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We are analyzing https://www.nature.com/articles/s41556-021-00656-3.

Title:
m6A-independent genome-wide METTL3 and METTL14 redistribution drives the senescence-associated secretory phenotype | Nature Cell Biology
Description:
Methyltransferase-like 3 (METTL3) and 14 (METTL14) are core subunits of the methyltransferase complex that catalyses messenger RNA N6-methyladenosine (m6A) modification. Despite the expanding list of m6A-dependent functions of the methyltransferase complex, the m6A-independent function of the METTL3 and METTL14 complex remains poorly understood. Here we show that genome-wide redistribution of METTL3 and METTL14 transcriptionally drives the senescence-associated secretory phenotype (SASP) in an m6A-independent manner. METTL14 is redistributed to the enhancers, whereas METTL3 is localized to the pre-existing NF-κB sites within the promoters of SASP genes during senescence. METTL3 and METTL14 are necessary for SASP. However, SASP is not regulated by m6A mRNA modification. METTL3 and METTL14 are required for both the tumour-promoting and immune-surveillance functions of senescent cells, which are mediated by SASP in vivo in mouse models. In summary, our results report an m6A-independent function of the METTL3 and METTL14 complex in transcriptionally promoting SASP during senescence. Here Liu et al. show that genome-wide redistribution of methyltransferase-like 3 and 14 transcriptionally promotes the senescence-associated secretory phenotype in an m6A-independent manner.
Website Age:
30 years and 10 months (reg. 1994-08-11).

Matching Content Categories {📚}

  • Education
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Custom-built

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🌆 Monumental Traffic: 20M - 50M visitors per month


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$536,300 per month
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Keywords {🔍}

data, pubmed, mettl, article, source, google, scholar, cells, cas, central, nature, fig, cell, sasp, analysis, genes, senescent, expression, extended, senescence, control, cancer, gene, nat, biol, statistical, independent, rna, modification, access, twotailed, senescenceassociated, calculated, knockdown, biologically, provided, methylation, research, experiments, imr, values, blots, mrna, mutant, cxcl, secretory, chromatin, gse, wildtype, represent,

Topics {✒️}

permissions reprints nature portfolio journals privacy policy nature portfolio pre-existing nf-κb sites advertising ovarian cancer research social media sa-β-gal-positive cells author information authors sa-β-gal activity nf-κb reporter activity medical research m6a-independent genome-wide mettl3 sa-β-gal staining situ genome-wide profiling rna n6-methyladenosine methyltransferase fast gapped-read alignment refined rip-seq protocol mettl3–eif3h enhances translation rna n6-methyladenosine methylation nf-κb p65 subunit peer reviewer reports nature+ nature 543 nature 555 nature 552 nature 567 nature 534 nature 550 nature 566 nature 479 nature 561 nature peer review extended data fig dsred-expressing shren control pancreatitis-induced inflammation contributes ectopically expressed wild-type d394a/w397a mutant mettl3 m6a-dependent translation control permissions ras-expressing imr90 cells source data fig rugang zhang sa-β-gal springerlink instant access author correspondence article liu inhibiting oncogene-induced senescence

Schema {🗺️}

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      description:Methyltransferase-like 3 (METTL3) and 14 (METTL14) are core subunits of the methyltransferase complex that catalyses messenger RNA N6-methyladenosine (m6A) modification. Despite the expanding list of m6A-dependent functions of the methyltransferase complex, the m6A-independent function of the METTL3 and METTL14 complex remains poorly understood. Here we show that genome-wide redistribution of METTL3 and METTL14 transcriptionally drives the senescence-associated secretory phenotype (SASP) in an m6A-independent manner. METTL14 is redistributed to the enhancers, whereas METTL3 is localized to the pre-existing NF-κB sites within the promoters of SASP genes during senescence. METTL3 and METTL14 are necessary for SASP. However, SASP is not regulated by m6A mRNA modification. METTL3 and METTL14 are required for both the tumour-promoting and immune-surveillance functions of senescent cells, which are mediated by SASP in vivo in mouse models. In summary, our results report an m6A-independent function of the METTL3 and METTL14 complex in transcriptionally promoting SASP during senescence. Here Liu et al. show that genome-wide redistribution of methyltransferase-like 3 and 14 transcriptionally promotes the senescence-associated secretory phenotype in an m6A-independent manner.
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         Stem Cells
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