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Double strand break repair protein TIRR regulates RNA metabolism in response to DNA damage and cell stress [RNA-Seq]

ABSTRACT: Double strand break repair protein TIRR regulates RNA metabolism in response to DNA damage and cell stress [RNA-Seq]

PROVIDER: PRJNA1041432 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26855159_1.fastq.gz	Fastqsanger.gz
	SRR26855159_2.fastq.gz	Fastqsanger.gz
	SRR26855160_1.fastq.gz	Fastqsanger.gz
	SRR26855160_2.fastq.gz	Fastqsanger.gz
	SRR26855161_1.fastq.gz	Fastqsanger.gz

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Double strand break repair protein TIRR regulates RNA metabolism in response to DNA damage and cell stress [RNA-Seq]

Project description:Tudor interacting repair regulator (TIRR) is a well-studied p53 binding protein 1 (53BP1) interactor in response to DNA double strand breaks (DSBs). TIRR is also an RNA binding protein, however its role in RNA regulation in response to cellular insults is not understood. Here we show that TIRR binds to specific group of mRNAs in response to DNA damage. TIRR bound transcripts encode for transcription factors and RNA polymerase II (RNAPII) transcription regulators. Furthermore, TIRR modulates the formation of RNA processing bodies (P bodies/PBs), in response to DSBs. TIRR also regulates the formation of the closely related but distinct compartments known as stress granules (SGs) in response to cell stress. Furthermore, TIRR dissociates from 53BP1 in response to sodium arsenite treatment independently of Ataxia Telangiectasia Mutated Protein (ATM) signalling. Finally, TIRR interacts with the nuclear export protein Exportin-1 (XPO1) upon DNA damage. TIRR bound RNA co-localises with PB and SGs and TIRR depletion leads to nuclear RNA retention. This work reveals that TIRR orchestrates mRNA nuclear export, metabolism and storage in PBs/SGs. Hence TIRR regulates RNA mediated DNA damage and cell stress responses independently of its canonical 53BP1 binding role.

2024-07-18 | GSE248032 | GEO

Double strand break repair protein TIRR regulates RNA metabolism in response to DNA damage and cell stress [RIP-seq]

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Double strand break repair protein TIRR regulates RNA metabolism in response to DNA damage and cell stress

Project description:Double strand break repair protein TIRR regulates RNA metabolism in response to DNA damage and cell stress

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Double strand break repair protein TIRR regulates RNA metabolism in response to DNA damage and cell stress [RIP-seq]

Project description:Double strand break repair protein TIRR regulates RNA metabolism in response to DNA damage and cell stress [RIP-seq]

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DNA double-strand break-derived RNA drives TIRR/53BP1 complex dissociation.

Project description: Not available

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p53 binding during the DNA double-strand break response

Project description:We used ChIP-seq to assess where p53 binds in the human genome and how that binding changes during the DNA double-strand break response. In particular, we considered the 1-Mb-wide window centered on the MYC locus. Contrary to previous reports, we found no evidence of p53 binding at the MYC promoter. Rather, we identified three locations downstream of MYC at which p53 was bound; binding at each of these regions increased during the DNA double-strand break response.

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Mechanisms of insertions at a double strand break

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