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FOXL2 and ESR1 binding sites in primary cells from mouse ovarian follicles

ABSTRACT: It has previously been shown that FOXL2 and ESR1 cooperate to repress the testis-determining gene Sox9 in murine granulosa cells, and suggested that FOXL2/ESR1 cooperation may be central to granulosa cell differentiation (Uhlenhaut et al., 2009). However, no study has so far compared the DNA-binding of FOXL2 and ESR1 at the genomic level or analyzed the impact of FOXL2 on ESR1 binding to its regulatory elements. Here, we have analyzed and compared the genomic locations recognized by ESR1 and FOXL2 in E2-treated primary murine granulosa cells. Input DNA, FOXL2 and ESR1 ChIP

ORGANISM(S): Mus musculus

SUBMITTER: Adrien Georges

PROVIDER: E-GEOD-62545 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Characterization of FOXL2 and five nuclear receptors transcriptional function in mouse granulosa cells

Project description:FOXL2 is a lineage determining transcription factor in the ovary, but its direct targets and modes of action are not fully characterized. Interaction of FOXL2 with several members of the nuclear receptor familly of transcription factors has been described, and many nuclear receptors play a key role in ovarian biology. Here, we explore the targets of FOXL2 and five nuclear receptors in murine primary follicular cells. siRNA targeting FOXL2 or control siRNA were used in conjunction with siRNAs targeting five different nuclear receptors or control siRNAs (2x6=12 conditions). Each condition was analysed in completely independent biological duplicates (i.e. cell from different animals grown independently)

2014-10-29 | E-GEOD-60764 | biostudies-arrayexpress

FOXL2 binding sites in primary cells from mouse ovarian follicles

Project description:FOXL2 is a lineage determining transcription factor in the ovary, but its direct targets and modes of action are not fully characterized. Here, we explore the genomic targets of FOXL2. We found in particular that FOXL2 directly modulates Esr2 expression through a newly identified intronic element. Input DNA and FOXL2 ChIP

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FOXL2 and ESR1 binding sites in primary cells from mouse ovarian follicles

Project description:It has previously been shown that FOXL2 and ESR1 cooperate to repress the testis-determining gene Sox9 in murine granulosa cells, and suggested that FOXL2/ESR1 cooperation may be central to granulosa cell differentiation (Uhlenhaut et al., 2009). However, no study has so far compared the DNA-binding of FOXL2 and ESR1 at the genomic level or analyzed the impact of FOXL2 on ESR1 binding to its regulatory elements. Here, we have analyzed and compared the genomic locations recognized by ESR1 and FOXL2 in E2-treated primary murine granulosa cells.

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FOXL2 interaction with different binding partners regulates the dynamics of granulosa cell differentiation across ovarian development

Project description:FOXL2 is a transcription factor essential for female fertility, expressed in somatic cells of the ovary, notably granulosa cells. In the mouse, Foxl2 deletion leads to partial sex reversal postnatally. However, deletion of the gene in 8-week-old females leads to granulosa to Sertoli cell transdifferentiation. We hypothesised that different outcomes of Foxl2 deletion in embryonic versus adult ovary may depend on a different role played across ovarian development. Therefore, we characterised the dynamics of gene expression and chromatin accessibility changes in purified murine granulosa cells across key developmental stages (E14.5, 1 and 8 weeks). We then performed genome-wide identification of FOXL2 target genes and on-chromatin interacting partners by ChIP-SICAP. We found that FOXL2 regulates more genes at postnatal stages, through the interaction with factors regulating primordial follicle activation (PFA), such as NR5A2, and others regulating steroidogenesis including AR and ESR2. As a proof of principle experiment, we chose one FOXL2 interactor, Ubiquitin specific protease 7 (USP7) and showed that deletion of this gene in granulosa cells leads to a blockage of PFA, impaired ovary development and sterility. Our study constitutes a comprehensive resource for exploration of the molecular mechanisms of ovarian development and causes of female infertility.

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A cellular model of the oncogenic FOXL2 somatic pathogenic variant C134W provides new insights in pathogenicity

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Genome wide identification of FOXL2 binding sites in mouse fetal ovaries

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