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Insights into the assembly and architecture of a Staufen-mediated mRNA decay (SMD)-competent mRNP

Author

Listed:
  • Manjeera Gowravaram

    (Freie Universität Berlin)

  • Juliane Schwarz

    (Max Planck Institute for Biophysical Chemistry
    University Medical Center Goettingen)

  • Sana K. Khilji

    (Freie Universität Berlin
    Max Planck Institute of Colloids and Interfaces)

  • Henning Urlaub

    (Max Planck Institute for Biophysical Chemistry
    University Medical Center Goettingen)

  • Sutapa Chakrabarti

    (Freie Universität Berlin)

Abstract

The mammalian Staufen proteins (Stau1 and Stau2) mediate degradation of mRNA containing complex secondary structures in their 3’-untranslated region (UTR) through a pathway known as Staufen-mediated mRNA decay (SMD). This pathway also involves the RNA helicase UPF1, which is best known for its role in the nonsense-mediated mRNA decay (NMD) pathway. Here we present a biochemical reconstitution of the recruitment and activation of UPF1 in context of the SMD pathway. We demonstrate the involvement of UPF2, a core NMD factor and a known activator of UPF1, in SMD. UPF2 acts as an adaptor between Stau1 and UPF1, stimulates the catalytic activity of UPF1 and plays a central role in the formation of an SMD-competent mRNP. Our study elucidates the molecular mechanisms of SMD and points towards extensive cross-talk between UPF1-mediated mRNA decay pathways in cells.

Suggested Citation

  • Manjeera Gowravaram & Juliane Schwarz & Sana K. Khilji & Henning Urlaub & Sutapa Chakrabarti, 2019. "Insights into the assembly and architecture of a Staufen-mediated mRNA decay (SMD)-competent mRNP," Nature Communications, Nature, vol. 10(1), pages 1-14, December.
  • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-13080-x
    DOI: 10.1038/s41467-019-13080-x
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    Cited by:

    1. Seungwon Jung & Seung Hwan Ko & Narae Ahn & Jinsam Lee & Chang-Hwan Park & Jungwook Hwang, 2024. "Role of UPF1-LIN28A interaction during early differentiation of pluripotent stem cells," Nature Communications, Nature, vol. 15(1), pages 1-14, December.

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