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Dev Biol. 2017 Jun 1;426(1):17-27. doi: 10.1016/j.ydbio.2017.04.010. Epub 2017 Apr 26.

Constitutive WNT/CTNNB1 activation triggers spermatogonial stem cell proliferation and germ cell depletion.

Author information

1
Université Côte d'Azur, CNRS, INSERM, iBV, France. Electronic address: chassot@unice.fr.
2
Université Côte d'Azur, CNRS, INSERM, iBV, France.
3
Department of Pharmacology, Graduate School of Medicine, Kyoto University Yoshida-Konoe-cho, Sakyo, Kyoto, Japan.
4
Department of Functional Genomics and Cancer, Institut de Génétique et de Biologie Moleculaire et Cellulaire (IGBMC), CNRS UMR7104, INSERM U964, Université de Strasbourg, F-67404 Illkirch, France.

Abstract

The differentiation of germ cells into oogonia or spermatogonia is the first step that eventually gives rise to fully mature gametes. In the female fetal gonad, the RSPO1/WNT/CTNNB1 signalling pathway is involved in primordial germ cell proliferation and differentiation into female germ cells, which are able to enter meiosis. In the postnatal testis, the WNT/CTNNB1 pathway also mediates proliferation of spermatogonial stem cells and progenitor cells. Here we show that forced activation of the WNT/CTNNB1 pathway in fetal gonocytes using transgenic mice leads to deregulated spermatogonial proliferation, and exhaustion of the spermatocytes by apoptosis, resulting in a hypoplastic testis. These findings demonstrate that a finely tuned timing in WNT/CTNNB1 signalling activity is required for spermatogenesis.

KEYWORDS:

CTNNB1; Canonical WNT signalling; Gonocytes; Proliferation; Spermatogenesis; Spermatogonia

PMID:
28456466
DOI:
10.1016/j.ydbio.2017.04.010
[Indexed for MEDLINE]
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