Saccharomyces cerevisiae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA387342 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Meiotic double-strand break end resection mapping by S1Seq
| PRJNA337955 | ENA
Project description:DNA double strand break (DSB) is a highly toxic lesion that can generate genome instability, a major source of tumorigenesis. DSBs are mainly repaired by nonhomologous end joining (NHEJ) or homologous recombination (HR). The selection of the DSB repair pathway primarily depends on the DNA resection of the DSB ends. Indeed, HR is initiated by resection at the DSB generating 3' single stranded extension. The shieldin complex prevents resection fostering DSB repair toward NHEJ. In the context of genome stability, NLRP3 was recently reported to interact with ATM and to enhance its activation in response to DNA DSBs. Whether NLRP3 controls the DSB repair machinery remains unknown. To further elucidate the function of NLRP3 in DNA repair, we sought NLRP3-binding partners by screening proteins that bind to FLAG-tagged NLRP3 (FLAG-NLRP3) in HeLa cells.
2025-07-14 | PXD058288 | Pride
Project description:In the bacterium Escherichia coli, RecG directs DNA synthesis during the repair of DNA double-strand breaks by homologous recombination. Examination of RecA binding during double-strand break repair in Escherichia coli in the presence and absence of RecG protein
2016-05-19 | E-GEOD-77181 | biostudies-arrayexpress
Project description:Sterile alpha motif and HD domain-containing protein 1 (SAMHD1) has a dNTPase-independent function in promoting DNA end resection to facilitate DNA double-strand break (DSB) repair by homologous recombination (HR); however, it is not known if upstream signaling events govern this activity. Here, we show that SAMHD1 is deacetylated by the SIRT1 sirtuin deacetylase, facilitating its binding with ssDNA at DSBs, to promote DNA end resection and HR. SIRT1 complexes with and deacetylates SAMHD1 at conserved lysine 354 (K354) specifically in response to DSBs. K354 deacetylation by SIRT1 promotes DNA end resection and HR but not SAMHD1 tetramerization or dNTPase activity. Mechanistically, K354 deacetylation by SIRT1 promotes SAMHD1 recruitment to DSBs and binding to ssDNA at DSBs, which in turn facilitates CtIP ssDNA binding, leading to promotion of genome integrity. Our findings define a mechanism governing the dNTPase-independent resection function of SAMHD1 by SIRT1 deacetylation in promoting HR and genome stability.
2023-03-11 | PXD031357 | Pride
Project description:The Bloom syndrome DNA helicase BLM contributes to chromosome stability through its roles in double-strand break repair by homologous recombination and DNA replication fork restart during the replication stress response. Loss of BLM activity leads to Bloom syndrome, which is characterized by extraordinary cancer risk and small stature. Here, we have analyzed the composition of the BLM complex in unperturbed cells and identified a direct physical interaction with the Mcm6 subunit of the minichromosome maintenance (MCM) complex by co-immunopecipitations using endogenous and recombinant proteins as well as two-hybrid analysis.
2022-02-15 | PXD018823 | Pride
Project description:DNA double strand break (DSB) repair through homologous recombination (HR) is crucial to maintain genome stability. DSB resection generates a single strand DNA intermediate, which is crucial for the HR process. We used a synthetic DNA structure, mimicking a resection intermediate, as a bait to identify proteins involved in this process. Among these, LC/MS analysis identified the RNA binding protein, HNRNPD. We found that HNRNPD was able to bind chromatin, although this binding occurred independently of DNA damage. However, upon damage, HNRNPD re-localized to γH2Ax foci and its silencing impaired CHK1 S345 phosphorylation and the DNA end resection process. Indeed, HNRNPD silencing reduced the ssDNA fraction upon camptothecin treatment and AsiSI-induced DSB resection and reduced RPA32 S4/8 phosphorylation. CRISPR/Cas9-mediated HNRNPD knockout impaired in vitro DNA resection and sensitized cells to camptothecin and olaparib treatment. We found that HNRNPD interacts with the heterogeneous nuclear ribonucleoprotein SAF-A previously associated with DNA damage repair. HNRNPD depletion resulted in an increased amount of RNA:DNA hybrids upon DNA damage . Both the expression of RNase H1 and RNA pol II inhibition recovered the ability to phosphorylate RPA32 S4/8 in HNRNPD knockout cells upon DNA damage, suggesting that RNA:DNA hybrid resolution likely rescues the defective DNA damage response of HNRNPD-depleted cells.
2019-02-26 | PXD012045 | Pride
Project description:Transient obstruction of DNA polymerase progression activates the ATR checkpoint kinase, which suppresses fork breakage, strand resection, and RPA accumulation. Herein, we use a developed DNA break-detection assay, BrITL, to identify replication-problematic loci (RPLs) that become processed into persistent double-strand breaks across the mammalian genome from ATR inhibition.
2018-10-04 | GSE115624 | GEO
Project description:Transient obstruction of DNA polymerase progression activates the ATR checkpoint kinase, which suppresses fork breakage, strand resection, and RPA accumulation. Herein, we use a developed DNA break-detection assay, BrITL, to identify replication-problematic loci that become processed into persistent double-strand breaks across the human genome from ATR inhibition.
2018-10-04 | GSE115623 | GEO
Project description:The choice between distinct DNA double-strand break (DSB) repair pathways is a central determinant of genome stability. This decision critically depends on DNA end resection, the nucleolytic processing of DSB ends that generates 3′ single-stranded DNA required for homologous recombination while simultaneously suppressing non-homologous end joining. Although the enzymatic mechanisms of resection have been well defined, its regulation by the dynamic, DSB-surrounding chromatin remains poorly understood. Here, we used the budding yeast cdc13-1 system to investigate how chromatin influences resection after telomere deprotection. Analysis of long-range resection nucleases revealed that Dna2 contributes to telomeric processing, particularly in the absence of Exo1, and acts in conjunction with the STR complex (Sgs1–Top3–Rmi1). Genetic removal of chromatin regulatory factors showed that H2A.Z incorporation did not significantly affect resection, whereas depletion of major nucleosome evictors RSC and SWI/SNF impaired telomere resection. These findings indicate that chromatin remodelling by RSC and SWI/SNF are involved in single-strand DNA formation after telomere deprotection and highlights utilisation of the cdc13-1 system to investigate chromatin regulators and their role in DSB repair pathway choice.
2026-06-22 | GSE325557 | GEO