Chemoreceptors are the primary interface of most organisms to their chemical environment. In animals, the chemoreceptor repertoire is particularly impressive, often including more than a thousand distinct genes. These genes encode multipass G-protein coupled receptors (GPCRs) that are expressed predominantly in specialized chemosensory neurons, such as olfactory and gustatory sensory neurons in mammals.
The nematode chemoreceptor superfamily
Worm Book Chapter (review)
Given their tiny organism size, the number and diversity of putative chemoreceptors in C. elegans and other closely related species is nothing less than astounding. In C. elegans, where estimates are most accurate, there are approximately 1,800 genes that potentially encode chemoreceptors, making them the largest gene superfamily. Perhaps 1/4 or so of these genes are defective in the sequenced N2 strain.
Table of families
Superfamily classification tree (huge, suggest downloading to view)
Most or all of the chemoreceptor families are subject to the process called birth-death evolution. New genes are born by duplication of existing genes, followed by gradual divergence of the two initially identical copies. Concurrently, existing genes are functionally lost via loss-of-function mutations and eventually are deleted from the genome altogether. The fact that the number of existing genes in each family is fairly stable over long periods of evolution indicates that the rates of birth and death are approximately equal (at least in the long term).
The process of gene birth balanced by death puts an interesting twist on the functional genetics interpretation of these genes. The simple idea interpretation is that any individual gene has a dispensable function, but the aggregate of genes have a critical function. This makes sense in terms of chemosensation if we imagine extensive functional overlap among closely related genes, perhaps both in ligand binding and in G-protein coupling.
This rather simple view has a number of important complications that I have not mentioned, including population diversity present at any particular moment in evolution, the relative rates of successful diversification and duplicate loss after an initial duplication event, and relationships among genetic drift, selection, and population size. None of these processes are well understood outside of mathematical models. We are actively interested in relating the sophisticated models describing these processes to the real patterns of duplication and loss that can be directly observed.
Thomas lab index page