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Microglia homeostasis mediated by epigenetic ARID1A to regulate neural progenitor cells response in brain development

ABSTRACT: We report the genomic characterization of H3K9me3 occupancy in microglia at E14 brain.CUT&Tag experiment was performed with antibody against H3K9me3. We generated genome-wide characterization of H3K9me3 occupancy in microglia and find that H3K9me3 was prone to bind the promoters and the intergenic regions. The number and proximity of H3K9me3 occupancy to the transcription start sites determined the probability of transcriptional regulation on genes expression.The genomic localization of H3K9me3 might reveal the importance role of ARID1A in chromatin landscape of microglia homeostatic state during cortical development. Detailed investigation of the binding profiles show that the enrichments of H3K9me3 peaks in the regulatory regions of Prg3 gene. This study provides a framework for the epigenetic regulation of ARID1A in microglia homeostasis.

ORGANISM(S): Mus musculus

PROVIDER: GSE190450 | GEO | 2021/12/15

REPOSITORIES: GEO

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Microglia homeostasis mediated by epigenetic ARID1A to regulate neural progenitor cells response in brain development [RNA-seq]

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Project description:Arid1a is the subunit of SWI/SNF complex, which was reported to guide SWI/SNF to DNA. Here, we found that loss of Arid1a in the liver results in improved liver regeneration after partial hepatectomy.Genome-wide analysis showed that after hepatectomy,loss of Arid1a reduces the recruitment and activity of E2F4 on target promoters, resulting in expression programs that favor regeneration during injury. Correspondingly, these promoters showed increased H3k4me2 and H3k27ac marks, indicating de-repression of these E2f target genes. The post partial hepatectomy mice liver cells were fixed and isolated, analysis of genomic occupancy of E2f4,H3K4me2,H3K27ac in hepatocytes from Arid1a WT and Arid1a liver specific KO mice by ChIP-seq.

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The ARID1A tumor suppressor controls global transcription via pausing of RNA Polymerase II

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EZH2 and H3K27me3 ChIP-seq in E14 mouse embryonic stem cells harboring wildtype or mutant EZH2.

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Histone ubiquitination-methylation crosstalk involving UHRF1 and SUV39H1/2 reinforces heterochromatin states in response to DNA hypomethylation

Project description:Histone H3 mono-ubiquitination, catalyzed by the RING E3 ubiquitin ligase UHRF1, is appreciated as a docking site for DNMT1 during DNA replication to facilitate DNA methylation maintenance. Its functions beyond this are unknown. Here, we identify simultaneous increases in UHRF1-dependent H3K18ub and SUV39H1/2-dependent H3K9me3 as prominent epigenetic alterations accompanying DNA hypomethylation induced by DNMT1 inhibition. Integrative epigenomics analyses reveal that transient accumulation of hemi-methylated DNA, resulting from incomplete DNA methylation maintenance, stimulates UHRF1-dependent H3K18ub at CpG islands that nucleates new domains of H3K9me3 and impedes PRC2 activity in these genomic regions. Notably, H3K18ub enhances the methyltransferase activity of SUV39H1/2, leading to increased H3K9me3 at these CpG island promoters. Blocking H3K18ub-dependent SUV39H1/2 activity enhances the efficacy of DNMT1 inhibitors. Collectively, these findings reveal a novel histone ubiquitination-methylation crosstalk mechanism that reinforces heterochromatin states in the absence of DNA methylation and proposes new strategies for improving cancer epigenetic therapy.

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