RNA甲基化
选择性拼接
核糖核酸
外显子剪接增强剂
RNA结合蛋白
内含子
分子生物学
N6-甲基腺苷
剪接体
剪接
外显子
SR蛋白
异相核糖核蛋白颗粒
作者
Mateusz Mendel,Kamila Delaney,Radha Raman Pandey,K.M. Chen,Joanna M. Wenda,Cathrine Broberg Vågbø,Florian A. Steiner,David Homolka,Ramesh S. Pillai
出处
期刊:Cell
[Elsevier]
日期:2021-06-10
卷期号:184 (12): 3125-
被引量:14
标识
DOI:10.1016/j.cell.2021.03.062
摘要
Summary The N6-methyladenosine (m6A) RNA modification is used widely to alter the fate of mRNAs. Here we demonstrate that the C. elegans writer METT-10 (the ortholog of mouse METTL16) deposits an m6A mark on the 3′ splice site (AG) of the S-adenosylmethionine (SAM) synthetase pre-mRNA, which inhibits its proper splicing and protein production. The mechanism is triggered by a rich diet and acts as an m6A-mediated switch to stop SAM production and regulate its homeostasis. Although the mammalian SAM synthetase pre-mRNA is not regulated via this mechanism, we show that splicing inhibition by 3′ splice site m6A is conserved in mammals. The modification functions by physically preventing the essential splicing factor U2AF35 from recognizing the 3′ splice site. We propose that use of splice-site m6A is an ancient mechanism for splicing regulation.
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