This is a repost from the old ERV. A retrotransposed ERV I dont trust them staying up at Blogger, and the SEED overlords are letting me have 4 reposts a week, so Im gonna take advantage of that!
I am going to try to add more comments to these posts for the old readers– Think of these as ‘directors cut’ posts
Several new readers have asked for more information on ERVs, and what exactly my blog subtitle ‘joke’ means. After finals next week I plan on writing more detailed posts, but until then, there are a few in the archives to tide you over
‘Mobile Elements’ was my third post ever. I tried to make it a brief overview on all the bits of mobile DNA in your genome:
- SINEs (13.6% of your genome)
- LINEs (20.9% of your genome)
- LTR elements, which includes the more complete ERVs (8.5% of your genome)
- DNA transposons (2.4% of your genome)
That adds up to ~45% of your genome. Now do you get the joke? If we are made in Gods image, God is a parasitic, selfish gene. LOL!
While the first post was on the mobile elements themselves, ‘Mobile Elements, Part Deux’ is about different ways your genome has evolved not just ‘because of‘ mobile elements, but ‘in response to’ mobile elements.
Mobile Elements: Drivers of Genome Evolution
This spring I sat in on a course in Viral Evolution. I quickly fell madly in love with Patrick Forterre hypothesis: that everything on Earth now evolved from and because of–viruses.
Of course, one of the booby-traps that scientists need to watch out for is… falling madly in love with a hypothesis. You have to look at the data objectively–regardless of how much you might like or dislike an idea.
So even though I cant get into a time machine, go back a few billion years, and watch what happened myself, we can look at our (and other organisms’ genomes) to see if we can find any clues. And that’s the topic of this first paper: Mobile Elements: Drivers of Genome Evolution.
Approximately half of the mammalian genome is composed of mobile elements, cousins of retroviruses. Mobile elements can be in the form of:
DNA transposons: Cut and paste themselves into DNA, normally staying close to the original insertion (‘Local Hopping’), but can move to a distant site in the genome
LTR retrotransposons: Duplicate themselves, rather than cut/paste. They do this by being transcribed into RNA, reverse transcribed into DNA, then inserted into DNA. They are very similar to retroviruses (have gag and pol) but lack a functional env. Endogenous retroviruses fall into this category.
Non-LTR retrotransposons: LINE-1s, or L1s. Only encode a nucleic acid binding protein, endonuclease, and RT. They are reverse transcribed right on the genomic DNA, not in a viral-like particle in the cytoplasm like LTR retrotransposons.
Oddballs: Look like bits from the other groups, but lack all of the genes necessary to be autonomous. They might be missing a protease/integrase/RT/etc.
Okay, well, that’s neat–but what do these bits of DNA have to do with the evolution of genomes? Well, these little guys can really screw around with your chromosomes. Humans have about 80-100 L1s, and about 1 in 50 people have a novel L1. These L1s can plop themselves in the middle of a gene. They can repair breaks in your DNA. Increase/Decrease the transcription of genes. And they (potentially) control X-chromosome inactivation in women! Trust me, that’s a good thing.
L1s also act in trans to activate Alu sequences, or SINES. Alus are only ~300 base pairs long, but they make up 11% of our genome! 1 in 30 people has a *new* Alu. Alus really have the ability to screw around with genomes–they can cause unequal crossovers (instead of two identical chromosomes splitting into two eggs/sperm, one is chromosome is larger, one is smaller), rearrange coding regions, and duplicating portions of chromosomes. And, L1s can do some rearranging of their own, as well.
So what are the effects of these chromosomal rearrangements? Obviously, screwing around with genes can lead to diseases. Alu insertions are the cause of over 20 diseases, and L1s cause some as well. Obviously, there can also be problems with chromosomal deletions, and L1s changing the transcription levels of genes can also have negative consequences.
But, changing transcription levels can also have evolutionarily beneficial consequences. After comparing our genome to the recently finished chimpanzee genome, we noticed that it wasn’t so much our genes that make us different from our chimpanzee cousins, but the transcription levels of the genes we share. Chromosomal duplications can also have a benefit–if you have two copies of a gene, then one of those genes is no longer under any evolutionary pressure. Its free to mutate, potentially creating a new useful gene, or mutate into a pseudogene.
So maybe I cant completely agree with Forterre yet, but obviously, viral elements have played a huge role in the evolution of our genome, and every other organism on this planet.
Moble Elements, Drivers of Genomic Evolution Part Deux
I didnt mean to make this a two parter (obviously, as ‘Part One’ was written several months ago), but I just came upon this article, and TEs impact on genomic evolution obviously needs another post. Its not just the TEs themselves that have directed the evolution of our genomes– how our genomes have reacted to TEs has also had far reaching effects.
As my blogs subtitle goes, if we’re made in Gods image, ‘God’ is made of gag, pol, and env. Up to 50% of our genome is made of transposable elements. Theyre egotistical bits of parasitic DNA that only care about themselves. Invite themselves into our genome, eat all our brownies, and leave the place a mess– inserting themselves in protein coding regions, breaking chromosomes, rearranging genes and chromosomes, messing up splicing, and screwing up transcription levels.
So, how are we still alive right now? If ~50% of our genome is made of these bastards, how is everything still working? Cause our genome evolved ways to make ‘God’ shut up. Lots of ways, actually, as Ive alluded to in my posts to Creationists and Deniers that want ERVs, in particular, to be active.
RNAi – A cellular function probably almost as old as TEs themselves. Maybe… *maybe*… RNAi was initially ‘invented’ strictly for control of TEs, and was eventually co-opted for use by the cell itself. See, most TEs have a little inverted repeat at the beginning and the end of their genome, so a transcript would invert itself into an RNA hairpin– exactly what dicers love to eat.
Experimental evidence of this control mechanism is that if you screw up RNAi proteins in eukaryotes, transcript levels of TEs jumps up. It also appears that C. elegans use the RNAi pathway as their main means of keeping TEs quiet.
Epigenetics – Making changes to histones causes DNA to twist up around them tight, or loosen up. Keep your DNA locked up tight, and genes arent transcribed, including TEs.
You can also make DNA wrap up around histones tighter by making little changes to DNA, called DNA methylation. Again, keeping the DNA wound up tight keeps the transcription machinery from getting in and making TE transcripts.
And, you can use chromatin remodeling proteins (like SWI/SNF in plants) to alter the structure of your chromatin, changing the loops and supercoils of your double-stranded DNA.
RNAi AND Epigenetics, Wondertwins, UNITE! - In some eukaryotes, RNAi is required for chromatin modifications, like in fission yeast. Sometimes RNAi and chromatin remodeling combine to actually cut out TEs, like in Tetrahymena and Paramecium!
So I missed half the picture in that first post!