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SRF promotes long-range chromatin loop formation and stem cell pluripotency

ABSTRACT: Serum response factor (SRF) is a transcription factor essential for cell proliferation, differentiation, and migration, and is required for primitive streak and mesoderm formation in the embryo. The canonical roles of SRF are mediated by a diverse set of context-dependent cofactors. Here we show that SRF physically interacts with CTCF and cohesin subunits at TAD boundaries and loop anchors. SRF reinforces the insulation of TADs and promotes the formation of long-range chromatin loops. In ES cells, SRF associates with Oct4, Sox2, and Nanog and contributes to the formation of 3D pluripotency hubs. Our findings reveal new roles of SRF in higher-order chromatin organization.

ORGANISM(S): Mus musculus

PROVIDER: GSE255733 | GEO | 2024/10/09

REPOSITORIES: GEO

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SRF is a new player in 3D genome organization and stem cell pluripotency

Project description:Serum response factor (SRF) is a transcription factor essential for cell proliferation, differentiation, and migration, and is required for primitive streak and mesoderm formation in the embryo. The canonical roles of SRF are mediated by a diverse set of context-dependent cofactors. Here we show that SRF physically interacts with CTCF and cohesin subunits at TAD boundaries and loop anchors. SRF reinforces the insulation of TADs and promotes the formation of long-range chromatin loops. In ES cells, SRF associates with Oct4, Sox2, and Nanog and contributes to the formation of 3D pluripotency hubs. Our findings reveal new roles of SRF in higher-order chromatin organization.

2024-10-14 | PXD049365 | Pride

SRF promotes long-range chromatin loop formation and stem cell pluripotency

Project description:SRF promotes long-range chromatin loop formation and stem cell pluripotency

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SRF-null neonatal cardiomyocytes

Project description:Serum Response Factor (SRF) is a transcriptional regulator required for mesodermal development. Numerous studies have implicated SRF as a central regulator of muscle gene expression and myogenesis. In this present study we used a loss of function approach to delineate the role of SRF in cardiac myocyte gene expression and function. In SRF null neonatal cardiomyocytes, we observe severe defects in the contractile apparatus, including Z-disc and stress fiber formation, as well as mislocalization and/or attenuation of sarcomeric proteins. Consistent with this, gene array and RT-PCR analyses show downregulation of genes encoding key cardiac transcriptional regulatory factors and proteins required for the maintenance of sarcomeric structure, function, and regulation. Chromatin IP analysis reveals that at least a subset of these proteins are likely regulated directly by SRF. Together the results presented here reveal new cellular and genetic mechanisms through which SRF exacts control over the contractile apparatus in cardiac myocytes. Keywords: genetic modification

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Srf conditional knockout in the mouse liver

Project description:Serum response factor (SRF) is a transcription factor that binds to the serum response element (SRE) of genes that are expressed in response to mitogens. SRF plays essential roles in muscle and nervous system development; however, little is known about the role of SRF during liver growth and function. To examine the function of SRF in the liver, we generated mice in which the Srf gene was specifically disrupted in hepatocytes. The survival of mice lacking hepatic SRF activity was lower than that of control mice; moreover, surviving mutant mice were smaller and had lower blood glucose and triglyceride levels compared with control mice. Srf-deficient livers were also smaller than control livers, hepatocyte morphology was abnormal, and liver-cell proliferation and viability was compromised. Gene array and quantitative RT-PCR analysis of SRF depleted livers revealed a reduction in mRNAs encoding components of the growth hormone/IGF1 pathway, cyclins, several metabolic regulators, and cytochrome p450 enzymes. Conclusion: SRF is essential for hepatocyte proliferation and survival, liver function, and control of postnatal body growth by regulating hepatocyte gene expression.

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Identification of SRF binding sites in Three Human Cell types

Project description:We used chromatin immunoprecipitation (ChIP) in combination with human promoter microarrays to identify 216 putative SRF binding sites in the human genome. We performed independent quantitative PCR validation at over half of these sites that resulted in 146 sites we assert to be true binding sites at over 90% confidence. Nearly half of the sites are bound by SRF in only one of the three cell types we tested, providing strong evidence for the diverse roles for SRF in different cell types. Keywords: ChIP-chip SRF binding was tested in three different cell lines. It was validated by qPCR. Using the proximal promoter arrays, we are assaying binding in approximately 19,000 human promoters.

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Project description:Srf is a MADS-box transcription factor that is critical for muscle differentiation. Its function in hematopoiesis has not yet been revealed. Mkl1, a cofactor of Srf, is part of the t(1;22) translocation in acute megakaryoblastic leukemia, and plays a critical role in megakaryopoiesis. In order to test the role of Srf in megakaryocyte development, we crossed Pf4-Cre mice, which express Cre recombinase in cells committed to the megakaryocytic lineage, to SrfF/F mice in which functional Srf is no longer expressed after Cre-mediated excision. Pf4-Cre/SrfF/F (KO) mice are born with normal mendelian frequency, but have significant macrothrombocytopenia with approximately 50% reduction in platelet count. In contrast, the BM has increased numbers and percentages of CD41+ megakaryocytes (WT: 0.41+/-0.06%; KO: 1.92+/-0.12%) with significantly reduced ploidy. KO mice show significantly increased megakaryocyte progenitors in the BM by both FACS analysis and CFU-Mk. Megakaryocytes lacking Srf have abnormal stress fiber and demarcation membrane formation and platelets lacking Srf have abnormal actin distribution. In vitro and in vivo assays reveal platelet function defects in KO mice. Critical actin cytoskeletal genes are downregulated in KO megakaryocytes. Thus, Srf is required for normal megakaryocyte maturation and platelet production, due at least in part, to regulation of cytoskeletal genes. C-kit+CD41+ megakaryocyte progenitors from PF4-Cre/SRF C57BL/6 SRF WT (3) and C57BL/6 SRF KO (3) mice were sorted by flow cytometry and cultured for three days in thrombopoietin.

2010-07-13 | E-GEOD-21859 | biostudies-arrayexpress

Identification of SRF binding sites in Three Human Cell types

2006-10-31 | GSE5998 | GEO

Transcription profiling of mouse Serum response factor (Srf) conditional knockout in the mouse liver

2009-03-07 | E-GEOD-13333 | biostudies-arrayexpress

SRF-VP16 overexpression in ES cells

Project description:Empty vector, SRF-dM-VP16 (control construct lacking the SRF DNA binding domain), or SRF-VP16 were expressed in wild-type ES cells (E14wt), SRF heterozygotes (E99-/+) or two SRF ko cell lines (E81-/-,E100-/-). RNA was harvested 72h after transfection. Each condition was performed in duplicate, except E100-/- vector transfected. Keywords: ordered

2004-11-15 | GSE1948 | GEO

Expression data in Srf KO and Srf WT murine muscle cells

Project description:The objective of the study is to caracherize the genes that are regulated by Srf in myoblasts at day 0 (J0) and in differentiated cells at day 1 (J1) and day 3 (J3). We used microarrays to investigate gene expression in Srf KO and Srf WT muscle cells at day 0 (J0), day 1 (J1) and day 3 (J3) of differentiation

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