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Hypoxia-induced SETX links replication stress with the unfolded protein response

ABSTRACT: Hypoxia-induced SETX links replication stress with the unfolded protein response

PROVIDER: PRJNA661072 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12573869_1.fastq.gz	Fastqsanger.gz
	SRR12573869_2.fastq.gz	Fastqsanger.gz
	SRR12573870_1.fastq.gz	Fastqsanger.gz
	SRR12573870_2.fastq.gz	Fastqsanger.gz
	SRR12573871_1.fastq.gz	Fastqsanger.gz

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Hypoxia-induced SETX links replication stress with the unfolded protein response

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Hypoxia-induced SETX links replication stress with the unfolded protein response.

Project description:Tumour hypoxia is associated with poor patient prognosis and therapy resistance. A unique transcriptional response is initiated by hypoxia which includes the rapid activation of numerous transcription factors in a background of reduced global transcription. Here, we show that the biological response to hypoxia includes the accumulation of R-loops and the induction of the RNA/DNA helicase SETX. In the absence of hypoxia-induced SETX, R-loop levels increase, DNA damage accumulates, and DNA replication rates decrease. Therefore, suggesting that, SETX plays a role in protecting cells from DNA damage induced during transcription in hypoxia. Importantly, we propose that the mechanism of SETX induction in hypoxia is reliant on the PERK/ATF4 arm of the unfolded protein response. These data not only highlight the unique cellular response to hypoxia, which includes both a replication stress-dependent DNA damage response and an unfolded protein response but uncover a novel link between these two distinct pathways.

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GNL3/nucleostemin links DNA replication homeostasis and replication forks stability

Project description:GNL3/nucleostemin links DNA replication homeostasis and replication forks stability

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Epigenomic profiling of SETX in meiotic germ cells by ChIP-seq

Project description:SETX is a DNA/RNA helicase that resolves R-loop, and lack of SETX in germ cells causes meiotic arrest. To investigate roles of SETX in transcription during meiosis, we perfomred ChIP-seq of SETX using antibodies.

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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

SETX attenuates the antiviral innate immune response and controls viral biogenesis (GRO-Seq)

Project description:The innate immune response is the first line of defense against pathogens, and factors that control this cellular response represent targets for treating both infectious and inflammatory diseases. Here, we reveal a novel role for the human helicase SETX, also previously implicated in amyotrophic lateral sclerosis (ALS4) and ataxia with oculomotor apraxia (AOA2), in controlling the magnitude of the antiviral response. Cells depleted for SETX and AOA2 patient-derived SETX-null cells show increased expression of antiviral mediators in response to infection. Mechanistically, this effect is achieved through SETX-mediated inhibition of RNAPII transcription of antiviral genes, and depends on SETX helicase activity. Our results suggest that SETX helps maintain the delicate balance between controlling viral infection and avoiding the potentially detrimental effects of an excessive antiviral response. More broadly, the observation that SETX can regulate the transcriptional activity of specific genes may have important implications for disorders where SETX function is compromised. A549 cells that were transfected with either control non-targeting or SETX-specific siRNAs were infected with the Influenza A virus (A/PR/8/34(ΔNS1) strain) at a multiplicity of infection (MOI) of 3 for 4 hours. Nuclei were then extracted and used to prepare Global Run-On Sequencing (GRO-seq) libraries.

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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

Epigenomic profiling of SETX and Rloops in meiotic germ cells by CUT&Tag

2023-12-31 | GSE224946 | GEO

Gene expression profiling in Setx shRNA P19 cells, wild type human Setx P19 transfected cells with and without retionoic acid

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