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Senataxin resolves R-loops forming at DNA double strand breaks to prevent translocations

ABSTRACT: Senataxin resolves R-loops forming at DNA double strand breaks to prevent translocations

PROVIDER: PRJEB24001 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2224140.fastq.gz	Fastqsanger.gz
	ERR2224141.fastq.gz	Fastqsanger.gz
	ERR2224142.fastq.gz	Fastqsanger.gz
	ERR2224143.fastq.gz	Fastqsanger.gz
	ERR2224144_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Senataxin resolves R-loops forming at DNA double strand breaks to prevent translocations

Project description:DNA Double Strands Breaks (DSBs) are highly detrimental since they can lead to mutations and chromosomes rearrangements (amplification, deletion, translocation and chromosome loss). Here, we set to assess the role of senataxin, a RNA:DNA helicase involved in the regulation of transcription and the maintenance of genome integrity, at sites of DNA Double Strand Breaks. We performed ChIP-Seq mapping of senataxin before and after damage, genome-wide DNA:RNA hybrids (DRIP) mapping before and after damage. We also performed RNA-Seq and RNA pol II mapping (total and phosphorylated on serine 2 of the CTD) by ChIP-Seq in undamaged cells to discriminate between damage in active versus inactive regions.

2018-02-20 | E-MTAB-6318 | biostudies-arrayexpress

Senataxin resolves RNA:DNA hybrids forming at DNA double-strand breaks to prevent translocations.

Project description: Not available

| S-EPMC5803260 | biostudies-literature

Senataxin and RNase H2 act redundantly to suppress genome instability during class switch recombination

Project description:Class switch recombination generates antibody distinct isotypes critical to a robust adaptive immune system and defects are associated with auto-immune disorders and lymphomagenesis. Transcription is required during class switch to recruit the cytidine deaminase AID—an essential step for the formation of DNA doublestrand breaks—and strongly induces the formation of R loops within the immunoglobulin heavy chain locus. However, the impact of R loops on double-strand break formation and repair during class switch recombination remains unclear. Here we report that cells lacking two enzymes involved in R loop removal— Senataxin and RNase H2—exhibit increased R loop formation and genome instability at the immunoglobulin heavy chain locus without impacting class switch recombination efficiency, transcriptional activity, or AID recruitment. Senataxin and RNase H2-deficient cells also exhibit increased insertion mutations at switch junctions, a hallmark of alternative end joining. Importantly, these phenotypes were not observed in cells lacking Senataxin or RNase H2B alone. We propose that Senataxin acts redundantly with RNase H2 to mediate timely R loop removal, promoting efficient repair while suppressing AID-dependent genome instability and insertional mutagenesis.

2022-12-14 | GSE201210 | GEO

INTS6-SOSS1 complex facilitates DNA:RNA hybrid autoregulation at double- strand breaks

Project description:This study shows that Integrator complex subunit 6 (INTS6) associates with the trimeric SOSS1 (comprising INTS3, INIP, and hSSB1) to form a tetrameric SOSS1 complex following DNA damage. INTS6 binds to DNA:RNA hybrids and plays a crucial role in Protein Phosphatase 2 (PP2A) recruitment to DNA double-strand breaks (DSBs), facilitating the dephosphorylation of RNAPII. Furthermore, INTS6 prevents the accumulation of damage-induced RNA transcripts and stabilizes DNA:RNA hybrids at DSB sites. INTS6 interacts with, and promotes the recruitment of Senataxin (SETX) to DSBs, facilitating the resolution of DNA:RNA hybrids/R-loops. These data demonstrate the significance of the SOSS1 complex in autoregulating DNA:RNA dynamics and the promotion of efficient DNA repair.

2025-05-06 | PXD048694 | Pride

Senataxin regulates cisplatin resistance through an R-loop mediated mechanism in HPV-associated Head and Neck Cancer

Project description:Resistance to cisplatin is a key clinical concern in HPV-independent (HPV-) and HPV-associated (HPV+) head and neck cancer. Upregulation of DNA repair is known to contribute to cisplatin resistance and a major source of endogenous DNA damage are DNA/RNA hybrids, known as R-loops. Following creation of HPV+ and HPV- cisplatin resistant cell lines, RNA-Sequencing revealed alterations in the expression of known R-loop regulators. Resistant cells had elevated global R-loop levels and in HPV+ resistant cells there was a corresponding upregulation of the R-loop resolving protein, senataxin. Depletion of senataxin led to increased sensitivity to cisplatin, an increase in DNA damage and elevated R-loops at specific genomic loci. In summary, using an in vitro model of cisplatin resistance, we identified that senataxin modulates sensitivity to cisplatin through an R-loop mediated mechanism in HPV+ cells. R-loops may represent a potential therapeutic target and warrant further investigation.

2025-07-29 | GSE279046 | GEO

RNase H2, mutated in Aicardi‐Goutières syndrome, resolves co-transcriptional R-loops to prevent DNA breaks and inflammation.

Project description:RNase H2, mutated in Aicardi‐Goutières syndrome, resolves co-transcriptional R-loops to prevent DNA breaks and inflammation.

| PRJNA612527 | ENA

Senataxin (SETX) prevents Myc-induced replicative stress [BLISS]

Project description:Here we investigated the RNA helicase Senataxin (SETX), an enzyme that resolve RNA-DNA hybrids and R-loops, to address its role in preventing replicative stress by oncogenic Myc. Silencing of SETX led to selective engagement of the DNA damage response (DDR) upon Myc activation, leading to a robust cytotoxicity. Pharmacological dissection of the upstream kinases regulating the DDR revealed a protective role of the ATR pathway, that once inactivated, boosted SETX driven-DDR. While loss of SETX did not lead to a genome-wide increase of R-loops, mechanistic analyses revealed enhanced R-loops localized at DDR-foci and newly replicated genomic loci, compatible with a selective role of SETX in resolving RNA-DNA hybrids to alleviate Myc-induced RS.

2025-03-19 | GSE275922 | GEO

Senataxin (SETX) prevents Myc-induced replicative stress [EU-seq]

2025-03-19 | GSE275924 | GEO

Senataxin (SETX) prevents Myc-induced replicative stress [DRIP-seq]

2025-03-19 | GSE275923 | GEO

Mechanism of SETX-BRCA1-BARD1 complex in resolution of R-loops and transcription-replication conflicts

Project description:Senataxin (SETX), a RNA-DNA helicase, is recruited to transcription pause sites via the tumor suppressor BRCA1. Here, we define the mechanism by which SETX-BRCA1 resolves transcription-associated R-loops to prevent deleterious outcomes. Specifically, we show that SETX unwinds R-loops, and that the complex of BRCA1 and its obligatory partner BARD1 binds R-loops and stimulates R-loop unwinding by SETX. Importantly, BRCA1-BARD1 alleviates the inhibitory effect of RAD52 on SETX-mediated R-loop unwinding. We also demonstrate that phosphorylation of Ser642 in SETX promotes its interaction with BRCA1 via the tandem BRCT domain of the latter. Accordingly, mutations in the catalytic domain or Ser642 in SETX lead to R-loop accumulation, transcription-replication conflicts, replication fork stalling, and DNA double strand breaks in human cells. Our results thus establish the molecular basis for functional synergy between SETX and BRCA1-BARD1 in R-loop resolution and the mitigation of transcription-replication conflicts to preserve genome integrity.

2026-01-16 | GSE292585 | GEO

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