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An experimental study on the causes of sex‐biased mortality in the black‐headed gull − the possible role of testosterone
Author(s) -
MÜLLER WENDT,
GROOTHUIS TON G. G.,
EISING CORINE M.,
DIJKSTRA COR
Publication year - 2005
Publication title -
journal of animal ecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.134
H-Index - 157
eISSN - 1365-2656
pISSN - 0021-8790
DOI - 10.1111/j.1365-2656.2005.00964.x
Subject(s) - flutamide , biology , testosterone (patch) , offspring , hatching , sexual dimorphism , medicine , endocrinology , androgen , physiology , in ovo , hormone , embryo , androgen receptor , ecology , pregnancy , genetics , prostate cancer , cancer
Summary1 During early development male offspring in avian species often suffer from enhanced mortality compared to female offspring. This has been attributed to different nutritional requirements, as sex‐biased mortality has been reported particularly in sexually size‐dimorphic species. However, other traits of the male phenotype, such as the embryonic hormone profile, have been suggested to contribute to this male disadvantage. In particular the negative effects of sex steroids on immune function may be causally involved. 2 We investigated the role of testosterone in the expression of male phenotype disadvantage through an experimental reduction of the availability of testosterone receptors by in‐ovo injection of an anti‐androgen (Flutamide©). Experimental nests contained a male and a female chick hatching from control treated eggs and a male and a female chick hatching from Flutamide treated eggs. 3 Male‐biased mortality occurred in control chicks at a stage where the sexes did not yet differ in their growth pattern, suggesting that sex‐specific nutritional requirements are not necessary for male‐biased mortality to occur. Control males and control females did not differ in their cell‐mediated immunity (CMI). This renders it unlikely that the observed skewed mortality was due to sex‐specific differences in the CMI. 4 Treatment of the eggs with flutamide antagonistically affected males and females. Flutamide treatment positively affected male development in particular through an enhanced growth rate, indicating that testosterone is involved in the expression of the male phenotype disadvantage. Female chicks hatching from Flutamide treated eggs were disadvantaged in growth and CMI. The possible pathways of this sex‐specific effect of Flutamide are discussed with regard to differential consequences of blocking the beneficial effects of maternal androgens and the interference with the process of sexual differentiation in males.