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In the chick embryo, estrogen can induce chromosomally male ZZ left gonad epithelial cells to form an ovarian cortex, which supports oogenesis
Author(s) -
Silvana Guioli,
Debiao Zhao,
Sunil Nandi,
Michael Clinton,
Robin Lovell-Badge
Publication year - 2020
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.15
H-Index - 36
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.181693
Subject(s) - biology , ovarian cortex , gonad , medulla , cortex (anatomy) , medicine , endocrinology , oogenesis , estrogen , ovary , estrogen receptor alpha , germ cell , embryonic stem cell , embryo , meiosis , sexual differentiation , microbiology and biotechnology , estrogen receptor , oocyte , genetics , neuroscience , gene , cancer , ovarian tissue , breast cancer
In chickens, the embryonic ovary differentiates into two distinct domains before meiosis: a steroidogenic core (the female medulla), overlain by the germ cell niche (the cortex). The differentiation of the medulla is a cell-autonomous process based on chromosomal sex identity (CASI). In order to address the extent to which cortex differentiation depends on intrinsic or extrinsic factors, we generated models of gonadal intersex by mixing ZW (female) and ZZ (male) cells in gonadal chimeras, or by altering oestrogen levels of ZW and ZZ embryos. We found that CASI does not apply to the embryonic cortex. Both ZW and ZZ cells can form the cortex and this can happen independently of the phenotypic sex of the medulla as long as oestrogen is provided. We also show that the cortex-promoting activity of oestrogen signalling is mediated via estrogen receptor alpha within the left gonad epithelium. However, the presence of a medulla with an 'intersex' or male phenotype may compromise germ cell progression into meiosis, causing cortical germ cells to remain in an immature state in the embryo.

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