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ASH1L-MRG15 methyltransferase deposits H3K4me3 and FACT for damage verification in nucleotide excision repair

ABSTRACT: ASH1L-MRG15 methyltransferase deposits H3K4me3 and FACT for damage verification in nucleotide excision repair

PROVIDER: PRJNA942778 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23760301_1.fastq.gz	Fastqsanger.gz
	SRR23760301_2.fastq.gz	Fastqsanger.gz
	SRR23760302_1.fastq.gz	Fastqsanger.gz
	SRR23760302_2.fastq.gz	Fastqsanger.gz
	SRR23760303_1.fastq.gz	Fastqsanger.gz

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ASH1L methyltransferase deposits H3K4me3 and FACT for damage verification in nucleotide excision repair [ChIP-Seq ASH1L-CTD]

Project description:To recognize DNA damage, nucleotide excision repair (NER) deploys a multipart mechanism by which the XPC sensor detects helical distortions followed by engagement of TFIIH for lesion verification. Accessory players ensure that this factor handover takes place on chromatin where DNA is wrapped around histones. We show that the histone methyltransferase ASH1L, once activated by MRG15, accelerates global-genome NER activity. Upon UV irradiation, ASH1L deposits H3K4me3 marks all over the genome (except in gene promoters), thus priming chromatin for relocations of XPC from native to damaged DNA. ASH1L further recruits the histone chaperone FACT to UV lesions. In the absence of ASH1L, MRG15 or FACT, XPC persists on damaged DNA without being able to deliver lesions to the TFIIH verifier. We conclude that ASH1L implements repair hotspots whose H3K4me3 and FACT occupancy confers an active promoter-like code and organization of histones that make DNA damage verifiable by the NER machinery.

2023-06-08 | GSE227008 | GEO

ASH1L methyltransferase deposits H3K4me3 and FACT for damage verification in nucleotide excision repair [ATAC-Seq]

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ASH1L methyltransferase deposits H3K4me3 and FACT for damage verification in nucleotide excision repair [ChIP-Seq]

2023-06-08 | GSE214182 | GEO

ASH1L methyltransferase deposits H3K4me3 and FACT for damage verification in nucleotide excision repair [ChIP-Seq ASH1L-CTD]

Project description:ASH1L methyltransferase deposits H3K4me3 and FACT for damage verification in nucleotide excision repair [ChIP-Seq ASH1L-CTD]

| PRJNA942905 | ENA

ASH1L methyltransferase deposits H3K4me3 and FACT for damage verification in nucleotide excision repair [ATAC-Seq]

Project description:ASH1L methyltransferase deposits H3K4me3 and FACT for damage verification in nucleotide excision repair [ATAC-Seq]

| PRJNA942903 | ENA

ASH1L-MRG15 methyltransferase deposits H3K4me3 and FACT for damage verification in nucleotide excision repair.

Project description:To recognize DNA adducts, nucleotide excision repair (NER) deploys the XPC sensor, which detects damage-induced helical distortions, followed by engagement of TFIIH for lesion verification. Accessory players ensure that this factor handover takes place in chromatin where DNA is tightly wrapped around histones. Here, we describe how the histone methyltransferase ASH1L, once activated by MRG15, helps XPC and TFIIH to navigate through chromatin and induce global-genome NER hotspots. Upon UV irradiation, ASH1L adds H3K4me3 all over the genome (except in active gene promoters), thus priming chromatin for XPC relocations from native to damaged DNA. The ASH1L-MRG15 complex further recruits the histone chaperone FACT to DNA lesions. In the absence of ASH1L, MRG15 or FACT, XPC is misplaced and persists on damaged DNA without being able to deliver the lesions to TFIIH. We conclude that ASH1L-MRG15 makes damage verifiable by the NER machinery through the sequential deposition of H3K4me3 and FACT.

| S-EPMC10314917 | biostudies-literature

ASH1L-MRG15 methyltransferase deposits H3K4me3 and FACT for damage verification in nucleotide excision repair

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-06-08 | GSE227009 | GEO

MRG15 interactome upon UV irradiation

Project description:The aim of this analysis is to identify the difference between interaction partners of MRG15 wild type and Chromodomain and MRG domain mutants upon UV irradiation. Therefore, MRG15 wild type and mutants (N-terminal FLAG tag) were overexpressed in U2OS cells. After UV irradiation, immunoprecipitation of the constructs was performed using FLAG M2 affinity gel. The constructs were eluted from the beads with 3xFLAG peptide.

2023-07-03 | PXD043089 | Pride

ASH1L links histone H3 lysine 36 di-methylation to leukemia

Project description:The histone methyltransferases MLL and ASH1L are trithorax-group proteins that interact genetically through undefined molecular mechanisms to regulate developmental and hematopoietic gene expression. Here we show that the lysine 36-dimethyl mark of histone H3 (H3K36me2) written by ASH1L is preferentially bound in vivo by LEDGF, an MLL-associated protein that co-localizes with MLL, ASH1L and H3K36me2 on chromatin genome wide. Furthermore, ASH1L facilitates recruitment of LEDGF and wild type MLL proteins to chromatin at key leukemia target genes, and is a crucial regulator of MLL-dependent transcription and leukemic transformation. Conversely KDM2A, an H3K36me2 demethylase and Polycomb-group silencing protein, antagonizes MLL-associated leukemogenesis. Our studies illuminate the molecular mechanisms underlying epigenetic interactions wherein placement, interpretation and removal of H3K36me2 contribute to the regulation of gene expression and MLL leukemia, and suggest ASH1L as a target for therapeutic intervention. Investigation of multiple transcription factors and histone modification marks in MV4-11 human leukemia cells.

2016-07-01 | E-GEOD-73528 | biostudies-arrayexpress

Phase Separation of MRG15 delays cellular senescence [CUT&Tag]

Project description:Phase separation, a biophysical process that segregates subcellular environments into condensates, is recognized for its role in regulating transcription. However, the extent of its influence on cellular senescence processes remains to be fully elucidated. Here, we have established that the depletion of MRG15, a conserved chromodomainprotein, leads to cellular senescence in human mesenchymal stem cells (hMSCs). MRG15 is capable of forming phase-separated liquid condensates via its intrinsically disordered region (IDR). Through the utilization of IDR deletion and replacement assays, we have shed light on the pivotal role that MRG15 condensation plays in the senescence of hMSCs. Through epigenomic and transcriptomic analysis, the depletion of MRG15 impacts pathways that are integral to the cell cycle and the senescence process, as evidenced by the diminished binding and the modified expression of key genes, including CDKN1A, LMNB1, CCNB1, NPM1, MYC, and HMGB2. Within a bleomycin-induced model of idiopathic pulmonary fibrosis in mice, hMSCs of the wild-type variety were able to ameliorate inflammation and fibrosis, a stark contrast to the outcomes observed in MSCs where MRG15 was knocked down or its IDR was deleted. Our findings establishes a link between phase separation and senescence regulation and could present a promising new therapeutic target for the alleviation of age-related diseases and the potential extension of lifespan.

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