actual observation!
Yeast link in #270 contains this quote, I highlight:
A smaller proportion of events resulted in apparently uniquely healed linear chromosomes in which the broken chromosome acquired a new telomere.
Acquisition of new telomere has been nearly observed in yeast and biologist stating that calls it apparently unique as an event. Hardly promising for mammalian parallels.
Second link is also - yeast (Saccaromyces cerevisiae - beer yeast).
Formation of ring chromosomes is great for continued life, but not so great for developing new chromosome pairs, at least not directly, but a ring has very little to go on when it comes to forming telomeres and centromeres as of mesocentric or acrocentric normal chromosomes:
Two cases show a missing chromosome 22 or 18 that is replaced by two centric ring products,
Centric ring products ....
a third case shows two chromosome-10-derived telocentric chromosomes,
Telocentric chromosomes are - as I said above - neither mesocentric nor acrocentric like the ones we usually find in mammals.
whereas a fourth case involves the formation of two chromosome-18-derived isochromosomes.
Isochromosomes, I admit to not knowing what it is.
OK, your modified scenario, via telocentrics is what, from say one or two extant chromosome pairs up to a new one with centromere in netween telomeres?
Posted by: lundahl.hans
|
November 7, 2011 5:49 AM
Note, we do not know that the person with chromosome 10 two telocentric ones has any more chances than the woman with stable split in chromosome 11 to both beget and carry through gestion.
http://www.ncbi.nlm.nih.gov/pubmed/21271652
Even this:
This is the first report on centric fission of chromosome 12 leading to stable telocentrics, each with a fully functional centromere. Our observation shows that the centric fission of chromosome 12 can be a new mechanism for generation of a partial centromere and trisomy 12p syndrome.
Article is from 2011, though.
Posted by: lundahl.hans
|
November 7, 2011 5:53 AM
And from Turkey - a country where Islamic scholars have been accused for dishonesty in accomodating science and Islam, where there are also anti-islamic powers, who might be dishonest too.
I wonder if it is apocryphic.
If not, I am a bit astonished.
Posted by: Nerd of Redhead, OM
|
November 7, 2011 6:55 AM
Oh gee, the unscientific crank is cranky. tl;dr, drivel.
Posted by: lundahl.hans
|
November 7, 2011 7:07 AM
But the Nerd prefers being Jerk to being Nerd ... Yadda, Yadda ...
Seriously, once the woman with split 11 got a viable baby, it was karyotype 2n=46.
BUt I saw sth about third generation split on medical literature, will look up!
C U L8r Lig8r ...
Posted by: lundahl.hans
|
November 7, 2011 7:39 AM
Meanwhile, I did add a link to three generations split chromosome 7 - author, year, publication, no text given - to a letter sent to three medical students, with appropriate questions.
Posted by: GiveMeLiberty
|
December 22, 2011 11:46 PM
This is a near perfect explanation, but there is one major problem. If the number of chromosomes does not give an individual animal an advantage nor make any change to the individual animal, then we'd expect to find that most species would exist with all different numbers of chromosomes, since all would have an equal chance of surviving.
Reality is quite different. Then number of chromosomes is fixed for each species. This strongly suggests an advantage in a certain number of chromosomes. The evidence is so strong that it can't be ignore.
I give the write props for trying to answer the question, but a more honest answer would be to admit that he either doesn't know or doesn't want to explain, because sadly he did not fully and completely answer the question.
Posted by: https://me.yahoo.com/a/tVh9ew8QguDfeGsPqebUjQKsBvKu2Q--#80755
|
January 1, 2012 1:52 PM
The survival value of a fixed chromosome number in mammals is:
not getting spontaneously aborted as a very small fetus
since, even a trisomy in chromosome pair one (a big chromosome pair, since all except sex chromosomes are numbered after size starting with biggest and getting small as we get to pair 22), unless absent from part of the cells, is enough clear overload distinction from mother's immunity tolerance to make a spontaneous abortion occur.