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YTHDC1 m6A-dependent and m6A-independent functions converge to preserve DNA damage response (Ythdc1 ChIP-Seq)

ABSTRACT: YTHDC1 m6A-dependent and m6A-independent functions converge to preserve DNA damage response (Ythdc1 ChIP-Seq)

PROVIDER: PRJNA998829 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25430173_1.fastq.gz	Fastqsanger.gz
	SRR25430173_2.fastq.gz	Fastqsanger.gz
	SRR25430174_1.fastq.gz	Fastqsanger.gz
	SRR25430174_2.fastq.gz	Fastqsanger.gz
	SRR25430175_1.fastq.gz	Fastqsanger.gz

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YTHDC1 m6A-dependent and m6A-independent functions converge to preserve DNA damage response (Ythdc1 ChIP-Seq)

Project description:Cells have evolved a robust and highly regulated DNA damage response to preserve their genomic integrity. Although increasing evidence highlights the relevance of RNA regulation, our understanding of its impact on a fully efficient DNA damage response remains limited. Here, through a targeted CRISPR-knockout screen, we identified RNA binding proteins and modifiers that participate in mediating the p53 response. Among the top hits, m6A reader YTHDC1 was identified as a master regulator of p53 expression. YTHDC1 binds to the transcription start sites ofTP53and other genes involved in DNA damage response, promoting their transcriptional elongation. YTHDC1 deficiency leads to reducedTP53expression, and also retention of introns leading to aberrant protein production of key DNA damage factors. While intron retention is dependent on m6A, YTHDC1 favoursTP53transcriptionalpause-release independently of m6A. Depletion of YTHDC1 causes genomic instability and aberrant cancer cell proliferation mediated by genes regulated by YTHDC1. Our results uncover YTHDC1 as an orchestrator of the DNA damage response through distinct mechanisms of co-transcriptional mRNA regulation.

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YTHDC1 m6A-dependent and m6A-independent functions converge to preserve the DNA damage response

Project description:Cells have evolved a robust and highly regulated DNA damage response to preserve their genomic integrity. Although increasing evidence highlights the relevance of RNA regulation, our understanding of its impact on a fully efficient DNA damage response remains limited. Here, through a targeted CRISPR-knockout screen, we identify RNA binding proteins and modifiers that participate in the p53 response. Among the top hits, we find the m6A reader YTHDC1 as a master regulator of p53 expression. YTHDC1 binds to the transcription start sites of TP53 and other genes involved in the DNA damage response, promoting their transcriptional elongation. YTHDC1 deficiency also causes the retention of introns and therefore aberrant protein production of key DNA damage factors. While YTHDC1-mediated intron retention requires m6A, TP53 transcriptional pause-release is promoted by YTHDC1 independently of m6A. Depletion of YTHDC1 causes genomic instability and aberrant cancer cell proliferation mediated by genes regulated by YTHDC1. Our results uncover YTHDC1 as an orchestrator of the DNA damage response through distinct mechanisms of co-transcriptional mRNA regulation.

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Project description:This SuperSeries is composed of the SubSeries listed below.

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