Sex Reversal in Birds

Abstract

Sexual differentiation in birds is controlled genetically as in mammals, although the sex chromosomes are different. Males have a ZZ sex chromosome constitution, while females are ZW. Gene(s) on the sex chromosomes must initiate gonadal sex differentiation during embryonic life, inducing paired testes in ZZ individuals and unilateral ovaries in ZW individuals. The traditional view of avian sexual differentiation aligns with that expounded for other vertebrates; upon sexual differentiation, the gonads secrete sex steroid hormones that masculinise or feminise the rest of the body. However, recent studies on naturally occurring or experimentally induced avian sex reversal suggest a significant role for direct genetic factors, in addition to sex hormones, in regulating sexual differentiation of the soma in birds. This review will provide an overview of sex determination in birds and both naturally and experimentally induced sex reversal, with emphasis on the key role of oestrogen. We then consider how recent studies on sex reversal and gynandromorphic birds (half male:half female) are shaping our understanding of sexual differentiation in avians and in vertebrates more broadly. Current evidence shows that sexual differentiation in birds is a mix of direct genetic and hormonal mechanisms. Perturbation of either of these components may lead to sex reversal.

Sex determination and gonadal sex differentiation in the chicken model

“…These findings are consistent with the finding that sexually dimorphic gene expression in chicken embryos can occur prior to the time of gonadal sex differentiation and hence predate any sexually dimorphic hormonal output (Ayers et al, 2013a, Lin et al, 2010, Major and Smith, 2016, O'Neill et al, 2000, Scholz et al, 2006, Zhang et al, 2010, Zhao et al, 2010. In a comparable experiment to that of Zhao et al, Maekawa et al, (2013) switched primordial brains between ZZ and ZW chicken embryos before gonadal sex differentiation (and vice versa) and raised birds to sexual maturity.…”

Two Doublesex1 mutants revealed a tunable gene network underlying intersexuality in Daphnia magna

“…Although sexual dimorphism can make male and female appear like two unrelated species, at genetic level, they differ only in genes on sex chromosome as in genetic sex determining species, or even in minuscule level if any as in environmental sex determining species. This similarity of genome between male and female may explain that sex change can happen naturally in several species [31,32]. These molecular and physiological evidence demonstrates that although sexual ambiguity is uncommon, it is a very natural manifestation of the genome and thus treating intersexes not as outliers but as an undeniable part of the population is very important.…”

Logical modelling uncovers developmental constraints for primary sex determination of chicken gonads

“…In mammals, sex determination results from two consecutive processes: (i) primary sex determination , which refers to the development of bi-potential gonads towards either male (testis) or female (ovary) pathways; and (ii) secondary sex determination , which refers to the development of the sexual dimorphic structures, directed by sex hormones produced in the differentiated gonads [ 13 , 14 ]. Sex reversal can be experimentally induced in chickens by oestrogen administration or production disturbance, indicating a role of this hormone in avian sex determination [ 15 ]. Vertebrate bi-potential gonads—along the evolutionary transition from lower to higher vertebrates—seem to display a gradual resistance to sex hormones.…”

“…Vertebrate bi-potential gonads—along the evolutionary transition from lower to higher vertebrates—seem to display a gradual resistance to sex hormones. Indeed, gonadal sex differentiation in fish [ 16 ] and amphibians [ 17 ] is generally susceptible to androgens and oestrogens; in reptiles [ 18 ], birds [ 15 ] and marsupials [ 19 ]; it is susceptible to oestrogens but not to androgens, whereas in eutherian mammals, gonadogenesis is resistant to hormone treatment [ 20 ].…”