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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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Identification of protein co-localized with Foxl2 on chromatin

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2022-07-11 | PXD024439 | Pride

CRISPR targeting of FOXL2 c.402C>G mutation reduces malignant phenotype in granulosa tumor cells and identifies anti-tumoral compounds

Project description:FOXL2 is a transcription factor that plays a key role in sex determination, ovary development and maintenance. Mutations related to this gene have been described in syndromes involving premature ovarian failure and granulosa cell tumors. This kind of rare cancer (less than 5% of diagnosed ovarian cancers) has been causally associated with the FOXL2 c.402C>G, p.C134W mutation in 97% of the adult cases (AGCTs). In this study, we have used CRISPR technology to specifically eliminate the FOXL2 c.402C>G mutation in granulosa tumor cells. Our results indicate that this Cas9-mediated strategy allows the specific elimination of the mutation with no activity on the wild type allele. Granulosa cells depleted on FOXL2 c.402C>G show a reduced malignant phenotype. Specifically, we detect changes in cell proliferation, invasion, and cell death levels. In addition, we show that granulosa tumor cells become more susceptible to Dasatinib and Ketoconazole treatments when FOXL2 c.402C>G allele is eliminated. Our transcriptomic and proteomic analyses indicate that CRISPR-modified granulosa tumor cells significantly change their expression signature towards a wild type like phenotype. Finally, this expression signature has led us to discover new compounds with antiproliferative and proapoptotic effects on granulosa cell tumor cells. Our results demonstrate the potential of CRISPR for specifically targeting and eliminating a granulosa cell tumor-causing mutation, as well as its therapeutic potential for the treatment of this rare ovarian cancer.

2025-03-15 | PXD053682 | Pride

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A genome-wide exploration of the targets of the transcription factors FOXL2 and ESR2 unveils their implication in cell migration, invasion and adhesion [ChIP-Seq]

Project description:To explore what FOXL2-dependent changes of gene expression observed in our RNA-seq data were directly related to FOXL2 binding, we performed ChIP-seq analysis in FOXL2-expressing granulosa cells (two data points). To explore the potential co-regulation between FOXL2 and ESR2 of several targets, we knocked-down Esr2 in granulosa cells and performed a ChIP-seq under the same conditions as those previously described for FOXL2.

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Transcription profiling of mouse KK1 granulosa cells transfected with Foxl2-VP16 and Foxl2-MAD

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