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Transcriptome and N6-methyladenosine RNA methylome analysis of YTHDF2 kockdown(KD) and wildtype(WT) cells in Multiple Myeloma

ABSTRACT: Transcriptome and N6-methyladenosine RNA methylome analysis of YTHDF2 kockdown(KD) and wildtype(WT) cells in Multiple Myeloma

PROVIDER: PRJNA682024 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13180967_1.fastq.gz	Fastqsanger.gz
	SRR13180967_2.fastq.gz	Fastqsanger.gz
	SRR13180968_1.fastq.gz	Fastqsanger.gz
	SRR13180968_2.fastq.gz	Fastqsanger.gz
	SRR13180969_1.fastq.gz	Fastqsanger.gz

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Genome-wide maps of chromatin state in YTHDF2 kockdown(KD) and wildtype(WT) cells in Multiple Myeloma

Project description:We found that the experssion of STAT5A was upregulated when the YTHDF2 was knocked down. To identify the function of STAT5A protein as a Transcription factor in YTHDF2 kockdown(KD) and wildtype(WT) cells in Multiple Myeloma. CHIP-seq was conducted to analyze changes in related signaling pathways and gene expression in Multiple Myeloma cells when YTHDF2 was knocked down.

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Project description:N6-methyladenosine (m6A) is the most abundant internal messenger (mRNA) modification in mammalian mRNA. This modification is reversible and non-stoichiometric, which potentially adds an additional layer of variety and dynamic control of mRNA metabolism. The m6A-modified mRNA can be selectively recognized by the YTH family “reader” proteins. The preferential binding of m6A-containing mRNA by YTHDF2 is known to reduce the stability of the target transcripts; however, the exact effects of m6A on translation has yet to be elucidated. Here we show that another m6A reader protein, YTHDF1, promotes ribosome loading of its target transcripts. YTHDF1 forms a complex with translation initiation factors to elevate the translation efficiency of its bound mRNA. In a unified mechanism of translation control through m6A, the YTHDF2-mediated decay controls the lifetime of target transcripts; whereas, the YTHDF1-based translation promotion increases the translation efficiency to ensure effective protein production from relatively short-lived transcripts that are marked by m6A. PAR-CLIP and RIP was used to identify YTHDF1 binding sites followed by ribosome profling and RNA seq to assess the consequences of YTHDF1 siRNA knock-down

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