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Publication : Somatic cell fate maintenance in mouse fetal testes via autocrine/paracrine action of AMH and activin B.

First Author  Rodriguez KF Year  2022
Journal  Nat Commun Volume  13
Issue  1 Pages  4130
PubMed ID  35840551 Mgi Jnum  J:326811
Mgi Id  MGI:7315897 Doi  10.1038/s41467-022-31486-y
Citation  Rodriguez KF, et al. (2022) Somatic cell fate maintenance in mouse fetal testes via autocrine/paracrine action of AMH and activin B. Nat Commun 13(1):4130
abstractText  Fate determination and maintenance of fetal testes in most mammals occur cell autonomously as a result of the action of key transcription factors in Sertoli cells. However, the cases of freemartin, where an XX twin develops testis structures under the influence of an XY twin, imply that hormonal factor(s) from the XY embryo contribute to sex reversal of the XX twin. Here we show that in mouse XY embryos, Sertoli cell-derived anti-Mullerian hormone (AMH) and activin B together maintain Sertoli cell identity. Sertoli cells in the gonadal poles of XY embryos lacking both AMH and activin B transdifferentiate into their female counterpart granulosa cells, leading to ovotestis formation. The ovotestes remain to adulthood and produce both sperm and oocytes, although there are few of the former and the latter fail to mature. Finally, the ability of XY mice to masculinize ovaries is lost in the absence of these two factors. These results provide insight into fate maintenance of fetal testes through the action of putative freemartin factors.
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