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Genetics. 2016 Feb;202(2):661-73. doi: 10.1534/genetics.115.177857. Epub 2015 Nov 27.

Wnt Signaling in Sexual Dimorphism.

Author information

1
Department of Molecular Biology, Princeton University, Princeton, New Jersey 08540 gdeshpan@princeton.edu pschedl@princeton.edu.
2
Department of Molecular Biology, Princeton University, Princeton, New Jersey 08540.
3
Department of Molecular Biology, Princeton University, Princeton, New Jersey 08540 Laboratory of Gene Expression Regulation in Development, Institute of Gene Biology, Russian Academy of Sciences, 119334 Moscow, Russia gdeshpan@princeton.edu pschedl@princeton.edu.

Abstract

The embryonic gonad of Drosophila melanogaster begins to display sexually dimorphic traits soon after its formation. Here we demonstrate the involvement of a wnt family ligand, wnt-2, in the induction of these sex-specific differences. We show that wnt-2 contributes to the survival of a male-specific population of somatic gonadal precursor cells (SGPs), the male-specific SGPs that are located at the posterior of the male gonad. We also show that the Wnt-2 ligand synergizes with the JAK-STAT ligand Upd, which is produced by SGPs at the anterior of the gonad to activate the STAT pathway in male germ cells. We suggest that the use of two spatially separated signaling systems to initiate the JAK-STAT stem cell maintenance pathway in germ cells provides a mechanism for increasing the pool of potential progenitors of the germline stem cells in the adult testes. Finally, we present evidence indicating that, like the JAK-STAT pathway, wnt-2 stimulates germ cells in male embryos to re-enter the cell cycle.

KEYWORDS:

Drosophila sex determination; Wnt pathway; nonautonomous signaling; sexual dimorphism

PMID:
26614739
PMCID:
PMC4788241
DOI:
10.1534/genetics.115.177857
[Indexed for MEDLINE]
Free PMC Article

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