Quantitative genetics of sexual size dimorphism in the collared flycatcher, Ficedula albicollis

Abstract

Quantitative genetic theory predicts that evolution of sexual size dimorphism (SSD) will be a slow process if the genetic correlation in size between the sexes is close to unity, and the heritability of size is similar in both sexes. However, there are very few reliable estimates of genetic correlations and sex-specific heritabilities from natural populations, the reasons for this being that (1) offspring have often been sexed retrospectively, and hence, selection acting differently with respect to body size in the two sexes between measuring and sex identification can bias estimates of SSD; and (2) in many taxa, parents may be incorrectly assigned to offspring either because of assignment errors or because of extrapair paternity. We used molecular sex and paternity identification to overcome these problems and estimated sex-specific heritabilities and the genetic correlation in body size between the two sexes in the collared flycatcher, Ficedula albicollis. After exclusion of the illegitimate offspring, the genetic correlation in body size between the sexes was 1.00 (SE = 0.22), implying a severe constraint on the evolution of SSD in this species. Furthermore, sex-specific heritability estimates were very similar, indicating that neither sex will be able to evolve faster than the other. By using estimated genetic parameters, together with empirically derived estimates of sex-specific selection gradients, we further demonstrated that the predicted selection response in female tarsus length is displaced about 200% in the opposite direction from that to be expected if there were no genetic correlation between the sexes. The correspondence between the biochemically estimated rate of extrapair paternity (about 15% of the young) and that estimated from the 'heritability method' (11%) was good. However, the estimated rate of extrapair paternity with the heritability method after exclusion of the illegitimate young was 22%, adding to increasing evidence that factors other than extrapair paternity (e.g., maternal effects) may be responsible for the commonly observed higher mother-offspring than father-offspring resemblance.