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We normally think of evolutionary change, such as that underlying differences between species of mammals, occurring over many tens of millions of years. Even 'rapid evolution', exemplified by the diversity that defines us as human individuals, occurs over tens or hundreds of thousands of years. But the extreme changes in dog morphology that have taken place over the last 150 years are exceptionally fast by normal evolutionary standards. What mechanism would allow for such accelerated change? One school of thought holds that adaptation occurs primarily through selection for single–base pair changes. Because these mutations tend to occur relatively infrequently, however, it seems unlikely that they could underlie the rapid changes in the dog. Another school of thought favors mutations in regulatory regions, leading to changes in levels and tissue specificity of gene expression, as means for rapid shifts in evolution.

Now, John Fondon and Harold Garner of the University of Texas at Dallas report evidence for selection acting on tandem repeats ( Sturtevant, A. H.Proc. Natl. Acad. Sci. USA 101, 18058–18063; 2004). Tandem repeats are plentiful, contributing to 3% of the human genome, and occur more frequently, 105 times as often as single-point mutations. Selection acting on this class of mutations may, therefore, explain a faster rate of evolution. Fondon's study examined variation in tandem-repeat length in 142 dogs, including 92 domesticated breeds. The authors sequenced 37 repeat regions of 17 genes homologous to human and mouse genes involved in development and found significant variation in the number of repeats, correlated to several morphological phenotypes. This may not reflect typical evolution in the wild, particularly because domesticated dogs have undergone intensive artificial breeding selection for traits desirable to their owners, including morphological changes.

Most of the tandem repeats analyzed were located in coding regions. Although the function of these changes in repeat length remains to be explored, previous studies have shown that repeat expansions or contractions can cause either loss of function or hypomorphic alleles. In the human genome, expansion of triplet repeats has been associated with several hereditary neurological diseases, including fragile X syndrome, Huntington disease, myotonic dystrophy and spinocerebellar ataxia. The function of repeat expansion or contraction in disease, as well as the relative prevalence and importance of tandem repeats compared with other types of mutations, are important questions to address in future studies in this emerging field.