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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression analysis of Wv/Wv fetal gonads

ABSTRACT: Following sex determination, XY and XX gonads develop into a testis and an ovary, respectively. Depending on the sex of the gonad, resident germ cells will subsequently be committed to either spermatogenesis or oogenesis. In this study we took advantage of the Wv/Wv mouse genetic model, in which gonads are almost devoided of germ cells, to uncover gene expression underlying fetal germ cell development. Male and Female gonads were collected at 12, 14 and 16 days post coitum (dpc) from wild-type and Wv/Wv mouse embryos. Total RNAs were extracted and hybridized on Affymetrix microarrays. Expression signals from male and female gonads or from wild-type and mutant gonads were compared to identify sexually dimorphic genes as well as genes expressed in germ cell during fetal gonad development.

ORGANISM(S): Mus musculus

SUBMITTER: Antoine ROLLAND

PROVIDER: E-GEOD-23908 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Uncovering gene regulatory networks during mouse fetal germ cell development.

Rolland Antoine D AD Lehmann Kim P KP Johnson Kamin J KJ Gaido Kevin W KW Koopman Peter P

Biology of reproduction 20101208 4

The commitment of germ cells to either oogenesis or spermatogenesis occurs during fetal gonad development: germ cells enter meiosis or mitotic arrest, depending on whether they reside within an ovary or a testis, respectively. Despite the critical importance of this step for sexual reproduction, gene networks underlying germ cell development have remained only partially understood. Taking advantage of the W(v) mouse model, in which gonads lack germ cells, we conducted a microarray study to ident ...[more]

PMID: 21148109

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Expression analysis of Wv/Wv fetal gonads

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2011-11-01 | E-GEOD-21650 | biostudies-arrayexpress

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Project description:Retinoic acid (RA) is a potent inducer of cell differentiation and plays an essential role in sex-specific germ cell development in the mammalian gonad. RA is essential for male gametogenesis and hence fertility. However, RA can also disrupt sexual cell fate in somatic cells of the testis, promoting transdifferentiation of male Sertoli cells to female granulosa-like cells when the male sexual regulator Dmrt1 is absent. The feminizing ability of RA in the somatic testis suggests that RA might normally play a role in somatic cell differentiation or cell fate maintenance in the ovary. To test for this possibility we disrupted RA signaling in somatic cells of the early fetal ovary using three genetic strategies and one pharmaceutical approach. We found that deleting all three RA receptors (RARs) in the XX somatic gonad at the time of sex determination did not significantly affect ovarian differentiation, follicle development, or female fertility. Transcriptome analysis of adult triple mutant ovaries revealed remarkably little effect on gene expression in the absence of somatic RAR function. Likewise, deletion of three RA synthesis enzymes (Aldha1-3) at the time of sex determination did not masculinize the ovary. A dominant-negative RAR transgene altered granulosa cell proliferation, likely due to interference with a non-RA signaling pathway, but did not affect granulosa cell specification or fertility. Finally, culture of fetal XX gonads with an RAR antagonist blocked germ cell meiotic initiation but did not disrupt sex-biased gene expression. We conclude that RA signaling, although crucial in the ovary for meiotic initiation, is not required for granulosa cell specification, differentiation, or reproductive function.

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