Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PXD005464
PROVIDER: PRJNA320432 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Fam60a defines a variant Sin3a-Hdac complex in embryonic stem cells required for self-renewal
| PRJNA343472 | ENA
Project description:Sin3a is the central scaffold protein of the prototypical Hdac1/2 chromatin repressor complex, crucially required during early embryonic development for the growth of pluripotent cells of the inner cell mass. Here, we explore the endogenous composition of the Sin3a-Hdac complex in pluripotent embryonic stem (ES) and differentiated cells. To do this, we established an endogenous double immunoprecipitation strategy coupled with quantitative mass spectrometry (ENDIP-MS) allowing us to define the precise composition of the Sin3a complex in multiple cell types. We identify the Fam60a subunit as a key defining feature of a variant Sin3a complex present in ES cells, but not in differentiated cells. Fam60a co-occupies H3K4me3 positive promoters with Sin3a and is essential to maintain it on chromatin. Consistent with this, Fam60a depletion phenocopies the loss of Sin3a, leading to decreased proliferation, an extended G1-phase and the deregulation of genes associated with differentiation. Taken together, our data characterise Fam60a as an essential core subunit of a variant Sin3a complex in ES cells required to promote rapid proliferation and to prevent unscheduled differentiation.
2017-05-19 | PXD005464 | Pride
Project description:ChIP coupled with NGS identifies genome-wide binding sites of a ES cells specific Sin3a/Hdac complex. The aim of these experiments is to study the role of Fam60a in the Sin3a/Hdac complex. ChIP-Seq experiments reveal that Fam60a is required to maintain high levels of Sin3a binding on target genes in mESCs. Depletion of Fam60a causes a drop of Sin3a binding to target sites. Underlining the function of Fam60a in mES cells, ChIP-seq analysis of Sin3a and Fam60a in mouse fibroblasts reveal strikingly low global binding level of Sin3a to its target genes while Fam60a is absent at these sites.
2017-04-24 | GSE81081 | GEO
Project description:RNA-Sequencing (RNA-seq). The aim of this RNA-seq experiment was to monitor the genome-wide transcriptional changes in mouse embryonic stem cells depleted of either Fam60a or Sin3a.
2017-05-16 | GSE87084 | GEO
Project description:The Sin3 histone deacetylase (HDAC) complex is a 1.2 MDa chromatin modifying complex that can repress transcription by binding to gene promoters and deacetylating histones. The Sin3/HDAC complex can affect cell cycle progression through multiple mechanisms and is among the targets of anticancer drugs, called HDAC inhibitors. We describe the identification of a new subunit of the Sin3 complex named family with sequence similarity 60 member A (FAM60A). We show that FAM60A/Sin3 complexes normally suppress the epithelial-to-mesenchymal transition (EMT) and cell migration. This occurs through transcriptional repression of genes that encode components of the TGF-beta signaling pathway. This work reveals that FAM60A and the Sin3 complex are upstream repressors of TGF-beta signaling, EMT and cell migration and extends the known biological roles of the Sin3 complex. This experiment investigates the role of FAM60A in gene expression by comparing A549 lung cancer cells treated with or without siRNA against FAM60A. The Sin3 histone deacetylase (HDAC) complex is a 1.2 MDa chromatin modifying complex that can repress transcription by binding to gene promoters and deacetylating histones. SDS3 is a core component of the Sin3 complex. The Sin3/HDAC complex can affect cell cycle progression through multiple mechanisms and is among the targets of anticancer drugs, called HDAC inhibitors. We describe the identification of a new subunit of the Sin3 complex named family with sequence similarity 60 member A (FAM60A). We show that FAM60A/Sin3 complexes normally suppress the epithelial-to-mesenchymal transition (EMT) and cell migration. This occurs through transcriptional repression of genes that encode components of the TGF-beta signaling pathway. This work reveals that FAM60A and the Sin3 complex are upstream repressors of TGF-beta signaling, EMT and cell migration and extends the known biological roles of the Sin3 complex. As a base line to better understand the relationship between FAM60A and the Sin3 complex, this experiment investigates the gene expression changes which occur in A549 lung cancer cells when the Sin3 complex is perturbed by knockdown of a core component via siRNA against SDS3. FAM60A siRNA knockdowns were compared to a non-targeting control in triplicate, for a total of 6 samples. SDS3 siRNA knockdowns were compared to a non-targeting control in triplicate, for a total of 6 samples.
2012-09-15 | E-GEOD-39733 | biostudies-arrayexpress
Project description:The Sin3 histone deacetylase (HDAC) complex is a 1.2 MDa chromatin modifying complex that can repress transcription by binding to gene promoters and deacetylating histones. The Sin3/HDAC complex can affect cell cycle progression through multiple mechanisms and is among the targets of anticancer drugs, called HDAC inhibitors. We describe the identification of a new subunit of the Sin3 complex named family with sequence similarity 60 member A (FAM60A). We show that FAM60A/Sin3 complexes normally suppress the epithelial-to-mesenchymal transition (EMT) and cell migration. This occurs through transcriptional repression of genes that encode components of the TGF-beta signaling pathway. This work reveals that FAM60A and the Sin3 complex are upstream repressors of TGF-beta signaling, EMT and cell migration and extends the known biological roles of the Sin3 complex. This experiment investigates the role of FAM60A in gene expression by comparing A549 lung cancer cells treated with or without siRNA against FAM60A. The Sin3 histone deacetylase (HDAC) complex is a 1.2 MDa chromatin modifying complex that can repress transcription by binding to gene promoters and deacetylating histones. SDS3 is a core component of the Sin3 complex. The Sin3/HDAC complex can affect cell cycle progression through multiple mechanisms and is among the targets of anticancer drugs, called HDAC inhibitors. We describe the identification of a new subunit of the Sin3 complex named family with sequence similarity 60 member A (FAM60A). We show that FAM60A/Sin3 complexes normally suppress the epithelial-to-mesenchymal transition (EMT) and cell migration. This occurs through transcriptional repression of genes that encode components of the TGF-beta signaling pathway. This work reveals that FAM60A and the Sin3 complex are upstream repressors of TGF-beta signaling, EMT and cell migration and extends the known biological roles of the Sin3 complex. As a base line to better understand the relationship between FAM60A and the Sin3 complex, this experiment investigates the gene expression changes which occur in A549 lung cancer cells when the Sin3 complex is perturbed by knockdown of a core component via siRNA against SDS3.
2012-09-15 | GSE39733 | GEO
Project description:Despite the requirement of Sin3a for survival of early embryos and embryonic stem cells (ESCs), mechanistic action of Sin3a in the maintenance and establishment of pluripotency remains unexplored. Here we report the transcriptional regulatory roles of Sin3a in maintaining ESC pluripotency and in reprogramming somatic cells towards full pluripotency. Sin3a/HDAC complex members were enriched in an extended Nanog interactome and exhibited a predominant transcriptional co-activator role at a global level in ESCs. We also established a critical role for Sin3a in efficient reprogramming of somatic cells towards full pluripotency. Nanog and Sin3a co-localize at almost all of their genome-wide targets in pre-iPSCs, and both factors are required to directly induce a synergistic transcriptional program wherein pluripotency genes are activated and reprogramming barrier genes are repressed. Our results, for the first time, establish positive roles of the Sin3a/HDAC complex in the maintenance and establishment of pluripotency.
2017-02-21 | GSE91021 | GEO
Project description:Despite the requirement of Sin3a for survival of early embryos and embryonic stem cells (ESCs), mechanistic action of Sin3a in the maintenance and establishment of pluripotency remains unexplored. Here we report the transcriptional regulatory roles of Sin3a in maintaining ESC pluripotency and in reprogramming somatic cells towards full pluripotency. Sin3a/HDAC complex members were enriched in an extended Nanog interactome and exhibited a predominant transcriptional co-activator role at a global level in ESCs. We also established a critical role for Sin3a in efficient reprogramming of somatic cells towards full pluripotency. Nanog and Sin3a co-localize at almost all of their genome-wide targets in pre-iPSCs, and both factors are required to directly induce a synergistic transcriptional program wherein pluripotency genes are activated and reprogramming barrier genes are repressed. Our results, for the first time, establish positive roles of the Sin3a/HDAC complex in the maintenance and establishment of pluripotency.
2017-02-21 | GSE90986 | GEO
Project description:The Sin3a/HDAC co-repressor complex cooperates with Nanog in promoting stem cell pluripotency and somatic cell reprogramming [ChIP-Seq]
| PRJNA356691 | ENA
Project description:The Sin3a/HDAC co-repressor complex cooperates with Nanog in promoting stem cell pluripotency and somatic cell reprogramming [Microarray Expression]
| PRJNA356573 | ENA