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Differential effects of m6A modification and YTHDF2 knockdown on global mRNA turnover

ABSTRACT: Differential effects of m6A modification and YTHDF2 knockdown on global mRNA turnover

PROVIDER: PRJNA753517 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15409627_1.fastq.gz	Fastqsanger.gz
	SRR15409627_2.fastq.gz	Fastqsanger.gz
	SRR15409628_1.fastq.gz	Fastqsanger.gz
	SRR15409628_2.fastq.gz	Fastqsanger.gz
	SRR15409629_1.fastq.gz	Fastqsanger.gz

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Effects of m6A modification and YTHDF2 knockdown on global mRNA turnover

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Effects of m6A modification and YTHDF2 knockdown on global mRNA turnover

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m6A modification profile in primary microglia with/without Igf2bp1 knockdown

Project description:Our study demonstrated that the expression of Igf2bp1 in activated microglia was significantly up-regulated, implying a role of Igf2bp1 in LPS-induced m6A modifications in microglia. To understand the roles of Igf2bp1 on LPS-induced m6A modification in microglia, we performed Igf2bp1 loss-of-function (LOF) approach. Microglia stimulated by LPS were transfected with either scrambled siRNA control or Igf2bp1 siRNA for 48 hours. To m6A modification profiles in control and Igf2bp1 LOF microglia were determined by MeRIP-seq analysis.

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Project description:The m6A modification regulates mRNA stability and translation. Here we show that transcriptomic m6A modification is dynamic and the m6A reader protein YTHDF2 promotes mRNA decay during the cell cycle. Depletion of YTHDF2 leads to the delay of mitotic entry due to overaccumulation of WEE1, a negative regulator of CDK1. We demonstrate that WEE1 transcripts contain m6A modification, which promotes their decay through the m6A reader YTHDF2. Moreover, we found that YTHDF2 protein stability is dependent on CDK1 activity. Thus, CDK1, YTHDF2, and WEE1 form a feedforward regulatory loop to promote mitotic entry. We further identified CUL1, CUL4A, DDB1, and SKP2 as components of E3 ubiquitin ligase complexes that mediate YTHDF2 proteolysis. Our study provides insights into how cell cycle mediators modulate transcriptomic m6A modification, which in turn regulates the cell cycle.

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