Tri-nucleotide CAG repeat number in the androgen receptor gene as a mechanism for inter-specific variation of sexual dimorphism in primates

Evolutionary models of sexual dimorphism link increased male size to male-male competition, while female size is tied to the nutritional requirements of reproduction. Molecular correlates of this model have not been explored. The androgen receptor gene, located on the X chromosome, mediates male reproductive development. Mutations of this gene interfere with virilization suggesting that this gene may be linked to the evolution of primate sexual dimorphism. A genetic mechanism for the evolution of dimorphism must account for the continuous inter-specific variation of dimorphism. Expansion of the tri-nucleotide CAG repeat in the androgen receptor gene is a possible mechanism for modulating dimorphism among primate species. The androgen receptor gene was sequenced from a convenience sample of Catarrhine primates including chimpanzee (n=6) gorilla (n=3), orangutan (n=l), gibbon (n=l), baboon (n=4), and macaque (n=3). The index of dimorphism was calculated as mean female weight divided by mean male weight for the species. Results show a negative correlation between repeat expansion and this index of dimorphism. This finding is consistent with a role for the expansion of this simple sequence repeat in the evolution of primate sexual dimorphism. Directional evolution toward an expanded CAG repeat has been proposed elsewhere. However, the causal link between the expanded tri-nucleotide repeat and several neuro-degenerative diseases indicates that excessive expansion has deleterious effects. One of the attractive features of this hypothesis is that it provides a genetic mechanism underlying variation in sexual dimorphism among species.