The Economist — IT IS not often that biologists have a chance to watch natural selection in action. The best-known cases—the evolution of resistance to antibiotics in bacteria and to pesticides in insects—are responses to deliberate changes people have made in the environment of the creatures concerned. But mankind has caused lots of accidental changes as well, and these also offer opportunities to study evolution.
Recently, two groups of researchers, one at New York University (NYU) and the other at the Woods Hole Oceanographic Institute in Massachusetts, have taken advantage of one of these changes to look at how fish evolve in response to environmental stress. The stress in question is pollution by polychlorinated biphenyls (PCBs). These chemicals—widely used in the middle decades of the 20th century to manufacture electrical insulation, coolants, sealants and plasticisers—often ended up dumped in lakes, rivers and coastal waters. Eventually, such dumping was banned (in America, this happened in 1977). But PCBs are persistent chemicals, and their effects are felt even today. In particular, they disrupt the immune systems of animals such as fish, cause hormonal imbalances and promote tumours.
As is the way of evolution, however, some fish species have developed resistance to PCB poisoning. Isaac Wirgin, at NYU, and Mark Hahn, at Woods Hole, have been studying PCB-resistant fish, to see how they do it. After that, the two researchers will be able to look at how these populations evolve yet again as the environment is cleaned up.
The species of interest to Dr Wirgin is the Atlantic tomcod of the Hudson river in upstate New York. Part of the Hudson was polluted with PCBs by two General Electric plants. Dr Hahn is looking at a different animal, the killifish (pictured), in New Bedford harbour, Massachusetts, which was polluted by other producers. Both Hudson tomcod and New Bedford killifish are able to tolerate levels of PCB far higher than those that would kill such fish in cleaner waters. The question is, why?
PCBs do their damage by binding to a protein called the aryl hydrocarbon receptor, or AHR, thus stopping it working properly. AHR is a transcription factor, meaning that it controls the process by which messenger molecules are copied from genes. These messenger molecules go on to act as the blueprints for protein production, so preventing a transcription factor from working can cause all sorts of problems. Both Hudson tomcod and New Bedford killifish, however, have unusual AHR molecules. And it is this that seems to explain their immunity.
A protein is a chain of chemical units called amino acids. In tomcods, AHR is composed of 1,104 such units. Except that in Hudson tomcod it frequently isn’t. These fish generally have 1,102 amino acids in their AHRs. The two missing links in the chain (a phenylalanine and a leucine, for aficionados) are encoded in the gene for ordinary tomcod AHR by six genetic “letters” that are missing from the DNA found in PCB-resistant Hudson tomcod. The shortened version of AHR does not bind nearly so easily to PCBs. It still, however, seems to work as a transcription factor. The result is fish that are more or less immune to PCB poisoning. (11/03/11)