Activation of Notch Signaling by Oocytes and Jag1 in Mouse Ovarian Granulosa Cells.
Journal
Endocrinology
ISSN: 1945-7170
Titre abrégé: Endocrinology
Pays: United States
ID NLM: 0375040
Informations de publication
Date de publication:
01 12 2019
01 12 2019
Historique:
received:
02
08
2019
accepted:
04
10
2019
pubmed:
15
10
2019
medline:
24
12
2019
entrez:
15
10
2019
Statut:
ppublish
Résumé
The Notch pathway plays diverse and complex roles in cell signaling during development. In the mammalian ovary, Notch is important for the initial formation and growth of follicles, and for regulating the proliferation and differentiation of follicular granulosa cells during the periovulatory period. This study seeks to determine the contribution of female germ cells toward the initial activation and subsequent maintenance of Notch signaling within somatic granulosa cells of the ovary. To address this issue, transgenic Notch reporter (TNR) mice were crossed with Sohlh1-mCherry (S1CF) transgenic mice to visualize Notch-active cells (EGFP) and germ cells (mCherry) simultaneously in the neonatal ovary. To test the involvement of oocytes in activation of Notch signaling in ovarian somatic cells, we ablated germ cells using busulfan, a chemotherapeutic alkylating agent, or investigated KitWv/Wv (viable dominant white-spotting) mice that lack most germ cells. The data reveal that Notch pathway activation in granulosa cells is significantly suppressed when germ cells are reduced. We further demonstrate that disruption of the gene for the Notch ligand Jag1 in oocytes similarly impacts Notch activation and that recombinant JAG1 enhances Notch target gene expression in granulosa cells. These data are consistent with the hypothesis that germ cells provide a ligand, such as Jag1, that is necessary for activation of Notch signaling in the developing ovary.
Identifiants
pubmed: 31609444
pii: 5586234
doi: 10.1210/en.2019-00564
pmc: PMC6850001
doi:
Substances chimiques
Jag1 protein, mouse
0
Jagged-1 Protein
0
Receptors, Notch
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
2863-2876Subventions
Organisme : NICHD NIH HHS
ID : P01 HD021921
Pays : United States
Organisme : NIGMS NIH HHS
ID : R25 GM086262
Pays : United States
Organisme : NIGMS NIH HHS
ID : K12 GM000678
Pays : United States
Organisme : NIGMS NIH HHS
ID : R25 GM079300
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM008061
Pays : United States
Informations de copyright
Copyright © 2019 Endocrine Society.
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