期刊
DEVELOPMENT
卷 139, 期 13, 页码 2283-2287出版社
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/dev.076307
关键词
AMH; Gonad; Medaka; Germ cells; Sex differentiation; Sex reversal
资金
- [21116509]
- [22132007]
- [21770072]
- [21370101]
- Grants-in-Aid for Scientific Research [22132007, 22132001] Funding Source: KAKEN
The function of AMH (Anti-Mullerian hormone), a phylogenetically ancient member of the TGF beta family of proteins, in lower vertebrates is largely unknown. Previously, we have shown that the gene encoding the type II anti-Mullerian hormone receptor, amhrII, is responsible for excessive germ cell proliferation and male-to-female sex reversal in the medaka hotei mutant. In this study, functional analyses in cultured cells and of other amhrII mutant alleles indicate that lack of AMH signaling causes the hotei phenotype. BrdU incorporation experiments identified the existence of both quiescent and mitotically active germ cells among the self-renewing, type I population of germ cells in the developing gonad. AMH signaling acts in supporting cells to promote the proliferation of mitotically active germ cells but does not trigger quiescent germ cells to proliferate in the developing gonad. Furthermore, we show that the male-to-female sex reversal phenotype in hotei mutants is not a direct consequence of AMH signaling in supporting cells, but is instead mediated by germ cells. Our data demonstrate that interfollicular AMH signaling regulates proliferation at a specific stage of germ cell development, and that this regulation is crucial for the proper manifestation of gonadal sex directed by sex determination genes.
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