Author:
Decorsière Adrien,Cayrel Anne,Vagner Stéphan,Millevoi Stefania
Abstract
Following DNA damage, mRNA 3′-end formation is inhibited, contributing to repression of mRNA synthesis. Here we investigated how DNA-damaged cells accomplish p53 mRNA 3′-end formation when normal mechanisms of pre-mRNA 3′-end processing regulation are inhibited. The underlying mechanism involves the interaction between a G-quadruplex structure located downstream from the p53 cleavage site and hnRNP H/F. Importantly, this interaction is critical for p53 expression and contributes to p53-mediated apoptosis. Our results uncover the existence of a specific rescue mechanism of 3′-end processing regulation allowing stress-induced p53 accumulation and function in apoptosis.
Publisher
Cold Spring Harbor Laboratory
Subject
Developmental Biology,Genetics
Cited by
146 articles.
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