Cephalopod venoms

i-e88a953e59c2ce6c5e2ac4568c7f0c36-rb.png

The history of venoms is a wonderful example of an evolutionary process. We're all familiar with the idea of venomous snakes, but the cool thing is that when we examine exactly what it is they're injecting into their prey, it's a collection of proteins that show a nested hierarchy of descent. Ancient reptiles had a small and nasty set of poisons they would use, and to improve their efficacy, more and more have been added to the cocktail; so some lizards produce venomous proteins, while the really dangerous members of the Serpentes produce those same proteins, plus a large array of others.

i-6cf230da0ba5a3497fce1fd797019ad6-lizard_venoms.jpg

So something like CRISP (Cystein RIch Secretory Protein) is common to all, but only the most refined predators add PLA2 (Phosopholipase A2) to the mix.

Now lethally poisonous snakes are nice and cute and all, but we all know where the interesting action really is: cephalopods. Let's leave the vertebrates altogether and look at a venomous protostome clade to see what they do.

i-ff97caf7d7970f57aa4b6dc82eace617-ceph_venom_glands.gif
Relative glandular arrangements of a cuttlefish and b octopus. Posterior gland is shown in green; anterior, in blue. Orange structure is the beak.

Brian Fry, who did all that excellent work characterizing and cataloging the
pharmacy of venoms secreted by poisonous snakes, has also turned his hand to the cephalopods. He examined the products of the venom glands of octopus, squid, and cuttlefish, and found a range of proteins, some unique, and others familiar: CAP (a CRISP protein), chitinase, peptidase S1, PLA2 and others. There are a couple of interesting lessons in that list.

First, evolution doesn't just invent something brand new on the spot to fill a function — what we find instead is that existing proteins are repurposed to do a job. This is how evolution generally operates, taking what already exists and tinkering and reshaping it to better fulfill a useful function. Phospholipase A2, for instance, is a perfectly harmless and extremely useful non-venomous protein in many organisms — we non-toxic humans also make it. We use it as a regulatory signal to control the inflammation response to infection and injury — in moderation, it's a good thing. What venomous animals can do, though, is inject us with an overdose of this regulator to send our local repair and recovery systems berserk, producing swelling that can incapacitate a tissue. Similarly, a peptidase is a useful enzyme for breaking down proteins in the digestive system…but a poisonous snake or cephalopod biting your hand can squirt it into the tissues, and now it's being used to digest your muscles and connective tissue. Some effective venoms are simply common proteins used inappropriately (from the perspective of the target).

Another interesting observation is that cephalopods and vertebrates have independently converged in using some of the same venoms. In part, this is a consequence of historical availability — all animals have phospholipases,, since they are important general signalling molecules, so it's part of the collection of widgets in the metazoan toolbox from which evolution can draw. It's also part of an inflammation pathway that can be exploited by predators, in the same way that we have shared proteins used in the operation of the nervous system that can be targeted by neurotoxins. So there is independent convergence on a specific use of these proteins as toxins, but one of the things that facilitates the convergence is a shared ancestry.

In fact, some very diverse groups seem to consistently settle on the same likely suspects in their venoms.

i-427acefb14a1c22ea42a523485acea91-venom_table.gif

But finally, there must also be physical and chemical proteins of these particular proteins that must also predispose them to use as toxins. After all, animals aren't coopting just any protein for venoms — they aren't injecting large quantities of tubulin or heat shock proteins into their prey. There must be something about each of the standard suspects in venoms that make them particularly dangerous. What the comparative evolutionary approach allows us to do is identify the common molecular properties that make for a good venom. As Fry explains it,

Typically the proteins chosen are from
widely dispersed multigene secretory protein families with
extensive cysteine cross-linking. These proteins are collectively much more numerous than globular enzymes,
transmembrane proteins, or intracellular protein. Although
the relative abundance of these protein types in animal
venoms may reflect stochastic recruitment processes, there
has not been a single reported case of a signal peptide
added onto a transmembrane or intracellular protein or a
hybrid protein expressed in a venom gland. A strong bias is
also evident for all of the protein-scaffold types, whether
from peptides or enzymes. Although the protein scaffolds
present in venoms represent functionally and structurally
versatile kinds, they share an underlying biochemistry that
would produce toxic effects when delivered as an "overdose". Toxic effects include taking
advantage of a universally present substrate to cause
physical damage or causing changes in physiological
chemistry though agonistic or antagonistic targeting. This allows the new venom gland protein to have an
immediate effect based on overexpression of the original
bioactivity. Furthermore, the features of widely dispersed
body proteins, particularly the presence of a molecular
scaffold amenable to functional diversification, are features
that make a protein suitable for accelerated gene duplication and diversification in the venom gland.

To simplify, killing something with a secreted poison typically involves reusing an extant protein, but not just any protein — only a subset of the proteins in an animal's proteome has just the right properties to make for a good venom. Therefore, we see the same small set of proteins get independently coopted into the venom glands of various creatures.


Fry BG, Roelants K, Norman JA (2009) Tentacles of venom: toxic protein convergence in the Kingdom Animalia. J Mol Evol Mar 18. [Epub ahead of print].

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Cool!

Have the proteins changed much since they took on the function of venom? And are the same changes found in different lineages at the protein level too?

I might have thought the cone snail would use more of the same proteins as the cephalopods than it does.

Maybe their rampant mutation rates mean that less turns into more quickly enough that they didn't need to start with as many proteins.

And yes, "strange" how animals use similar proteins, while plants have significantly different toxins in most cases. Almost as if one could not evoke common design.... Not that the IDiots will ever address such glaring difficulties, which are predicted by non-telic evolution.

Glen D
http://tinyurl.com/6mb592

Nothing like reading about venoms while munching lunch. Very interesting the way the same protein families get used over widely different organisms. Good find.

By Nerd of Redhead, OM (not verified) on 02 Apr 2009 #permalink

Glen: The differences between toxic plants and venomous animals might be due more to the toxic/venomous difference than the plant/animal. The plant's getting passively eaten, so the toxin doesn't need to be secreted (or even concentrated in any particular organ). That, presumably, gives plants a wider choice of options.

The new digestive enzymes of carnivorous plants might behave more like venoms, perhaps?

Interesting. I was told once that the venoms of various sea creatures tend to be proteins. Hence, the remedy for a sting is to get your friend to pee on it, thus changing the pH and denaturing the protein. I haven't had the joy of testing this remedy out, however.

By ShaggyManiac (not verified) on 02 Apr 2009 #permalink

Time for the Christian Cobra Coalition to unite once again!

The problem has been that cobras and black mambas heard the good news of Christ much later in the Cenozoic era.

It's reading stuff like THIS that fill me with that awe and wonder you're supposed to only feel when contemplating deities.

Urine is normally only slightly acidic to neutral in pH. However, high concentrations of urea can also denature proteins, and if the pee-on-the-stung-spot therapy works I'd suspect urea is the more likely mechanism.

By Sven DiMilo (not verified) on 02 Apr 2009 #permalink

It's funny how the divergence tree for venomous protiens is remarkably similar to the morphological and genetic evolutionary trees. I guess it must all be part of g0d's design.

How do you know it is not a nested hierarchy of descent and not a nested hierarchy of creation, smart guy? Everyone knows that the Designer gets His proteins from the same supplier and what you call the mutation rate is really just the expected structural failure rate.

I'm so ahead of those IDiots at the Disco Institute. I'm already working on a theory of intelligent supply chains!

The differences between toxic plants and venomous animals might be due more to the toxic/venomous difference than the plant/animal. The plant's getting passively eaten, so the toxin doesn't need to be secreted (or even concentrated in any particular organ). That, presumably, gives plants a wider choice of options.

Well, certainly that could make a significant difference. But if you think of a toxin like atropine, it could readily work as a venom. Nightshade plants "use it" because it's a secondary metabolite. Animals don't "use it," because they didn't evolve to make it.

Of course there may be issues of secretion, etc. That shouldn't be a grave problem for the god-like designer (no, don't say God), which, after all, was my main point, not the differences in the evolution of toxins vs. venoms.

I agree, though, that there would be significant differences in the evolution of toxins vs. the evolution of venoms.

Glen D
http://tinyurl.com/6mb592

This is all nicely explained by the Fall Contingency PZ blogged about a while back. God made everything good and wonderful, but then Adam and Eve fucked up, and then snakes decided to take their normal proteins like phospholipase A2 and use them for eeeevil. Science validates Genesis!

*mmlp* ...just threw up in my mouth a little.

Only the first image seems to be coming through. Are they being hosted on different sites?

I tend to think that animals live closer to the energy edge and they must conserve energy, so they tend to make use of what is available.
Plants can work on a more diverse set of chemicals, since their source of energy is the sun, which can provide more energy than they really need. So if they can find some molecule that makes them unpalatable to insects and/or animals, they gain a huge advantage over their neighbors. Plus, plants also wage chemical warfare on their neighbors, so they are primed to make interesting structures.

By Nerd of Redhead, OM (not verified) on 02 Apr 2009 #permalink

Marcus Ranum (#$): "I thought the cuttlefish's poison was in his pen!"

You mean keyboard :)

Anyway, this research is damn cool. Glad I don't have to work with these toxins in the lab though (but who knows, maybe someday I will if I ever finish school).

It's long been my theory that in general, plants don't want to kill animals, they just want to not be eaten by them. But they don't want the animals to take their valuable nitrogen elsewhere.

So the plants' goal is primarily to crash the appetite of forages, and most of the 'toxic' plants deploy substances that achieve this - from atropines and other adrenergic chemistry; through irritants like capsicum and salicin; to stupificants like marijuana and the rest. These are fairly harmless in small doses, but the tend to reduce the amount of the plant that an animal can eat.

Such a relatively delicate effect - more subtle than straight poison - can have some medical uses, but is far from botanical benevolence.

I can haz doctorate nao?

By Chris Davis (not verified) on 02 Apr 2009 #permalink

Frasque @ 9:

Ah, but you see that awe you're feeling is REALLY just awe at the glory of god's creation and it's the holy spirit trying to move through you if only you'd open your heart and Kent Hovind has a prize why aren't you claiming it and anyway why are there still monkeys??!!??!!11111!

Sigh. I'd try to channel Ray Comfort, too, but I'm afraid I wouldn't be able to reinstall my brain properly.

...to stupificants like marijuana and the rest...

Mmm...stupificants... *drool*

Therefore, we see the same small set of proteins get independently coopted into the venom glands of various creatures.

You're sure it's not due to that Empedoclean thingy Wilkins was on about yesterday?

Plants make themselves distasteful using a bewildering variety of secondary metabolites rather than killing things with these conserved proteins, as Chris pointed out. Since all sorts of things could come along and eat them, they will find a broad spectrum of deterrents useful and they can play with the nuances of deterrence and attraction without necessarily resorting to brute force digestion of other creatures' tissues. That's why I study them for a living, plant secondary metabolites are so much fun.

Maybe the driving difference between plants and animals is that animals have a huge range of options for killing other organisms, while plants are rooted in one spot, giving them either thorns or poisons?

Just as how plants have huge metabolic changes (and therefore many have huge genomes) in response to weather changes, while animals just move to where the temperature is currently better suited?

It's long been my theory that in general, plants don't want to kill animals, they just want to not be eaten by them. But they don't want the animals to take their valuable nitrogen elsewhere.

Dogbane has no qualms about killing anything that eats it. Socrates found about the same with hemlock. And while it's not a plant, Death's Angel Amanita presumably has about the same "concerns" as does a plant, and it will "happily" kill us.

Whatever fixes the problem of getting eaten. And I realize that various mushrooms and plants may have evolved such intense toxins in arms races with particular herbivores. There is, though, no need to do anything other than to kill us off as "general herbivores," along with putting off the "specific herbivores."

My guess is that limiting herbivory is often the "tactic" used by plants not because it is "preferable" to killing the herbivore, since the latter probably does the best job of it. It's just easier to merely interfere with the herbivore's actions than it is to kill it, especially since interference doesn't provoke natural selection to the same degree.

Glen D
http://tinyurl.com/6mb592

Small correction PZ, maybe:

...there must also be physical and chemical proteins of these particular proteins

I think the first instance of the word 'proteins' was meant to be 'properties'.

Great article. As usual.

Great post, PZ!

It seems like the more I learn about evolution- I see things are "repurposed" from normal, benign things in the body.

The electric eel, for example- uses an electrical charge we all have in our bodies and simply redirects the energy outward, stunning fish.

evolution rarely invents new things. It repurposes old things.

So the plants' goal is primarily to crash the appetite of forages, and most of the 'toxic' plants deploy substances that achieve this - ... like marijuana and the rest.

Hmmm... not my experience. Where'd I put those Doritos?

Sometimes it's actually detrimental to kill off the animal. A lot of night-blooming flowers are pollinated by adult hawkmoths, but the caterpillars are herbivorous... so the plants need to deter the herbivory, but not kill off the pollinators, possibly by convincing the adults to drink their nectar but oviposit elsewhere. Pretty complicated stuff. Of course deadly poisonous plants exist, but those pretty red berries that will kill you may be delicious to the birds that will spread the seeds far and wide. And then there are those that just kill anything that nibbles, nasty things, but AFAIK they're in the minority. Not that anyone has managed to survey every plant that ever lived, of course. It just seems to me that the small metabolites would offer more versatility in function for less energy.

Speaking of poetic venom,

Wislawa Szymborska, Nobel Prize winner in literature, begins one of my favorite poems:

"The buzzard never says it is to blame.
The panther wouldn't know what scruples mean.
When the piranha strikes, it feels no shame.
If snakes had hands, they'd claim their hands were clean."

To read the satisfying conclusion:

http://web.archive.org/web/20030102022610/http://www.isla.pt/goncalo/Po…

By the way, Cuttlefish has published some of her/his poems; go to the blog, Digital Cuttlefish. And hoping for a Cuttlefish poem to adorn this PZ post.

By ThirtyFiveUp (not verified) on 02 Apr 2009 #permalink

Aren't there various insects and animals that taste bad? Again, like plants, they're not trying to kill prey per se, just not get eaten. What mechanisms (chemically) are used, and is it any relation to either venoms or (plant) toxins?

Glen D said:
"It's just easier to merely interfere with the herbivore's actions than it is to kill it, especially since interference doesn't provoke natural selection to the same degree."

I like the idea!

I'm impressed with that demure look the cuttlefish has: appearing so innocent while packing a lethal sting. Just look at those eyes!

Yeah, blf, there are similar mechanisms. In fact, the monarch tastes so bad because it accumulates distasteful metabolites by feeding on its distasteful host plant, essentially stealing the toxins. Not sure if animals co-opt each others' venom in the same way, anyone know of an example?

I can't speak to the cephalopod data, but the phylogeny used for Fry's squamate venom evolution paper is still very much in flux. Squamate phylogeny is a mess, has been for years, and a stable topology may show a very different history than that presented here. As more molecules and more fossils get added to the analysis, the tree keeps changing. That is not saying that this tree isn't correct. I only mean to point out that what appears to be a really cool story here may end up being very different, though no less cool.

By c-serpent (not verified) on 02 Apr 2009 #permalink

Venom? Pshaw! Who needs venom when the very visage of a creature is enough to promote fevered dreams that drive animals howling mad accompanied by the discordant sound of blind, idiot flute players piping insanity at the heart of all chaos?

Iä! Iä!

. . . 'course, venom is certainly an added bonus . . . .

No kings,

Robert

By Desert Son (not verified) on 02 Apr 2009 #permalink

What I would like to know is how the data about venomous proteins can be interpreted to deduce common descent. Since a lot of factors can give rise to convergent use of a protein, common descent seems a bit hard to point out. How does one even approach such a problem?

The evolutionary explanation for the convergence of these proteins is amazingly elegant: these venomous little bastards didn't have to evolve anything particularly new, they just had to play around a bit with what metazoans already have.

Shalom from Israel,
Freidenker.

I think it's really cool that venoms only work because all cellular processes have a common ancestor and therefore work fundamentally the same.

You can't have a poisonous anything if the proteins in the venom don't work in or on your metabolism!

Although of course there are exceptions to everything, notably the presence of cyanide in almonds (oh there I go again!)

Thanks, Robert -- I think every thread should have at least one Lovecraft reference!

Supercool.

Not sure if animals co-opt each others' venom in the same way, anyone know of an example?

Nudibranchs eating Portuguese Men O'War, and using their venom for themselves. Other sea slugs "recycle" anemone venom for their own protection.

Actually, this example has been used by creationists arguing that it's all "just too complex," oblivious to the fact that the most straightforward explanation for the existence of venom, then co-option of that very venom by the predator, is evolution.

Arguing that god gave anemones and Portuguese Men O'War for their protection, and then to give sea slugs the ability to eat them anyway, and to use the poor anemones' venom for themselves, gives us a god as sensible as Behe's god who gave P. falciparum humans to parasitize, then gave us defenses against god's little pathogens, but had the foresight to make sure that malaria could evade many of our defenses so that they can still kill little children.

Gee, it's funny how design always ends up doing what evolution is expected to do. But it's all too complex to evolve, so the purposeless arms races in the biological realm must have been designed.

Glen D
http://tinyurl.com/6mb592

Pay attention, all you boys 'n
Girls, and stay away from poison!
Toxic proteins work for me,
Because I use a pen, you see.
This poison poet always mocks in
Toxic ink, or inky toxin.
(That line appears intoxicated;
Maybe I'm just addle-pated.)
I think up verses, then I pen 'em,
Dripping with my protein venom.

I bite, or write; my victims curse.
Remember, poison could be verse!

Not sure if animals co-opt each others' venom in the same way, anyone know of an example?

There are probably insects that do it. One example I know is a snake that eats toads and sequesters the toad toxins in special "glands" on the snake's back.
Here's the article.

By Sven DiMilo (not verified) on 02 Apr 2009 #permalink

So, would bile be a form a venom without a delivery method?
I like the idea of being venomous outside of language usage. ;)

Hopefully I am not repeating anyone here, but what strikes me really cool about all this is the selection of a toxic (as an overdoes) protein that is difficult if not impossible to evolve against. If the venom protein was some purely toxic material that did NOT have a valid function in the target's body, then the target could evolve a defense against the toxin. But the target needs the toxic protein (in the correct amounts) so there is a reverse pressure to maintain the a sensitivity to the toxin because it plays a role in the target under normal circumstances.

Thus, this is an excellent indication that evolution took place because it is a toxin overdose for which immunity will be nearly impossible to develop.

Extra cool!

By And-U-Say (not verified) on 02 Apr 2009 #permalink

Nudibranchs eating Portuguese Men O'War, and using their venom for themselves. Other sea slugs "recycle" anemone venom for their own protection.

A bit different because the nudibranchs are co-opting whole cells (the cnidocytes) rather than the chemical toxin per se. But obviously a similar strategem and very cool anyway.

By Sven DiMilo (not verified) on 02 Apr 2009 #permalink

Here's the first 'graph of the snake article I linked above, with more examples:

Many invertebrates sequester dietary toxins for use in their
own defense (1–4), including such classic cases as milkweed
insects (4) and sea slugs (1). However, vertebrate examples
of toxin sequestration, especially from vertebrate prey, are rare.
The brilliantly colored neotropical poison frogs (Dendrobatidae),
their Malagasy analogues (Mantellidae), and a few other
anurans sequester defensive alkaloids from arthropods (5–11);
the same is suspected for two genera of New Guinean birds (12).
Accumulation of defensive toxins from vertebrate prey is known
only from some populations of gartersnakes (Thamnophis sirtalis),
which may incur a defensive advantage because of the
transitory storage of tetrodotoxin from ingested newts (13).

By Sven DiMilo (not verified) on 02 Apr 2009 #permalink

@Merrydol: Thanks a bunch for the input on plant deterrents. Do you happen to know if anyone's addressed this specific issue of plants evolving mechanisms to reduce herbivory by attacking appetite? I've been looking for something on the subject for ages.

Thing is - it seems to me that if such a situation exists (in which plants want to limit, rather than prevent, herbivory by large animals in order to benefit from their nitrogenous wastes), and they are doing this in some cases by attacking appetite, then it could lead to some interesting predictions:

  • * The physiological effect needs to be more subtle than would be achieved by straight poison. They have to carry out a biochemical adjustment on the herbivore
  • * That adjustment might include: putting the animal into an adrenergic stage (which shuts down appetite); inducing vomiting; confusion; local anaethesia; soporifics; and a variety of gastric irritants, etc.
  • * Many of the true 'medicinal' plants seem to do these very things.
  • * The effect, being subtle, may have benefits in some disease situation and in controlled doses.
  • * Of course, a mechanism that was somehow specific to appetite without extraneous effects would be the most efficient. The fact that no such 'clean' appetite suppression is found (that I know of, anyway)suggests that the animals long since evolved protection systems for their hunger - precisely to protect themselves.
  • * Which suggests that the current search for such a side-effect-free appetite suppressant to help the obesity epidemic has a hard task ahead of it.

I'm sure that if these rambling are correct, I'm not the first person to come up with them. But I've never seen anything that discusses the matter. So - are my notions all stoopid or wot?

CD

By Chris Davis (not verified) on 02 Apr 2009 #permalink

@39: Convergence means that the proteins _aren't_ being used by very different animals because the common ancestor had them, but because they're handy. Among the lizards/serpents we have one nested heirarchy of common descent in venom protein use, among the cephalopods we have another heirarchy, but the use of the same classes of protein by the two groups is a convergence.

By Stephen Wells (not verified) on 02 Apr 2009 #permalink

Thanks for the interesting post. Love to see more like this (and maybe a little less about God).

Nice, thanks Glen and Sven (congrats on the Molly, btw).

As I understand the plant poison bit, plants are in an evolutionary arms race with small herbivores: mites, insects, nematodes, etc. Small herbivores tend to focus on a small array of food plants. I doubt there is any plant so poisonous that some small herbivore is not specialized on eating it.

On the other hand, large herbivores tend to be more generalists and have a number of low level antipoison devices. I have Hippeastrum plants, which are poison, in my yard. Deer, when times are hard, will eat them. They will eat an inch of leaf tonight, and another inch of leaf tomorrow night.

By Jim Thomerson (not verified) on 02 Apr 2009 #permalink

An excellent article but another small quibble: venomous snakes aren't necessarily poisonous and poisonous snakes aren't necessarily venomous.

Re: Cone snails and cephalopods. Toxins have more components than the protein ones the study discusses, there are chemical toxins in there too. For eg mu-conotoxin strongly binds voltage gated sodium channels in skeletal muscle (tetrodotoxin from pufferfish has the opposite specificity, it binds most tightly to channels in nerve rather than muscle). IIRC the blue ringed octopus has a toxin similar to mu-conotoxin. There's more than one way to kill something and proteins are just part of the lethal toolbox, and the most easily analysed. To do the chemical ones you have isolate and analyse the components of the synthesis pathway, in the creature or their bacterial symbionts . . .

By Peter Ashby (not verified) on 02 Apr 2009 #permalink

Conotoxins are peptides, essentially small proteins. The blue-ringed octopus has tetrodotoxin of bacterial origin. But your real point is valid; not all "venoms" are peptides.

By Sven DiMilo (not verified) on 02 Apr 2009 #permalink

@Jim Thomerson #54: Yeah, that was one of the things that set me thinking about this. I live on a farm, and the field next to my house had a grove of small willows growing on it, which the farmer hoped to sell as fuel to an eco power station.

The idea fell through, and they moved some cows onto the field instead. They rapidly grazed all the grass and small plants, but before bringing in feed the farmer waited until they were hungry enough to start on the willows. "They don't loike 'em, but they'll eat 'em if they're 'ungry,' he told me. It suddenly struck me what salicin might be for...

By Chris Davis (not verified) on 02 Apr 2009 #permalink

Samphire: Yes, Stephen Fry mentioned this in a recent episode of QI, asking the panel to name "poisonous" snakes. Cue the alarm bells!

According to Fry, poisonous means it is deadly if eaten, as opposed to venomous which kills you with - well, venom!

Logical, I suppose.

By Elwood Herring (not verified) on 02 Apr 2009 #permalink

This is such a great paradigm for a well-written researchblogging article!

Hopefully I am not repeating anyone here, but what strikes me really cool about all this is the selection of a toxic (as an overdoes) protein that is difficult if not impossible to evolve against. If the venom protein was some purely toxic material that did NOT have a valid function in the target's body, then the target could evolve a defense against the toxin. But the target needs the toxic protein (in the correct amounts) so there is a reverse pressure to maintain the a sensitivity to the toxin because it plays a role in the target under normal circumstances.

Thus, this is an excellent indication that evolution took place because it is a toxin overdose for which immunity will be nearly impossible to develop.

Extra cool!

And I think this comment by And-U-Say (#47) makes one of the more astute observations of this example of evolutionary cooption.

Very cool indeed!

Posted by: Merrydol @ 36 "Yeah, blf, there are similar mechanisms. In fact, the monarch tastes so bad because it accumulates distasteful metabolites by feeding on its distasteful host plant, essentially stealing the toxins. ...?"

Monarchs don't just taste bad. When I was at uni, a while ago, my honors supervisor told a group of us a story of when she was doing a study on monarchs. She had to carry 9 butterflies somewhere and gently slotted their closed together wings between each of her fingers and the last one carefully between her lips. By the time she got them to where she wanted her lips were numb.

By Katkinkate (not verified) on 02 Apr 2009 #permalink

Interesting paper.

oh wow, fascinating stuff. I like the concept of defense (or attack) mechanisms that don't get evolved against. never ocurred to me that it might be of evolutionary advantage to have an opponent adapt slower.

"taking what already exists and tinkering and reshaping it to better fulfill a useful function" != Directed by any intelligent/magical/mystical/ephemeral entity.

I know what you mean, but surprisingly, there are some people who will leap on any metaphor that may promise to add support to their crackpot beliefs.

My favorites are still the sea snails; many gorgeous conchs in the tropics are deadly. I've been lucky enough only to ever pick up empty shells as a kid (or shells with hermit crabs) - some old timers confirmed that there were indeed deadly snails in the areas I'd been to; I wish the locals would tell me that sort of thing without me asking.

By MadScientist (not verified) on 03 Apr 2009 #permalink

A lot of plants contain nasty tasting things to repel herbivores:
Brocoli for example !

Love your blog, love the paper and the community of interested and intelligent commenters is a credit to you and your writing! keep up the good work!

m

In regard to PZ’s comments:

“So something like CRISP (Cystein RIch Secretory Protein) is common to all, but only the most refined predators add PLA2 (Phosopholipase A2) to the mix.”

and

“First, evolution doesn’t just invent something brand new on the spot to fill a function — what we find instead is that existing proteins are repurposed to do a job. This is how evolution generally operates, taking what already exists and tinkering and reshaping it to better fulfill a useful function.”

Yes, this is the big dilema for your failed theory. Where did the existing and/or added proteins come from?

For PZ’s (and Dawkin’s) problematic explanation for the origin of an eye, go to Example #2 & #3:
http://www.whoisyourcreator.com/how_does_evolution_occur.html

“Professing themselves to be wise, they became fools …”
- Romans 1:22

I'm wondering about the platypus, where does it fit in?

Wait, there are venomous mammals?

Since octopi and cuttlefish are so amazing, it stands to reason that they're not just venomous, their venom has the broadest range of toxins listed. Killing sharks, opening bottles, fitting through tiny holes, flashing like neon signs, mimicking anything and everything; is there anything they *can't* do?

Yes, this is the big dilema for your failed theory. Where did the existing and/or added proteins come from?

Duplication. Insertion. Deletion. Exon shuffling. Point mutations. Horizontal transfer.

What is a "dilema"?

By Sven DiMilo (not verified) on 03 Apr 2009 #permalink

Sven DiMilo,
re: urine on stings #10
Urea is not very high in human urine, I think around 5 mM. The amount of urea needed to denature a protein is quite substantial (depending on the protein). High concentrations (6-8 M) are used to get a mixture of proteins to precipitate.

Good point ray. Blood urea is 2-5 mM, and the kidneys concentrate it quite a bit, but not to 6 M, that's for damn sure.
Guess in that case I doubt that peeing on a sting does anything that water wouldn't.

By Sven DiMilo (not verified) on 05 Apr 2009 #permalink

If anyone would like a copy of the article, feel free to email me for it (bgf AT unimelb.edu.au)

The journal changed the box view and I didn’t catch it in the proofs. Insects were supposed to be divided into three layers in the one box: bristle, probiscis and stinger. These each represent independent evolution of venom within the insects. And the use of the probiscis to deliver venom is something that almost certainly has been convergently utilised on several occasions but it was beyond the scope of this article to go into that. We do, however, have a very lengthy article coming out soon(ish) in Annual Review of Genomics and Human Genetics in which we explore this in greater detail. The abstract for the ARGHG article is as follows:

Convergently recruited proteins were compared from the venoms of centipedes, cephalopods, cone snails, fish, insects (e.g. ants, bees, Lonomia caterpillars, wasps), platypus, scorpions, shrew, spiders, toxicoferan reptiles (lizards and snakes) and sea anemones. Proteins types that have been convergently recruited into disparate venoms are AVIT/Colipase/Prokineticin, CAP, Chitinase, Cystatin, Defensins, Hyaluronidase, Kunitz, Lectin, Lipocalin, Natriuretic, Peptidase S1, Phospholipase A2, Sphingomyelinase D and SPRY. Many of these same venom protein types have also been convergently recruited for use in the hematophagous gland secretions of bloodmeal-feeding invertebrates (e.g. fleas, leeches, kissing bugs, mosquitos, ticks) and vertebrates (Vampire Bats). We discuss a number of overarching structural, functional and evolutionary generalities of these protein families from which toxins have been frequently recruited and propose a revised and expanded working-definition for venom. Given the large number of striking similarites between the protein compositions of conventional venoms and hematophagous secretions, we argue that the latter should also fall under the same definition.

Cheers
Bryan

Posted by: Hendi | April 3, 2009 7:27 AM

A lot of plants contain nasty tasting things to repel herbivores:
Brocoli for example !

Don't be cute!
Broccoli is tasty. At least to this omnivore.
Brussel sprouts on the other hand bring back olfactory memories of when changing nappies on my sons when they were babies.