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

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

PROVIDER: PRJNA1016278 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26049135_1.fastq.gz	Fastqsanger.gz
	SRR26049135_2.fastq.gz	Fastqsanger.gz
	SRR26049136_1.fastq.gz	Fastqsanger.gz
	SRR26049136_2.fastq.gz	Fastqsanger.gz
	SRR26049137_1.fastq.gz	Fastqsanger.gz

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METTL3-mediated chromatin contacts promote phase separation during senescence.

Project description:METTL3-mediated chromatin contacts promote phase separation during senescence.

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

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

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

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

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.

2024-04-22 | GSE243044 | GEO

METTL3-mediated chromatin contacts promote phase separation during senescence [H3K27Ac-HiChIP-seq]

Project description:METTL3-mediated chromatin contacts promote phase separation during senescence [H3K27Ac-HiChIP-seq]

| PRJNA1016279 | ENA

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

2024-04-22 | GSE243046 | GEO

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

2024-04-22 | GSE243042 | GEO

METTL3-mediated chromatin contacts promote phase separation during senescence [H3K27Ac-HiChIP-seq]

2024-04-22 | GSE243043 | GEO

METTL3-mediated chromatin contacts promote phase separation during senescence.

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

2024-04-22 | GSE243047 | GEO

m6A independent genome-wide METTL3 and METTL14 redistribution drives senescence-associated secretory phenotype [rna.M3]

Project description:Methyltransferase-like 3 (METTL3) and 14 (METTL14) are core subunits of the methyltransferase complex (MTC) that catalyzes mRNA N6-methyladenosine (m6A) modification. Despite the expanding list of m6A-dependent function of the MTC, m6A independent function of the METTL3 and METTL14 complex remains poorly understood. Here we show that genome-wide redistribution of METTL3 and METTL14 drives senescence-associated secretory phenotype (SASP) in a m6A-independent manner. METTL3 and METTL14 are necessary for SASP. However, SASP is not regulated by m6A mRNA modification. METTL14 is redistributed to the enhancers, while METTL3 is localized to the pre-existing NF-B sites within the promoters of the SASP genes during senescence. METTL3 interacts with NF-B and they are mutually dependent on their associations with the promoters of SASP genes. METTL14 but not METTL3 is necessary for function of SASP gene enhancers. METTL3 and METTL14 are required for both the tumor-promoting and immune surveillance functions of senescent cells mediated by SASP in vivo in mouse models. In summary, our results report a m6A independent function of the METTL3 and METTL14 complex in promoting SASP through regulating transcription by genome-wide redistribution of METTL14 to enhancers and METTL3 to promoters of SASP genes during senescence.

2020-12-10 | GSE159551 | GEO

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