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Post-slippage cells increase expression of factors associated with SASP.

ABSTRACT: Post-slippage cells increase expression of factors associated with SASP.

PROVIDER: PRJNA471655 | ENA |

REPOSITORIES: ENA

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Post-slippage cells increase expression of factors associated with SASP.

Project description:Human transcriptome analysis of U2OS cells treated with nocodazole or DMSO (Control). The gene expression profiling will reveal senescence-associated genes induced upon nocodazole treatment. Our preliminary data show that antimitotic drugs treatment promote post-slippage senescence.

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Unique human beta-cell senescence-associated secretory phenotype (SASP) reveal conserved signaling pathways and heterogeneous factors

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Effect of SASP factors on mouse intestinal organoids

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Mitochondrial RNA cytosolic leakage drives the SASP

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Mettl14-driven senescence-associated secretory phenotype (SASP) facilitates somatic reprogramming

Project description:The METTL3-METTL14 complex, as the "writer" of N6-methyladenosine (m6A), plays an important role in many biological processes. Previous studies have shown that overexpression of Mettl3 can increase the level of m6A and promotes somatic cell reprogramming. Here, we demonstrate that Mettl14, another component of the methyltransferase (MTase) complex, can significantly enhance the generation of induced pluripotent stem cells (iPSCs) in m6A independent manner. Cooperating with Oct4, Sox2, Klf4 and c-Myc (OSKM), Mettl14 transiently increased the senescence-associated secretory phenotype (SASP) gene expression in the non-reprogramming cells at the late reprogramming stage. The conditional medium in reprogramming intermediates overexpressing Mettl4 or its mutant could enhanced the reprogramming, so do IL-6, a component of SASP. Corespondingly, blocking of SASP using senolytic agent or NF-κB inhibitor impairs the effect of Mettl14 on reprogramming. . Our work highlights the m6A independent function of Mettl14 and provides new insight into the interplay between senescence and reprogramming in vitro.

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Mitochondrial RNA cytosolic leakage drives the SASP [CRISPR/Cas9]

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Unique human beta-cell senescence-associated secretory phenotype (SASP) reveal conserved signaling pathways and heterogeneous factors

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Effect of SASP factors at single nucleus level of mouse intestinal organoids [snRNA-seq]

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