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

Author

Listed:
  • 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)

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.

Suggested Citation

  • David M. Burns & Andrea D’Ambrogio & Stephanie Nottrott & Joel D. Richter, 2011. "CPEB and two poly(A) polymerases control miR-122 stability and p53 mRNA translation," Nature, Nature, vol. 473(7345), pages 105-108, May.
    • Handle: RePEc:nat:nature:v:473:y:2011:i:7345:d:10.1038_nature09908
    DOI: 10.1038/nature09908
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