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BTG2 bridges PABPC1 RNA-binding domains and CAF1 deadenylase to control cell proliferation

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  • Benjamin Stupfler

    (Institut de Génétique et de Biologie Moléculaire et Cellulaire
    Centre National de la Recherche Scientifique UMR7104
    Institut National de la Santé et de la Recherche Médicale U964
    Université de Strasbourg)

  • Catherine Birck

    (Institut de Génétique et de Biologie Moléculaire et Cellulaire
    Centre National de la Recherche Scientifique UMR7104
    Institut National de la Santé et de la Recherche Médicale U964
    Université de Strasbourg)

  • Bertrand Séraphin

    (Institut de Génétique et de Biologie Moléculaire et Cellulaire
    Centre National de la Recherche Scientifique UMR7104
    Institut National de la Santé et de la Recherche Médicale U964
    Université de Strasbourg)

  • Fabienne Mauxion

    (Institut de Génétique et de Biologie Moléculaire et Cellulaire
    Centre National de la Recherche Scientifique UMR7104
    Institut National de la Santé et de la Recherche Médicale U964
    Université de Strasbourg)

Abstract

While BTG2 plays an important role in cellular differentiation and cancer, its precise molecular function remains unclear. BTG2 interacts with CAF1 deadenylase through its APRO domain, a defining feature of BTG/Tob factors. Our previous experiments revealed that expression of BTG2 promoted mRNA poly(A) tail shortening through an undefined mechanism. Here we report that the APRO domain of BTG2 interacts directly with the first RRM domain of the poly(A)-binding protein PABPC1. Moreover, PABPC1 RRM and BTG2 APRO domains are sufficient to stimulate CAF1 deadenylase activity in vitro in the absence of other CCR4–NOT complex subunits. Our results unravel thus the mechanism by which BTG2 stimulates mRNA deadenylation, demonstrating its direct role in poly(A) tail length control. Importantly, we also show that the interaction of BTG2 with the first RRM domain of PABPC1 is required for BTG2 to control cell proliferation.

Suggested Citation

  • Benjamin Stupfler & Catherine Birck & Bertrand Séraphin & Fabienne Mauxion, 2016. "BTG2 bridges PABPC1 RNA-binding domains and CAF1 deadenylase to control cell proliferation," Nature Communications, Nature, vol. 7(1), pages 1-11, April.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms10811
    DOI: 10.1038/ncomms10811
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    Cited by:

    1. Fabian Poetz & Joshua Corbo & Yevgen Levdansky & Alexander Spiegelhalter & Doris Lindner & Vera Magg & Svetlana Lebedeva & Jörg Schweiggert & Johanna Schott & Eugene Valkov & Georg Stoecklin, 2021. "RNF219 attenuates global mRNA decay through inhibition of CCR4-NOT complex-mediated deadenylation," Nature Communications, Nature, vol. 12(1), pages 1-19, December.

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