12) Darwin’s Galapagos finches
When Charles Darwin visited the Galapagos Islands, he recorded the presence of several species of finch that all looked very similar except for their beaks. Ground finches have deep and wide beaks; cactus finches have long, pointed beaks; and warbler finches have slender, pointed beaks, reflecting differences in their respective diets. Darwin speculated that all the finches had a common ancestor that had migrated to the islands. Close relatives of the Galapagos finches are known from the South American mainland, and the case of Darwin’s finches has since become the classic example of how natural selection has led to the evolution of a variety of forms adapted to different ecological niches from a common ancestral species — termed ‘adaptive radiation’. This idea has since been reinforced by data showing that even small differences in the depth, width or length of the beak can have major consequences for the overall fitness of birds.
To find out what genetic mechanisms underlie the changes in beak shape that mark each species, Harvard University’s Arhat Abzhanov and his colleagues examined numerous genes that are switched on in the developing beaks of finch chicks; their study was published in 2006. The researchers discovered that shape differences coincide with differing expression of the gene for calmodulin, a molecule involved in calcium signalling that is vital in many aspects of development and metabolism. Calmodulin is expressed more strongly in the long and pointed beaks of cactus finches than in the more robust beaks of other species. Artificially boosting the expression of calmodulin in the embryonic tissues that give rise to the beak causes an elongation of the upper beak, similar to that seen in cactus finches. The results show that at least some of the variation in beak shape in Darwin’s finches is likely to be related to variation in calmodulin activity, and implicates calmodulin in the development of craniofacial skeletal structures more generally.
The study shows how biologists are going beyond the mere documentation of evolutionary change to identify
the underlying molecular mechanisms.
Reference
Abzhanov, A. et al. Nature 442, 563–567 (2006).
Author websites
Clifford Tabin: http://www.hms.harvard.edu/dms/bbs/fac/tabin.html
Peter Grant: http://www.eeb.princeton.edu/FACULTY/Grant_P/grantPeter.html
13) Microevolution meets macroevolution
Darwin conceived of evolutionary change as happening in infinitesimally small steps. He called these ‘insensible gradations’, which, if extrapolated over long periods of time, would result in wholesale changes of form and function. There is a mountain of evidence for such small changes, called microevolution — the evolution of drug resistance, for instance, is just one of many documented examples. We can infer from the fossil record that larger species-to-species changes, or macroevolution, also occur, but they are naturally harder to observe in action. That said, the mechanisms of macroevolution can be seen in the here-and-now, in the architecture of genes. Sometimes genes involved in the day-to-day lives of organisms are connected to, or are even the same as, those that govern major features of animal shape and development. So everyday evolution can have large effects.
Sean Carroll from the Howard Hughes Medical Institute in Chevy Chase, Maryland, and his colleagues looked at a molecular mechanism that contributes to the gain of a single spot on the wings of male flies of the species Drosophila biarmipes; they reported their findings in 2005. The researchers showed that the evolution of this spot is connected with modifications of an ancestral regulatory element of a gene involved in pigmentation. This regulatory element has, over time, acquired binding sites for transcription factors that are ancient components of wing development. One of the transcription factors that binds specifically to the regulatory element of the yellow gene is encoded by engrailed, a gene fundamental to development as a whole.
This shows that a gene involved in one process can be co-opted for another, in principle driving
macroevolutionary change.
Reference
Gompel, N., Prud’homme, B., Wittkopp, P. J., Kassner, V. A. & Carroll, S. B. Nature 433, 481–487 (2005).
Additional resources
Hendry, A. P. Nature 451, 779–780 (2008).
Prud’homme, B. et al. Nature 440, 1050–1053 (2006).
Author website
Sean Carroll: http://www.hhmi.org/research/investigators/carroll_bio.html
14) Toxin resistance in snakes and clams
Biologists are increasingly coming to understand the molecular mechanisms that underlie adaptive evolutionary change. In some populations of the newt Taricha granulosa, for example, individuals accumulate the nerve poison tetrodotoxin in their skin, apparently as a defence against garter snakes (Thamnophis sirtalis). Garter snakes that prey on the newts that produce tetrodotoxin have evolved resistance to the toxin. Through painstaking work, Shana Geffeney at the Stanford School of Medicine in California and her colleagues uncovered the underlying mechanism; their study was published in 2005. Variation in the level of resistance of garter snakes to their newt prey can be traced to molecular changes that affect the binding of tetrodotoxin to a particular sodium channel.
Similar selection for toxin resistance apparently occurs in softshell clams (Mya arenaria) in areas of the North American Atlantic coast, as reported by Monica Bricelj at the Institute for Marine Biosciences in Nova Scotia, Canada, and her colleagues in the same issue of Nature. The algae that produce ‘red tides’ generate saxitoxin — the cause of paralytic shellfish poisoning in humans. Clams are exposed to the toxin when they ingest the algae. Clams from areas subject to recurrent red tides are relatively resistant to the toxin and accumulate it in their tissues. Clams from unaffected areas have not evolved such resistance.
Resistance to the toxin in the exposed populations is correlated with a single mutation in the gene that encodes a sodium channel, at a site already implicated in the binding of saxitoxin. It seems likely, therefore, that the saxitoxin acts as a potent selective agent in the clams and leads to genetic adaptation.
These two studies show how similar selective pressures can lead to similar adaptive responses even in very
different taxa.
References
Geffeney, S. L., Fujimoto, E., Brodie, E. D., Brodie, E. D. Jr, & Ruben, P. C. Nature 434, 759–763 ( 2005).
Bricelj, V. M. et al. Nature 434, 763–767 (2005).
Additional resources
Mitchell-Olds, T. & Schmitt, J. Nature 441, 947–952 (2006).
Bradshaw, H. D. & Schemske, D. W. Nature 426, 176–178 (2003).
Coltman, D. W., O’Donoghue, P, Jorgenson, J. T., Hogg, J. T. Strobeck, C. & Festa-Bianchet, M. Nature 426, 655–658 (2003).
Harper Jr, G. R. & Pfennig, D. W. Nature 451, 1103–1106 (2008).
Ellegren, H. & Sheldon, B. Nature 452, 169–175 (2008).
Author websites
Shana Geffeney: http://wormsense.stanford.edu/people.html
Monica Bricelj: http://marine.biology.dal.ca/Faculty_Members/Bricelj,_Monica.php
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