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Kruppel-like factor 4-dependent Staufen1-mediated mRNA decay regulates cortical neurogenesis

Author

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  • Byoung-San Moon

    (University of Southern California
    Nankai University)

  • Jinlun Bai

    (University of Southern California)

  • Mingyang Cai

    (University of Southern California)

  • Chunming Liu

    (University of Kentucky)

  • Jiandang Shi

    (Nankai University)

  • Wange Lu

    (University of Southern California)

Abstract

Kruppel-like factor 4 (Klf4) is a zinc-finger-containing protein that plays a critical role in diverse cellular physiology. While most of these functions attribute to its role as a transcription factor, it is postulated that Klf4 may play a role other than transcriptional regulation. Here we demonstrate that Klf4 loss in neural progenitor cells (NPCs) leads to increased neurogenesis and reduced self-renewal in mice. In addition, Klf4 interacts with RNA-binding protein Staufen1 (Stau1) and RNA helicase Ddx5/17. They function together as a complex to maintain NPC self-renewal. We report that Klf4 promotes Stau1 recruitment to the 3′-untranslated region of neurogenesis-associated mRNAs, increasing Stau1-mediated mRNA decay (SMD) of these transcripts. Stau1 depletion abrogated SMD of target mRNAs and rescued neurogenesis defects in Klf4-overexpressing NPCs. Furthermore, Ddx5/17 knockdown significantly blocked Klf4-mediated mRNA degradation. Our results highlight a novel molecular mechanism underlying stability of neurogenesis-associated mRNAs controlled by the Klf4/Ddx5/17/Stau1 axis during mammalian corticogenesis.

Suggested Citation

  • Byoung-San Moon & Jinlun Bai & Mingyang Cai & Chunming Liu & Jiandang Shi & Wange Lu, 2018. "Kruppel-like factor 4-dependent Staufen1-mediated mRNA decay regulates cortical neurogenesis," Nature Communications, Nature, vol. 9(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-017-02720-9
    DOI: 10.1038/s41467-017-02720-9
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