SUMO safeguards somatic and pluripotent cell identities by enforcing distinct chromatin states [SUMO-ChIP-seq]
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ABSTRACT:
PROVIDER: PRJNA476248 | ENA |
REPOSITORIES: ENA
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Project description:Mouse embryonic fibroblasts (MEFs) were generated from Ubc9fl/- and Ubc9+/+ embryos (E13.5). MEFs were treated with tamoxifen for six days to cause CreERT2 activation, and induce Ubc9 floxed allele deletion. We determined the ChIP-seq profiles of SUMO-1 and SUMO-2 using chromatin of wild-type MEFs Ubc9+/+ and of the corresponding Ubc9 KO MEFs which are entirely depleted for sumoylation. The analysis revealed the nearly complete absence of genome-wide binding of SUMO-1 and SUMO-2 in Ubc9-/- MEFs, attesting for antibody specificities.
2018-10-24 | GSE115842 | GEO
Project description:Purposes: (1) compare the SUMO chromatin landscape between mouse embryonic fibroblasts (MEFs) and embryonic stem cells (ESc) (2) Decipher how hyposumoylation enhances MEF to induced pluripotent stem cells (iPSc) reprogramming (3) Decipher how hyposumoylation enhances ESc to 2C-like cells conversion. Methods : (1) ChIP-seq in MEFs and ESc for SUMO isoforms and histone marks. (2) ChIP-seq for transcription factors and histone marks at day 4 of MEF to iPSc reprogramming comparing wild type (shCtrl) and hyposumoylated cells (shUbc9). ATAC-Seq at day 4 of MEF to iPSc reprogramming comparing wild type (shCtrl) and hyposumoylated cells (shUbc9). RNA-Seq in MEFs, iPSc, at day 4 and day 7 of MEF to iPSc reprogramming comparing wild type (shCtrl) and hyposumoylated cells (shUbc9). (3) RNA-Seq in ESc comparing wild-type (siCtrl) and hyposumoylated cells (siUbc9). Results: (1) SUMO chromatin landscape is highly different between MEFs and ESc and associates to distinct chromatin marks. (2) Hyposumoylation enhances MEFs to iPSc reprogramming by favoring the extinction of the MEF transcriptional program and redistributing pluripotency factors from MEF enhancers toward ES enhancers. (3) Hyposumoylation enhances ES to 2C-like conversion by destabilizing heterochromatin thus resulting in an activation of the 2-cell transcriptional program. Conclusion: SUMO at chromatin is gate-keeper of cell-identity.
2018-10-24 | GSE99009 | GEO
Project description:SUMO safeguards somatic and pluripotent cell identities by enforcing distinct chromatin states
| PRJNA386997 | ENA
Project description:The post-translational modification of proteins by SUMO acts as a key gatekeeper of cell identity. In mouse embryonic fibroblast (MEFs), SUMO impedes reprogramming to pluripotency, while in embryonic stem cells (ESCs), it represses the emergence of totipotent-like cells, suggesting that SUMO targets distinct sets of substrates to preserve the somatic and pluripotent states. Using MS-based proteomics, we show here that the composition of the endogenous SUMOylomes differs dramatically between MEFs and ESCs. In MEFs, SUMOylated proteins organize in a rather diffuse functional network enriched in nuclear factors with general cellular functions. In contrast, in ESCs, SUMOylated proteins form a tightly interconnected network mainly composed of repressive chromatin complexes. We also characterized several SUMOylated pluripotency factors and show that SUMO modification of Dppa2 and Dppa4 hampers their ability to induce a totipotent-like state. Altogether, we propose that rewiring the repertoire of SUMO target networks is a major driver of cell fate transition during embryonic development.
2020-09-04 | GSE144881 | GEO
Project description:Similar to ubiquitin, SUMO forms chains, but the identity of SUMO-chain-modified factors and the purpose of this modification remain largely unknown. Here, we identify budding yeast SUMO protease Ulp2, able to disassemble SUMO chains, as a DDK interactor enriched at replication origins that promotes DNA replication initiation. Replication-engaged DDK is SUMOylated on chromatin, becoming a degradation-prone substrate when Ulp2 no longer protects it against SUMO-chain assembly. Specifically, SUMO chains channel DDK for SUMO-targeted ubiquitin ligase Slx5/Slx8-mediated and Cdc48 segregase-assisted proteasomal degradation. Importantly, the SUMOylation-defective ddk-KR mutant rescues inefficient replication onset and MCM activation in cells lacking Ulp2, suggesting that SUMO chains time DDK degradation. Using two unbiased proteomic approaches, we further identify subunits of the MCM helicase and other factors as SUMO-chain-modified degradation-prone substrates of Ulp2 and Slx5/Slx8. We thus propose SUMO-chain-/Ulp2-protease-regulated proteasomal degradation as a mechanism that times the availability of functionally-engaged SUMO-modified protein pools during replication and beyond.
2019-09-10 | GSE113835 | GEO
Project description:Transgenic C. elegans strains that express human SUMO-1 under the control of pan-neuronal (aex-3) or pan muscular (myo-4) promoters were assayed for gene expression changes. Control N2 non transgenic worms were compared to aex-3::His-SUMO-1 and myo-4::His-SUMO-1 worms in 3 biological replicate populations
2011-01-31 | E-GEOD-19972 | biostudies-arrayexpress
Project description:Analysis of changes in SUMO-2 binding to chromatin in response to heat shock in human U2OS cells
2015-07-13 | E-MTAB-2368 | biostudies-arrayexpress
Project description:Post-translational modification by SUMO is a key regulator of cell identity. In mouse embryonic fibroblasts (MEFs), SUMO impedes reprogramming to pluripotency, while in embryonic stem cells (ESCs), it represses the emergence of totipotent-like cells, suggesting that SUMO targets distinct substrates to preserve somatic and pluripotent states. Using MS-based proteomics, we show that the composition of endogenous SUMOylomes differs dramatically between MEFs and ESCs. In MEFs, SUMO2/3 targets proteins associated with canonical SUMO functions, such as splicing, and transcriptional regulators driving somatic enhancer selection. In contrast, in ESCs, SUMO2/3 primarily modifies highly interconnected repressive chromatin complexes, thereby preventing chromatin opening and transitioning to totipotent-like states. We also characterize several SUMO-modified pluripotency factors and show that SUMOylation of Dppa2 and Dppa4 impedes the conversion to 2-cell-embryo-like states. Altogether, we propose that rewiring the repertoire of SUMO target networks is a major driver of cell fate decision during embryonic development.
2020-09-16 | PXD017697 | Pride
Project description:Transient brain ischemia massively activates global SUMOylation. A large fraction of SUMO targets are nuclear proteins involved in gene expression. However, gene expression profile modulated by ischemia-induced SUMOylation has not been studied. Using a SUMO knockdown (SUMO-KD) mouse model and microarray technique, we investigated how SUMOylation modulated gene expression after brain ischemia. Wild-type and SUMO-KD mice were subjected to transient forebrain ischemia or sham surgery. The hippocampal CA1 subfield samples collected at 3 hours reperfusion were analyzed using Affymetrix microarrays.
2016-08-01 | E-GEOD-80681 | biostudies-arrayexpress
Project description:Post-translational modification by SUMO is a key regulator of cell identity. In mouse embryonic fibroblasts (MEFs), SUMO impedes reprogramming to pluripotency, while in embryonic stem cells (ESCs), it represses the emergence of totipotent-like cells, suggesting that SUMO targets distinct substrates to preserve somatic and pluripotent states. Using MS-based proteomics, we show that the composition of endogenous SUMOylomes differs dramatically between MEFs and ESCs. In MEFs, SUMO2/3 targets proteins associated with canonical SUMO functions, such as splicing, and transcriptional regulators driving somatic enhancer selection. In contrast, in ESCs, SUMO2/3 primarily modifies highly interconnected repressive chromatin complexes, thereby preventing chromatin opening and transitioning to totipotent-like states. We also characterize several SUMO-modified pluripotency factors and show that SUMOylation of Dppa2 and Dppa4 impedes the conversion to 2-cell-embryo-like states. Altogether, we propose that rewiring the repertoire of SUMO target networks is a major driver of cell fate decision during embryonic development.
2020-09-16 | PXD020287 | Pride