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METTL3-mediated chromatin contacts promote phase separation during senescence [Mettl3-HiChIP-seq]

ABSTRACT: METTL3-mediated chromatin contacts promote phase separation during senescence [Mettl3-HiChIP-seq]

PROVIDER: PRJNA1016277 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26048979_1.fastq.gz	Fastqsanger.gz
	SRR26048979_2.fastq.gz	Fastqsanger.gz
	SRR26048980_1.fastq.gz	Fastqsanger.gz
	SRR26048980_2.fastq.gz	Fastqsanger.gz

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Project description:Cellular senescence is a stable state of growth arrest that emerges as a response to stress. The methyltransferase complex (MTC) has been shown to facilitate the expression of the senescence-associated secretion phenotype (SASP) factors via genome-wide redistribution. However, whether and how MTC impacts on the three-dimensional (3D) chromatin organization and its functional implications during senescence remain largely unknown. Here we show that the MTC complex coordinates its enzymatic activity-dependent and -independent functions to enforce cellular senescence. Specifically, METTL3-mediated chromatin loops induce Hexokinase 2 (HK2) expression during senescence. The elevated HK2 expression subsequently promotes liquid-liquid phase separation (LLPS), manifesting as stress granules. These phase-separated stress granules act as reservoirs to sequester cell-cycle related mRNAs harboring polymethylated m6A sites, impeding their efficient translation. Overall, we uncover a mechanism by which senescent cells utilize phase-separated stress granules, facilitated by MTC-mediated HK2 activation, to sequester cell-cycle related mRNAs in governing senescence-associated stable growth arrest.

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