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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

SLFN11 blocks stressed replication forks independently of ATR

Project description:SLFN11 blocks stressed replication forks independently of ATR

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SLFN11 blocks stressed replication forks independently of ATR

Project description:SLFN11 sensitizes cancer cells to a broad range of DNA-targeted therapies. Here we show that, in response to replication stress induced by camptothecin, SLFN11 tightly binds chromatin at stressed replication foci via RPA1 together with the replication helicase subunit MCM3. Unlike ATR, SLFN11 neither interferes with the loading of CDC45 and PCNA nor inhibits the initiation of DNA replication but selectively blocks fork progression while inducing chromatin opening across replication initiation sites. The ATPase domain of SLFN11 is required for chromatin opening, replication block and cell death but not for the tight binding of SLFN11 to chromatin. Replication stress by the CHK1 inhibitor Prexasertib also recruits SLFN11 to nascent replicating DNA together with CDC45 and PCNA. We conclude that SLFN11 is recruited to stressed replication forks carrying extended RPA filaments where it blocks replication by changing chromatin structure across replication sites.

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SLFN11 blocks stressed replication forks independently of ATR

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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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SLFN11 blocks stressed replication forks independently of ATR (NS-Seq)

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PARP1 proximity proteomics reveals interaction partners at stressed replication forks

Project description:PARP1 mediates poly-ADP-ribosylation of proteins on chromatin in response to different types of DNA lesions. PARP inhibitors are used for the treatment of BRCA1/2-deficient breast, ovarian, and prostate cancer. Loss of DNA replication fork protection is proposed as one mechanism that contributes to the vulnerability of BRCA1/2-deficient cells to PARP inhibitors. However, the mechanisms that regulate PARP1 activity at stressed replication forks remain poorly understood. Here, we performed proximity proteomics of PARP1 and isolation of proteins on stressed replication forks to map putative PARP1 regulators. We identified TPX2 as a direct PARP1-binding protein that regulates the auto-ADP-ribosylation activity of PARP1. TPX2 interacts with DNA damage response proteins and promotes homology-directed repair of DNA double-strand breaks. Moreover, TPX2 mRNA levels are increased in BRCA1/2-mutated breast and prostate cancers, and high TPX2 expression levels correlate with the sensitivity of cancer cells to PARP-trapping inhibitors. We propose that TPX2 confers a mitosis-independent function in the cellular response to replication stress by interacting with PARP1.

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

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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.

| S-EPMC9974760 | biostudies-literature

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