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METTL3 and N6-methyladenosine Promotes Homologous Recombination Mediated Repair of DSBs by Facilitating R-loop Formation [RIP-Seq]

ABSTRACT: METTL3 and N6-methyladenosine Promotes Homologous Recombination Mediated Repair of DSBs by Facilitating R-loop Formation [RIP-Seq]

PROVIDER: PRJNA625054 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11540633_1.fastq.gz	Fastqsanger.gz
	SRR11540633_2.fastq.gz	Fastqsanger.gz
	SRR11540634_1.fastq.gz	Fastqsanger.gz
	SRR11540634_2.fastq.gz	Fastqsanger.gz
	SRR11540635_1.fastq.gz	Fastqsanger.gz

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METTL3 and N6-methyladenosine Promotes Homologous Recombination Mediated Repair of DSBs by Facilitating R-loop Formation

Project description:METTL3 and N6-methyladenosine Promotes Homologous Recombination Mediated Repair of DSBs by Facilitating R-loop Formation

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METTL3 and N6-methyladenosine Promotes Homologous Recombination Mediated Repair of DSBs by Facilitating R-loop Formation [other]

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Dsk1 repairs DSBs by homologous recombination via Rad52 in Schizosaccharomyces pombe

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METTL3 and N6-methyladenosine Promotes Homologous Recombination Mediated Repair of DSBs by Facilitating R-loop Formation

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

2020-04-14 | GSE148573 | GEO

METTL3 and N6-methyladenosine Promotes Homologous Recombination Mediated Repair of DSBs by Facilitating R-loop Formation [other]

Project description:Examination of R-loop formation at I-PpoI cutting site (28S rDNA and DAB1) and other uncut genome in NC or siMETTL3 transferred HEK293T with or without I-PpoI cutting

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METTL3 and N6-methyladenosine Promotes Homologous Recombination Mediated Repair of DSBs by Facilitating R-loop Formation [RIP-Seq]

Project description:The goals of this study are to compare the level of YTHDC1 associated nascent RNA at chromatin between DMSO and zeocin treatment.

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A complex of BRCA2 and PP2A-B56 is required for homologous recombination-mediated DNA repair

Project description:Mutations in the tumour suppressor BRCA2 are associated with predisposition to breast and ovarian cancers. BRCA2 has a central role in genome integrity by facilitating the repair of toxic DNA double-strand breaks (DSBs) by homologous recombination. BRCA2 acts by promoting RAD51 nucleofilament formation on resected single-stranded DNA, but how BRCA2 activity is regulated during HR is not fully understood. Here, we delineate a pathway where ATM and ATR kinases phosphorylate a highly conserved region in BRCA2 in response to DNA DSBs. These phosphorylations stimulate the binding of the protein phosphatase PP2A-B56 to BRCA2 through a conserved binding motif. We show that the phosphorylation-dependent formation of the BRCA2-PP2A-B56 complex is required for efficient RAD51 loading to sites of DNA damage and HR-mediated DNA repair. Moreover, we find that several cancer-associated mutations in BRCA2 deregulate the BRCA2-PP2A-B56 interaction and sensitize cells to PARP inhibition. Collectively, our work uncovers PP2A-B56 as a positive regulator of BRCA2 function in HR with clinical implications for BRCA2 and PP2A-B56 mutated cancers.

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HELZ promotes R loop resolution to facilitate DNA double-strand break repair by homologous recombination

Project description:Successful R-loop homeostasis consists of its timely biogenesis and removal throughout the genome to regulate diverse cellular processes. Yet, they are considered hazardous source to our genome when their turnover goes awry. Here, we report HELZ, a novel player in R-loop homeostasis and DNA repair pathway. HELZ mediates resistance to several DNA damaging agents, and localizes to DSBs and its depletion increases R-loops fostering genomic instability. Loss of HELZ results in impaired homologous recombination (HR) due to R-loops accumulation, with an increase in classical-non-homologous end joining (c-NHEJ), suggesting a role for HELZ in regulating DSB repair pathway choice. Rad51 retention at DSBs is governed by HELZ mediated R-loop accumulation. Mechanistically, our data show that HELZ complexes with BRCA1 and facilitates its recruitment to DSBs in an R-loop dependent manner. Collectively, our data support a model in which HELZ recruits BRCA1 and facilitates R loop resolution at DSBs to promote HR and therefore maintains genome stability.

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BRCA1 functions independently of homologous recombination in DNA interstrand crosslink repair

Project description:Brca1 is required for DNA repair by homologous recombination (HR) and normal embryonic development. Here we report that deletion of the DNA damage responsefactor 53BP1 overcomes embryonic lethality in Brca1-nullizygous mice, and rescues HR deficiency, as measured by hypersensitivity to PARP (polyADPribose polymerase) inhibition. However, Brca1,53BP1 double-deficient cells are hypersensitive to DNA interstrand crosslinks (ICLs), indicating that BRCA1 has an additional role in DNA cross-link repair that is distinct from HR. Disruption of the non-homologous end-joining (NHEJ) factor, Ku, promotes DNA repair in Brca1-deficient cells; however deletion of either Ku or 53BP1 exacerbates genomic instability in cells lacking FANCD2, a mediator of the Fanconi Anemia pathway for ICL repair. Brca1 therefore has two separate roles in ICL repair, whereas FANCD2 provides a key activity that can not be bypassed by ablation of 53BP1 or Ku. B cells were stimulated to undergo class switch recombination in vitro. Chromatin from B cells was harvested 72 hours post-stimulation and used for RPA ChIP to study the extent of resection of DNA DSBs.

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Mettl3-m6A-YTHDF1 axis promotion of mitochondrial dysfunction in metabolic dysfunction–associated steatotic liver disease (MASLD)

Project description:The N6-methyladenosine (m6A) mRNA modification and the mitochondrial respiratory chain (MRC) hold paramount importance in the advancement of MASLD. This study thoroughly investigates the relationship and impact of m6A mRNA modification and mitochondrial function in the progression of MASLD. Here we report that the mRNA and protein levels of mitochondrial respiratory chain (MRC) subunits showed inconsistent trends in vivo experiments. Abnormal m6A modification and mitochondrial dysfunction in MASLD were attributed to the upregulation of methyltransferase like 3 (Mettl3) and the downregulation of YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) induced by high-fat foods. Mettl3 promoted the MRC's function. However, knockout of the reader protein YTHDF1, which plays a crucial role in the m6A modification process, counteracted the effect of Mettl3 and suppressed MRC. In MASLD, damage to the MRC may be regulated by the Mettl3-m6A-YTHDF1 complex axis, especially by the role of YTHDF1. Our research has offered a novel perspective on the involvement of m6A mRNA methylation in the pathogenesis of MASLD.

2024-09-20 | PXD047819 | Pride

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