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Dsk1 repairs DSBs by homologous recombination via Rad52 in Schizosaccharomyces pombe

ABSTRACT: Dsk1 repairs DSBs by homologous recombination via Rad52 in Schizosaccharomyces pombe

PROVIDER: PRJNA1099302 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28637411_1.fastq.gz	Fastqsanger.gz
	SRR28637411_2.fastq.gz	Fastqsanger.gz
	SRR28637412_1.fastq.gz	Fastqsanger.gz
	SRR28637412_2.fastq.gz	Fastqsanger.gz
	SRR28637413_1.fastq.gz	Fastqsanger.gz

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Dsk1 repairs DSBs by homologous recombination via Rad52 in Schizosaccharomyces pombe

Project description:To investigate the different of gene expression between dsk1Δ and wild strain, and then, we performed the gene expression analysis from the RNA-Seq data.

2024-12-25 | GSE263826 | GEO

Different SWI/SNF complexes coordinately promote R-loop- and RAD52- dependent transcription-coupled homologous recombination

Project description:The SWI/SNF family of ATP-dependent chromatin remodeling complexes are implicated in multiple DNA damage response mechanisms and frequently mutated in cancer. The BAF and PBAF complexes are two major types of SWI/SNF complexes that are functionally distinguished by their exclusive subunits. Accumulating evidence suggests that double-strand breaks (DSBs) in transcriptionally active DNA are preferentially repaired by a dedicated homologous recombination pathway. We show that different BAF and PBAF subunits promote homologous recombination and are rapidly recruited to DSBs in a transcription-dependent manner. The PBAF complex promotes RNA polymerase II eviction near DNA damage to rapidly initiate transcriptional silencing, while the BAF complex helps to maintain this transcriptional silencing. Furthermore, ARID1A-containing BAF complexes promote RNaseH1 and RAD52 recruitment to facilitate R-loop resolution and DNA repair. Our results highlight how multiple SWI/SNF complexes perform different functions to enable DNA repair in the context of actively transcribed genes.

2023-07-31 | PXD035140 | Pride

PolySUMOylation of PCNA and Rad52 restricts centromeric recombination in fission yeast

Project description:SUMOylation, a conserved post-translational modification in eukaryotes, regulates protein function, localization, and stability. One of the least understood aspects of SUMOylation is formation of polymeric chains and their impact on DNA metabolism. Here, using Schizosaccharomyces pombe, we show that loss of SUMO chains results in elevated spontaneous replication stress and DNA damage. Notably, SUMO chains are required for proper centromeric organization; their absence leads to aberrant recruitment of recombination factors and increased recombination within centromeres. To explore site-specific SUMOylation connected with recombination repair, we established a split-SUMO-ID proteomics approach that allowed identification of SUMO- and Rad52-dependent interactomes. This revealed an enrichment of polySUMOylated proteins at the sites of Rad52 repair, including the essential replication factor PCNA. We demonstrate that SUMO chain-modified PCNA counteracts Rad8-mediated PCNA polyubiquitination, thereby regulating the channeling toward the template-switch branch of post-replication repair at stalled forks within centromeres. In the absence of SUMO chains, excessive template-switching drives elevated recombination at centromeres. Finally, we show that artificial tethering of a SUMO chain to Rad52 suppresses centromeric recombination caused by loss of SUMO chains. Together, our findings uncover an essential role for SUMO chains in maintaining centromere stability by modulating DNA repair pathway choice under endogenous replication stress.

2024-09-15 | GSE276805 | GEO

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

| PRJNA625048 | ENA

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.

2023-11-01 | GSE242527 | GEO

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

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

| PRJNA625049 | ENA

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.

2012-09-30 | E-GEOD-35698 | biostudies-arrayexpress

Ectopic expression of RAD52 and dn53BP1 improves homology-directed repair during CRISPR/Cas9 genome editing

Project description:Gene disruption by CRISPR/Cas9 is highly efficient and relies on the error-prone non-homologous end-joining (NHEJ) pathway. Conversely, precise gene editing requires homology-directed repair (HDR), which occurs at a lower frequency than NHEJ in mammalian cells. Here, by testing whether manipulation of DNA repair factors would improve HDR efficacy, we show that transient ectopic co-expression of RAD52 and a dominant-negative 53BP1 (dn53BP1) synergize to enable efficient HDR using a single-stranded oligonucleotide DNA donor template at multiple loci in human cells, including patient-derived induced pluripotent stem (iPS) cells. Co-expression of RAD52 and dn53BP1 improves multiplexed HDR-mediated editing, whereas expression of RAD52 alone enhances HDR with Cas9 nickase. Our data show that the frequency of NHEJ-mediated DSB repair in the presence of these two factors is not suppressed, and suggest that dn53BP1 competitively antagonizes 53BP1 to augment HDR in combination with RAD52. Importantly, co-expression of RAD52 and dn53BP1 does not alter Cas9 off-target activity. These findings support the use of RAD52 and dn53BP1 co-expression to overcome bottlenecks that limit HDR in precision genome editing.

2017-11-23 | GSE103241 | GEO

Reappearance from Obscurity: Mammalian Rad52 in Homologous Recombination.

Project description:Homologous recombination (HR) plays an important role in maintaining genomic integrity. It is responsible for repair of the most harmful DNA lesions, DNA double-strand breaks and inter-strand DNA cross-links. HR function is also essential for proper segregation of homologous chromosomes in meiosis, maintenance of telomeres, and resolving stalled replication forks. Defects in HR often lead to genetic diseases and cancer. Rad52 is one of the key HR proteins, which is evolutionarily conserved from yeast to humans. In yeast, Rad52 is important for most HR events; Rad52 mutations disrupt repair of DNA double-strand breaks and targeted DNA integration. Surprisingly, in mammals, Rad52 knockouts showed no significant DNA repair or recombination phenotype. However, recent work demonstrated that mutations in human RAD52 are synthetically lethal with mutations in several other HR proteins including BRCA1 and BRCA2. These new findings indicate an important backup role for Rad52, which complements the main HR mechanism in mammals. In this review, we focus on the Rad52 activities and functions in HR and the possibility of using human RAD52 as therapeutic target in BRCA1 and BRCA2-deficient familial breast cancer and ovarian cancer.

| S-EPMC5042393 | biostudies-literature

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

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

| PRJNA625054 | ENA

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