Global Profiling of Activin Target Genes in Mouse Granulosa Cells
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE20583 | GEO | 2011/03/02
SECONDARY ACCESSION(S): PRJNA125279
REPOSITORIES: GEO
Similar Datasets
Project description:In order to understand the mechanisms and pathways by which activin regulates follicle function, we performed a microarray study and identified activin regulated genes in mouse ovarian granulose cells. Primary cultured ovarian granulosa cells collected from day 21-23 old immature mice were treated with Activin A (A), Activin A plus its antagonist follistatin (AplusF), and PBS (P, vehicle) for 24 h. RNA from each treatment group was isolated and the experiments were repeated four times. Samples from experiment one were assigned as P1, A1 and A+F1, samples from experiment two as P2, A2 and A+F2, and so on. About 100 ng of each RNA sample was amplified using a modified Eberwine T7-based amplification protocol and hybridized to the Illumina Sentrix Mouse-6 Expression BeadChip (Illumina, Inc., San Diego, CA) that contains 48,000 sets of oligonucleotides.
2011-03-02 | E-GEOD-20583 | biostudies-arrayexpress
Project description:Compares activin deficient granulosa cells (Inhba flox/-; Inhbb-/-; Amhr2cre/+) to wild type granulosa cells Keywords: Genetic Modificaton
2007-12-28 | GSE7150 | GEO
Project description:The Foxo transcription factors regulate multiple cellular functions. Foxo1 and Foxo3 are highly expressed in granulosa cells of ovarian follicles. Selective depletion of the Foxo1 and Foxo3 genes in granulosa cells revealed a novel ovarian-pituitary endocrine feedback loop characterized by: 1) undetectable levels of serum FSH but not LH, 2) reduced expression of the pituitary Fshb gene and its transcriptional regulators and 3) ovarian production of a factor(s) that suppresses pituitary cell Fshb. Equally notable and independent of FSH, depletion of Foxo1/3 altered the expression of specific genes associated with follicle growth versus apoptosis by disrupting critical regulatory interactions of Foxo1/3 with the activin and BMP2 pathways, respectively. As a consequence, granulosa cell proliferation and apoptosis were decreased. These data provide the first evidence that Foxo1/3 divergently regulate follicle growth or death by interacting with the activin and BMP pathways in granulosa cells and by modulating pituitary FSH production. A direct comparison of ovarian granulosa cells from wild type d25, Foxo1/3 dKO d25 and Foxo1/3 dKO 2 month mice.
2013-02-16 | E-GEOD-35593 | biostudies-arrayexpress
Project description:The Foxo transcription factors regulate multiple cellular functions. Foxo1 and Foxo3 are highly expressed in granulosa cells of ovarian follicles. Selective depletion of the Foxo1 and Foxo3 genes in granulosa cells revealed a novel ovarian-pituitary endocrine feedback loop characterized by: 1) undetectable levels of serum FSH but not LH, 2) reduced expression of the pituitary Fshb gene and its transcriptional regulators and 3) ovarian production of a factor(s) that suppresses pituitary cell Fshb. Equally notable and independent of FSH, depletion of Foxo1/3 altered the expression of specific genes associated with follicle growth versus apoptosis by disrupting critical regulatory interactions of Foxo1/3 with the activin and BMP2 pathways, respectively. As a consequence, granulosa cell proliferation and apoptosis were decreased. These data provide the first evidence that Foxo1/3 divergently regulate follicle growth or death by interacting with the activin and BMP pathways in granulosa cells and by modulating pituitary FSH production.
2013-02-16 | GSE35593 | GEO
Project description:Activin signalling controls the pluripotency of human embryonic stem cells (hESCs) by inducing the formation of nuclear Smad2/3-Nanog complexes that bind to and regulate several downstream targets. We aimed to clarify the transcriptional dynamics to the inhibition of Activin in hPSCs. To this end we performed microarray analysis of hPSCs treated with SB431542 (SB), an antagonist of the ALK4 and ALK7 type I Activin receptors, for early (2h, 4h and 8h) and late (24h and 48h) time points. Moreover, given our finding that Activin signalling regulates H3K4me3 of its target genes, we tested the transcriptional effect to the knock-down of the Mll/Set1 complex subunit Dpy30 by using shRNA. Finally, we also evaluated the transcriptional response to the knock-down of the Smad2/3 cofactor Nanog by using shRNA.
2015-01-01 | E-MTAB-2749 | biostudies-arrayexpress
Project description:Compares activin deficient granulosa cells (Inhba flox/-; Inhbb-/-; Amhr2cre/+) to wild type granulosa cells Experiment Overall Design: Three replicate wild type granulosa cell samples compared to 2 activin-deficient granulosa cell samples. Each replicate is derived from 2-3 females.
2008-06-15 | E-GEOD-7150 | biostudies-arrayexpress
Project description:Nodal and Activin are morphogens of the TGFbeta superfamily of signaling molecules that direct differential cell fate decisions in a dose- and distance-dependent manner. During early embryonic development the Nodal/Activin pathway is responsible for the specification of mesoderm, endoderm, node and mesendoderm. In contradiction to this drive towards cellular differentiation, the pathway also plays important roles in the maintenance of self-renewal and pluripotency in embryonic and epiblast stem cells. The molecular basis behind stem cell interpretation of Nodal/Activin signaling gradients and the undertaking of disparate cell fate decisions remains poorly understood. Here, we show that any perturbation of endogenous signaling levels in mouse ES cells leads to their exit from self renewal towards divergent differentiation programs. Increasing Nodal signals above basal levels by direct stimulation with Activin promotes differentiation towards the mesendodermal lineages while repression of signaling with the specific Nodal/Activin receptor inhibitor SB431542 induces trophectodermal differentiation. To address how quantitative Nodal/Activin signals are translated qualitatively into distinct cell fates decisions, we performed chromatin immunoprecipitation of phospho-Smad2 the primary downstream transcriptional factor of the Nodal/Activin pathway followed by massively parallel sequencing and show that phospho-Smad2 binds to and regulates distinct subsets of target genes in a dose-dependent manner. Crucially, Nodal/Activin signaling directly controls the Oct4 master regulator of pluripotency by graded phospho-Smad2 binding in the promoter region. Hence stem cells interpret and carry out differential Nodal/Activin signaling instructions via a corresponding gradient of Smad2 phosphorylation that selectively titrates self-renewal against alternative differentiation programs by direct regulation of distinct target gene subsets and Oct4 expression. Four biological replicates consisting of 4 different passages of E14TG2a ES cells at P20, P21, P23 and P24
2011-06-30 | E-GEOD-23239 | biostudies-arrayexpress
Project description:Ovarian follicle development is a complex and well orchestrated biological process. Chromatin spatial organization has emerged as an important regulator of gene expression, but how these changes during follicle development are still unknown. Here, we integrated RNA-seq and Hi-C analyses of chicken follicular granulosa cells of 10 developmental stages. Our data revealed that SWF, F1, and POF had the greatest transcriptome differences from other stages. Our results provide a genome-wide atlas of chromatin interactions during chicken ovarian follicle development.
2021-11-10 | GSE167064 | GEO
Project description:Nodal and Activin are morphogens of the TGFbeta superfamily of signaling molecules that direct differential cell fate decisions in a dose- and distance-dependent manner. During early embryonic development the Nodal/Activin pathway is responsible for the specification of mesoderm, endoderm, node and mesendoderm. In contradiction to this drive towards cellular differentiation, the pathway also plays important roles in the maintenance of self-renewal and pluripotency in embryonic and epiblast stem cells. The molecular basis behind stem cell interpretation of Nodal/Activin signaling gradients and the undertaking of disparate cell fate decisions remains poorly understood. Here, we show that any perturbation of endogenous signaling levels in mouse ES cells leads to their exit from self renewal towards divergent differentiation programs. Increasing Nodal signals above basal levels by direct stimulation with Activin promotes differentiation towards the mesendodermal lineages while repression of signaling with the specific Nodal/Activin receptor inhibitor SB431542 induces trophectodermal differentiation. To address how quantitative Nodal/Activin signals are translated qualitatively into distinct cell fates decisions, we performed chromatin immunoprecipitation of phospho-Smad2 the primary downstream transcriptional factor of the Nodal/Activin pathway followed by massively parallel sequencing and show that phospho-Smad2 binds to and regulates distinct subsets of target genes in a dose-dependent manner. Crucially, Nodal/Activin signaling directly controls the Oct4 master regulator of pluripotency by graded phospho-Smad2 binding in the promoter region. Hence stem cells interpret and carry out differential Nodal/Activin signaling instructions via a corresponding gradient of Smad2 phosphorylation that selectively titrates self-renewal against alternative differentiation programs by direct regulation of distinct target gene subsets and Oct4 expression.
2011-06-30 | GSE23239 | GEO
Project description:The ovarian follicle is devoid of direct blood supply because of a blood follicle barrier. The intra follicular compartments are hypothesized to have low oxygen level. As the diameter of an ovarian follicle substantially increases during follicular development, the oxygen concentration is likely to decrease in the follicular fluid and reaches lowest levels in the ovulatory follicles. During the present investigation, transcriptome differences induced by low oxygen levels were comprehensively analyzed to understand the specific significance of low oxygen levels in ovulatory follicles.
2018-08-01 | GSE112070 | GEO