CPEB and two poly(A) polymerases control miR-122 stability and p53 mRNA translation

David M. Burns, Andrea D’Ambrogio, Stephanie Nottrott and Joel D. Richter ()
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David M. Burns: Program in Molecular Medicine, University of Massachusetts Medical School
Andrea D’Ambrogio: Program in Molecular Medicine, University of Massachusetts Medical School
Stephanie Nottrott: Program in Molecular Medicine, University of Massachusetts Medical School
Joel D. Richter: Program in Molecular Medicine, University of Massachusetts Medical School

Nature, 2011, vol. 473, issue 7345, 105-108

Abstract: Control of p53-linked cell senescence Messenger RNAs are capped at their 3′ ends by a non-templated run of adenines — the polyA tail — that enhances their translation. The polyA polymerase Gld2 is guided to 3′ untranslated regions by the sequence-specific CPEB protein. Richter and colleagues have now found that the p53 tumour suppressor is not simply polyadenylated by Gld2. Rather, Gld2 can add a single A to the miR-122 microRNA, thereby stabilizing it. This adenylated miR-122/RISC complex then downregulates CPEB expression by binding target sites in its 3′ untranslated region. If CPEB is not downregulated by miR-122, CPEB binds the p53 3′ untranslated region and recruits a different polyA polymerase, Gld4. The data demonstrate a previously unknown hierarchy of translational control of p53 mRNA leading to cellular senescence.

Date: 2011
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DOI: 10.1038/nature09908

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