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TCAF1 Promotes TRPV2-mediated Ca2+ Release in Response to Cytosolic DNA to Protect Stressed Replication Forks

ABSTRACT: TCAF1 Promotes TRPV2-mediated Ca2+ Release in Response to Cytosolic DNA to Protect Stressed Replication Forks

PROVIDER: PRJNA1021654 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26198477.fastq.gz	Fastqsanger.gz
	SRR26198478.fastq.gz	Fastqsanger.gz
	SRR26198479.fastq.gz	Fastqsanger.gz
	SRR26198480.fastq.gz	Fastqsanger.gz
	SRR26411923.fastq.gz	Fastqsanger.gz

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TCAF1 Promotes TRPV2-mediated Ca2+ Release in Response to Cytosolic DNA to Protect Stressed Replication Forks

Project description:The protection of the replication fork structure under stress conditions is essential for genome maintenance and cancer prevention. A key signaling pathway for fork protection involves TRPV2-mediated Ca2+ release from the ER, which is triggered after the generation of cytosolic DNA and the activation of cGAS/STING. The resulting CaMKK2/AMPK activation and subsequent Exo1 phosphorylation prevent aberrant fork processing, thereby ensuring genome stability. However, it remains poorly understood how the TRPV2 channel is activated by the presence of cytosolic DNA. Here we show that the TRPM8 channel-associated factor 1 (TCAF1) plays a key role in promoting TRPV2-mediated Ca2+ release under replication stress or other conditions that activate cGAS/STING. Mechanistically, TCAF1 promotes Ca2+ release by facilitating the dissociation of STING from TRPV2, thereby relieving TRPV2 repression. Consistent with this function, TCAF1 is required for fork protection, chromosomal stability and cell survival after replication stress.

2024-04-24 | GSE244205 | GEO

Transcription profiling by array of Arabidopsis seedlings response to oscillations and prolonged increases in cytosolic Ca2+

Project description:Comparison of two types of calcium signature produced by application of voltage in Arabidopsis thaliana seedlings; namely oscillations or prolonged increase in cytosolic Ca2+ , each treatment is a biological dyeswap compared to untreated control

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Transcription profiling by array of Arabidopsis seedlings response to three oscillating levels in cytosolic Ca2+

Project description:Comparison of 3 oscillating elevations in cytosolic Ca2+ (created using electrical stimulation and measured using aequorin luminescence) in Arabidopsis seedlings. Treatment 1; high frequency high amplitude osc., Treatment 2; high frequency low amplitude osc., Treatment 3; low frequency low amplitude osc. One biological sample per experiment processed as technical dye swaps against intreated control.

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Transcription profiling by array of Arabidopsis seedlings response to transient and prolonged increases in cytosolic Ca2+

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2010-07-01 | E-MEXP-2661 | biostudies-arrayexpress

Cytosolic DNA sensing by cGAS/STING promotes TRPV2-mediated Ca<sup>2+</sup> release to protect stressed replication forks.

Project description:The protection of DNA replication forks under stress is essential for genome maintenance and cancer suppression. One mechanism of fork protection involves an elevation in intracellular Ca2+ ([Ca2+]i), which in turn activates CaMKK2 and AMPK to prevent uncontrolled fork processing by Exo1. How replication stress triggers [Ca2+]i elevation is unclear. Here, we report a role of cytosolic self-DNA (cytosDNA) and the ion channel TRPV2 in [Ca2+]i induction and fork protection. Replication stress leads to the generation of ssDNA and dsDNA species that, upon translocation into cytoplasm, trigger the activation of the sensor protein cGAS and the production of cGAMP. The subsequent binding of cGAMP to STING causes its dissociation from TRPV2, leading to TRPV2 derepression and Ca2+ release from the ER, which in turn activates the downstream signaling cascade to prevent fork degradation. This Ca2+-dependent genome protection pathway is also activated in response to replication stress caused by oncogene activation.

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Senataxin associates with replication forks to protect fork integrity across RNAPII transcribed genes

Project description:Here we analysed the role of yeast Senataxin (Sen1) in coordinating replication with transcription and in protecting genome integrity. Senataxin is mutated in the two severe neurodegenerative diseases AOA2 and ALS4. We show that a fraction of Sen1/Senataxin DNA/RNA helicase associates with replication forks and protects the integrity of those fork encountering highly expressed RNAPII genes. sen1 mutants accumulate aberrant DNA structures and RNA-DNA hybrids while forks clash head-on with RNAPII transcription units and counteract recombinogenic events and accumulation of checkpoint signals. Nrd1, which acts togheter with Sen1 in trascription temination, is not recruited at replication forks. nrd1 mutants does not display replication defects, high genome instability and checkpoint activation observed in sen1 mutants The Sen1 function in replication can be therefore separable from its role in RNA processing. We propose a role for Sen1/Senataxin during chromosome replication in facilitating replisome progression across RNAPII transcribed genes thus preventing DNA-RNA hybrids accumulation when forks encounter nascent transcripts on the lagging strand template. Chip on chip analysis was carried out as described (Bermejo et al., 2011), employing anti-Flag monoclonal antibody M2 (Sigma-Aldrich) Labelled probes were hybridized to Affymetrix S.cerevisiae Tiling 1.0 (P/N 900645) arrays and processed with TAS software.

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2025-12-10 | GSE309492 | GEO

Senataxin associates with replication forks to protect fork integrity across RNAPII transcribed genes

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SLFN11 blocks stressed replication forks independently of ATR

Project description:SLFN11 blocks stressed replication forks independently of ATR

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Dormant origins and fork protection mechanisms rescue sister forks arrested by transcription

Project description:Yeast Sen1Senataxin is a RNA/DNA helicase that preserves replication forks across RNA Polymerase II-transcribed genes by counteracting RNA:DNA hybrids accumulation. We show that in Sen1-depleted cells early forks clashing head-on with transcription halt, and impair progression of sister forks within the same replicon. Unsolved replication-transcription collisions trigger the local firing of dormant origins that rescue arrested forks. In sen1 mutants the MRX and Mrc1/Ctf4-complexes protect those forks clashing with transcription by preventing genotoxic fork-resection events mediated by the Exo1 nuclease. Hence, sister forks within the same replicon remain coupled when one of the two forks halts. This is different when forks encounter double strand breaks. Moreover, the local firing of dormant origins is not prevented by checkpoint activation but depends on delayed adjacent forks. Furthermore, a productive head-on clash between replication and transcription requires the tuning of origin firing and coordination between Sen1, the MRX and Mrc1/Ctf4-complexes and Exo1.

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