期刊
CELL REPORTS
卷 41, 期 11, 页码 -出版社
CELL PRESS
DOI: 10.1016/j.celrep.2022.111784
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资金
- Grenoble research communities
- French Agence National pour la Recherche (ANR)
- MSDAVENIR (ERiCAN, Epigenetic Reprogramming of Cancer Cell Plasticity and Resilience)
- ProFI [ANR-10-INBS-08-01]
- ANRS
- MSDAVENIR
- European Research Council (CoG RNAmedTGS)
Heat stress leads to changes in gene expression, and YTHDC1 plays a crucial role in this process. YTHDC1 redistributes across the genome and binds to m6A-modified transcripts, promoting the expression of heat shock proteins. Additionally, YTHDC1 interacts with m6A-modified non-coding RNAs in stress bodies, contributing to gene expression reprogramming.
Heat stress (HS) induces a cellular response leading to profound changes in gene expression. Here, we show that human YTHDC1, a reader of N6-methyladenosine (m6A) RNA modification, mostly associates to the chro-matin fraction and that HS induces a redistribution of YTHDC1 across the genome, including to heat-induced heat shock protein (HSP) genes. YTHDC1 binding to m6A-modified HSP transcripts co-transcriptionally promotes expression of HSPs. In parallel, hundreds of the genes enriched in YTHDC1 during HS have their transcripts undergoing YTHDC1-and m6A-dependent intron retention. Later, YTHDC1 concentrates within nuclear stress bodies (nSBs) where it binds to m6A-modified SATIII non-coding RNAs, produced in an HSF1-dependent manner upon HS. These findings reveal that YTHDC1 plays a central role in a chromatin -associated m6A-based reprogramming of gene expression during HS. Furthermore, they support the model where the subsequent and temporary sequestration of YTHDC1 within nSBs calibrates the timing of this YTHDC1-dependent gene expression reprogramming.
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