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METTL3-mediated m6A modification controls splicing factor abundance and contributes to CLL progression [MeRIP-seq]

ABSTRACT: METTL3-mediated m6A modification controls splicing factor abundance and contributes to CLL progression [MeRIP-seq]

PROVIDER: PRJNA927821 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23229750_1.fastq.gz	Fastqsanger.gz
	SRR23229750_2.fastq.gz	Fastqsanger.gz
	SRR23229751_1.fastq.gz	Fastqsanger.gz
	SRR23229751_2.fastq.gz	Fastqsanger.gz
	SRR23229752_1.fastq.gz	Fastqsanger.gz

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METTL3-mediated m6A modification controls splicing factor abundance and contributes to CLL progression [MeRIP-seq]

Project description:RNA splicing dysregulation is a hallmark of cancers, promoting the onset and progression of disease. In chronic lymphocytic leukemia (CLL), spliceosome mutations leading to aberrant splicing occur in ~20% of patients. However, the underlying mechanism for splicing defects in spliceosome unmutated CLL cases remains elusive. Through an integrative transcriptomic and proteomic analysis, we discover proteins involved in RNA splicing are post-transcriptionally upregulated in CLL cells, resulting in splicing dysregulation. The abundance of splicing (factors) complexes is an independent risk factor and associated with poor prognosis in CLL. Moreover, increased splicing factor expression is highly correlated with METTL3, an RNA methyltransferase that modifies N6-methyladenosine (m6A) on mRNA. METTL3 is essential for cell growth in vitro and in vivo, and controls splicing factor protein expression in a methyltransferase-dependent manner through m6A modification mediated ribosome recycling and decoding process. Our results uncover a novel regulatory axis of METTL3 for splicing dysregulation in CLL and highlight m6A modification as a major contributor to spliceosome mutation-independent splicing defects that lead to CLL progression.

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METTL3-mediated m6A modification controls splicing factor abundance and contributes to CLL progression [RNA-seq]

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METTL3-mediated m6A modification controls splicing factor abundance and contributes to CLL progression

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Project description:METTL3-mediated m6A modification controls splicing factor abundance and contributes to CLL progression [RNA-seq]

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Project description:METTL3-mediated m6A modification controls splicing factor abundance and contributes to CLL progression [Ribo-seq]

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Project description:We use MeRIP-sequencing to evaluate the effect of METTL3 knockdown on the gene changes in H1975 cells.

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