mayko
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Molecular Evolution Thread
You heard me.
Post your favorite tales of the genome over deep time.
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Convergent evolution of antifreeze glycoproteins in Antarctic notothenioid fish and Arctic cod
Liangbiao Chen, Arthur L. DeVries, and Chi-Hing C. Cheng
Proc Natl Acad Sci U S A. 1997 April 15; 94(8): 3817–3822.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC20524/
Evolution of antifreeze glycoprotein gene from a trypsinogen gene in Antarctic notothenioid fish.
Chen L, DeVries AL, Cheng CH.
Proc Natl Acad Sci U S A. 1997 Apr 15;94(8):3811-6.
http://www.ncbi.nlm.nih.gov/pubmed/9108060
So I have been reading these papers; there was also a very good bit in Sean B. Carroll's The Making of the Fittest about it. The story is
rather fascinating.
So the story dates back to the opening of the Drake Passage between South America and Antarctica. This led to the circumpolar current, which insulated
and ultimately froze the continent.
The freezing temperatures meant that fish had to adapt so that they would not freeze when they ingested nucleating ice crystals from their
environment.
What happened? Gene duplication, a common mechanism of new gene formation. A gene for trypsinogen was duplicated, then it mutated, losing introns and
exons and duplicating a repetitive sequence through a process called http://en.wikipedia.org/wiki/Slipped_strand_mispairing.
The result was a gene for repetitive Alanine/Threonine proteins, separated by spacers. A saccharide is added posttranslationally, resulting in AFGP:
AntiFreeze GlycoProtein. That's right: the fish freakin evolved themselves an antifreeze molecule which binds to and inactivates ice crystals!
What's more, fish in the Arctic have also discovered this protein. They did so independently, an example of convergent evolution. How do we know? The
Threonine/Alanine motif is the same, but they have different spacers! I even just ran across this paper which suggests that the gene sequence can be
used to infer descent.
Functional antifreeze glycoprotein genes in temperate-water New Zealand nototheniid fish infer an Antarctic evolutionary origin.
Cheng CH, Chen L, Near TJ, Jin Y.
Mol Biol Evol. 2003 Nov;20(11):1897-908. Epub 2003 Jul 28.
http://www.ncbi.nlm.nih.gov/pubmed/12885956
Pretty zany!
al-khemie is not a terrorist organization
"Chemicals, chemicals... I need chemicals!" - George Hayduke
"Wubbalubba dub-dub!" - Rick Sanchez
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mayko
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Dramatic variation of the vomeronasal pheromone receptor gene repertoire among five orders of placental and marsupial mammals
Wendy E. Grus, Peng Shi, Ya-ping Zhang, and Jianzhi Zhang
10.1073/pnas.0501589102
PNAS April 19, 2005 vol. 102 no. 16 5767-5772
http://www.pnas.org/content/102/16/5767.long
So pheremones are these special class of odorant which are picked up by the vomeronasal or Jacobson's organ. There, a specialized class of receptor proteins coded for by two superfamilies of genes, V1R an V2R.
Gene families, including the vomeronasal receptor genes and other olfactory receptor genes, undergo a sort of evolution called birth and death evolution, wherein new members of the gene family are constantly appearing via gene duplication and diversification, survive for a
while, then are converted into pseudogenes by mutation and persist as genetic fossils.
As you might expect, some mammals, such as mice, have a lot of genes. What is a little unusual about the human genome is that we have a significant
number of genes in the V1R family, about 200. That's more than dogs, rats, cows, and opossums... HOWEVER, all but four of those genes have mutated
into dysfunctionality in humans. Of the mammalian V1R repertoires studied, we have the smallest percentage of functional genes. And indeed, human
Jacobson's organs are vestigial and probably non-functional.
The authors of the paper don't know why rodents should have a relatively higher number of functional (or total) genes, compared to other mammals.
However, the psuedogenization event which wiped out human V1R genes may have had something to do with the evolution of primate vision and its
replacement of pheremonal signals in mating.
al-khemie is not a terrorist organization
"Chemicals, chemicals... I need chemicals!" - George Hayduke
"Wubbalubba dub-dub!" - Rick Sanchez
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mayko
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A slightly different class of chemoreceptor genes...
Niimura, Y., & Nei, M. (2007). Extensive gains and losses of olfactory receptor genes in mammalian evolution. PloS one, 2(8), e708.
doi:10.1371/journal.pone.0000708
Vertebrate olfactory receptors (ORs) are proteins that detect odor molecules in the environment. OR genes form the largest multigene family in
vertebrates, but the numbers are variable and many members are pseudogenes. Humans have ~800 OR genes but ~50% are pseudogenes, whereas mice have
~1400 such genes and 20-25% are pseudogenes. There are thus ~2.7 times more functional OR genes in mice than in humans. The genes are scattered in
clusters across the genome. Although the count number of OR genes differ between mice and humans, their genomic organization is conserved. Some gene
families have expanded and some have been lost in the tetrapod lineage; OR genes appear to undergo birth and death evolution.
8 mammal species were compared, including a monotreme and a marsupial. The primates and platypi have considerably fewer OR s. They estimate the genome
for the ancestral species at each evolutionary branching using parsimony principle. The mammalian OR genes are classified into Class I and Class II
genes, the latter of which have many subclades. Some of these clades have undergone dramatic additions and losses, while others have been
evolutionarily stable, but “dynamic change of the number of OR genes was the general rule.”, including a simultaneous gain of 416 genes to the
rodent order and loss of 290 genes to the primate order after their divergence (Fig 2). Gene birth and death is such that although mammal species may
have similar numbers of genes, the gene repertoires are highly variable. Similar order-specific expansions and contractions reported for other sensory
receptor genes.
Why do OR genes vary so much? Adaptation? Trichromatic vision in primates? Semiaquatic lifestyle of platypus and electrosensory organ? Dynamic
expansion of OR genes during terrestrial adaptation. Results suggest that expansion continued until ~100 myears ago.
The brain is as important as the sensory organ; could human brain expansion make up for reduced OR repertoire? Why is the OR family stable in
Drosophila but unstable in mammals – difference in expression mechanics?
al-khemie is not a terrorist organization
"Chemicals, chemicals... I need chemicals!" - George Hayduke
"Wubbalubba dub-dub!" - Rick Sanchez
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mayko
International Hazard
Posts: 1218
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Modern chemistry has given a vast arsenal of biocidal compounds to humans, with mixed results. Dosed with insecticide, what's a poor mosquito to do?
Weill, M., Lutfalla, G., & Mogensen, K. (2003). Comparative genomics: Insecticide resistance in mosquito vectors. Nature. Retrieved from
http://www.nature.com/nature/journal/v423/n6936/abs/423136b....
One possibility is for the population to adapt such that the insecticide's target changes. A toxin often interferes with some target enzyme; for
example, organophosphates like Malathion inactivates the enzyme acetylcholinesterase. This is a molecule which degrades acetylcholine, an important
neurotransmitter involved in muscular signaling. Without the degradation enzyme, the neurotransmitter will build up in the synapses, essentially
locking the nerve signal in the 'on' position; this is why the closely related organophosphate nerve agents cause the twitching, convulsing reaction in humans, ultimately paralyzing the lung muscles and causing death. (By
contrast, the tropane alkaloid atropine targets and inactivates the acetylcholine receptor, blocking the 'on' signal; while organophosphates kill by
overexcitation, the acetylcholinergics kill by overrelaxation. However, because they work in opposite directions, atropine is used to treat organophosphate poisoning)
So you're a population of Anopheles mosquitoes. You get sprayed with Malathion. Some of you die. Some of you live. But here's the twist: most of the
mozzies have mutations of one sort or other, and a few of the mozzies have a specific mutation in their acetylcholinesterase gene, a single nucleotide
replacement, where GGC has flipped to AGC, thus changing a glycine residue in the enzyme to a serine. This residue happens to be near the active site
of the acetylcholinesterase, thus the change modulates its activity and its sensitivity to organophosphate insecticide.
Only a small percentage of the original population might have this particular mutation, but after the spraying, their frequency increases -
because individuals lacking that mutation are preferentially poisoned. And if you keep spraying willy-nilly, perhaps as part of a poorly thought out
agricultural program, one thing leads to another, and soon Darwinian magick has been worked and your pesticide loses its effectiveness.
It's not just organophosphates. Organochlorines have seen resistance evolve against them as well.
Daborn, P., Yen, J., Bogwitz, M., & Goff, G. Le. (2002). A single P450 allele associated with insecticide resistance in Drosophila.
Science. Retrieved from http://www.sciencemag.org/content/297/5590/2253.short
DDT operates on sodium ion channels in insect neurons; it causes them to fire spontaneously, leading to convulsions and death. Like the mutation to the
acetylcholinesterase, mutations to the sodium ion channel protein can confer resistance.
However, there is another possibility which they also exploit: secretion of degradation enzymes to break down the poison before it can do its damage.
And indeed, among Drosophila fruit flies resistant to DDT, there was found overexpression of a cytochrome gene whose enzyme product is involved in toxin metabolism. Unlike the traditional mutation we saw in the organophosphate resistance,
this adaptation occurred because a transposable element, presumably carrying a promoter, inserted itself upstream of the cytochrome gene.
A surprise from this particular study was that the resistance did not appear to carry any particular fitness cost: even in the absence of selection,
it persisted in laboratory populations for years.
Müller, P., Warr, E., Stevenson, B. J., Pignatelli, P. M., Morgan, J. C., Steven, A., … Donnelly, M. J. (2008). Field-caught
permethrin-resistant Anopheles gambiae overexpress CYP6P3, a P450 that metabolises pyrethroids. (D. L. Stern, Ed.)PLoS genetics, 4(11), e1000286.
doi:10.1371/journal.pgen.1000286
Permethrin is another sodium-channel targetting organochlorine compound, and guess what? Mozzies have figured out the cytochrome trick too.
Evolution is more than a theoretical abstraction: all of this has very real consequences. Misuse of DDT as a general agricultural chemical fueled
preexisting mosquito resistance in Sri Lanka during the 1960's; by the time a malaria epidemic struck in the early 70's, the insecticide was useless as a public health measure and they had to switch to more expensive alternatives.
al-khemie is not a terrorist organization
"Chemicals, chemicals... I need chemicals!" - George Hayduke
"Wubbalubba dub-dub!" - Rick Sanchez
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