Selection for rapid embryo development correlates with embryo exposure to maternal androgens among passerine birds.

SCHWABL, H.; PALACIOS, M. G.; MARTIN, T. E.

AMERICAN NATURALIST

UNIV CHICAGO PRESS

Año: 2007 vol. 170 p. 96 - 106

0003-0147

Greater offspring predation favors evolution of faster development among species. The proximate mechanisms underlying evolved variation in rate of development are unknown. We hypothesized that greater offspring predation exerts selection on mothers to deposit increased levels of anabolic androgens in egg yolks to achieve faster development. Here, we tested if: a) increased offspring predation was associated with increased concentrations of androgens in egg yolks of passerine species, and b) increased levels of androgens were associated with faster embryo and nestling development. We examined three androgens that increase in potency along the androgen synthesis pathway: androstenedione (A4) < testosterone (T) < 5á-dihydrotestosterone (5á-DHT). Order of potency differs along other (e.g., estrogenic) pathways, thereby allowing examination of the relative importance of the three androgens and possible effect pathways. Concentrations of none of these steroids were related to clutch size; only A4 was allometrically related to egg volume. Species that experience greater predation rates showed higher concentrations of T and 5á-DHT in their yolks. Higher concentrations of T and particularly 5á-DHT were strongly correlated with faster development during the embryonic period and less so during the nestling stage, suggesting that androgens act most strongly early in development. Development rates were most strongly correlated with 5á-DHT, suggesting that potency of androgens and strength of their effects on development increases along the androgen synthesis pathway and is mediated by the androgen receptor pathway. These results are consistent with the hypothesis that selection for faster development by time-dependent offspring mortality may be achieved epigenetically by varying embryo exposure to maternal anabolic steroids.