FOXL2 and BMP2 act cooperatively to regulate follistatin gene expression during ovarian development

Follistatin is a secreted glycoprotein required for female sex determination and early ovarian development, but the precise mechanisms regulating follistatin (Fst) gene expression are not known. Here, we investigate the roles of bone morphogenetic protein 2 (BMP2) and forkhead-domain transcription f...

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Vydáno v:Endocrinology (Philadelphia) Ročník 152; číslo 1; s. 272
Hlavní autoři: Kashimada, Kenichi, Pelosi, Emanuele, Chen, Huijun, Schlessinger, David, Wilhelm, Dagmar, Koopman, Peter
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 01.01.2011
Témata:
Animals
Bone Morphogenetic Protein 2 - genetics
Bone Morphogenetic Protein 2 - metabolism
Cell Line, Tumor
Female
Fetal Development
Follistatin - genetics
Follistatin - metabolism
Forkhead Box Protein L2
Forkhead Transcription Factors - genetics
Forkhead Transcription Factors - metabolism
Gene Expression Regulation, Developmental - physiology
Genetic Markers
Mice
Ovary - embryology
Ovary - metabolism
ISSN:1945-7170, 1945-7170
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Shrnutí:Follistatin is a secreted glycoprotein required for female sex determination and early ovarian development, but the precise mechanisms regulating follistatin (Fst) gene expression are not known. Here, we investigate the roles of bone morphogenetic protein 2 (BMP2) and forkhead-domain transcription factor L2 (FOXL2) in the regulation of Fst expression in the developing mouse ovary. Bmp2 and Fst showed similar temporal profiles of mRNA expression, whereas FOXL2 protein and Fst mRNA were coexpressed in the same ovarian cells. In a cell culture model, both FOXL2 and BMP2 up-regulated Fst expression. In ex vivo mouse fetal gonad culture, exogenous BMP2 increased Fst expression, but this effect was counteracted by the BMP antagonist Noggin. Moreover, in Foxl2-null mice, Fst expression was reduced throughout fetal ovarian development, and Bmp2 expression was also reduced. Our data support a model in which FOXL2 and BMP2 cooperate to ensure correct expression of Fst in the developing ovary. Further, Wnt4-knockout mice showed reduced expression of Fst limited to early ovarian development, suggesting a role for WNT4 in the initiation, but not the maintenance, of Fst expression.
Bibliografie:ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:1945-7170
1945-7170
DOI:10.1210/en.2010-0636