EIF3D safeguards the homeostasis of key signaling pathways in human primed pluripotency

DOI Web Site 参考文献84件 オープンアクセス
  • Chikako Okubo
    Department of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto, 606-8507, Japan.
  • Michiko Nakamura
    Department of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto, 606-8507, Japan.
  • Masae Sato
    Department of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto, 606-8507, Japan.
  • Yuichi Shichino
    RNA Systems Biochemistry Laboratory, RIKEN Cluster for Pioneering Research, Saitama, 351-0198, Japan.
  • Mari Mito
    RNA Systems Biochemistry Laboratory, RIKEN Cluster for Pioneering Research, Saitama, 351-0198, Japan.
  • Yasuhiro Takashima
    Department of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto, 606-8507, Japan.
  • Shintaro Iwasaki
    RNA Systems Biochemistry Laboratory, RIKEN Cluster for Pioneering Research, Saitama, 351-0198, Japan.
  • Kazutoshi Takahashi
    Department of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto, 606-8507, Japan.

書誌事項

公開日
2025-04-11
資源種別
journal article
DOI
  • 10.1126/sciadv.adq5484
公開者
American Association for the Advancement of Science (AAAS)

説明

<jats:p>Although pluripotent stem cell (PSC) properties, such as differentiation and infinite proliferation, have been well documented within the frameworks of transcription factor networks, epigenomes, and signal transduction, they remain unclear and fragmented. Directing attention toward translational regulation as a bridge between these events can yield additional insights into previously unexplained mechanisms. Our functional CRISPR interference screen–based approach revealed that EIF3D, a translation initiation factor, is crucial for maintaining primed pluripotency. Loss of EIF3D disrupted the balance of pluripotency-associated signaling pathways, thereby compromising primed pluripotency. Moreover, EIF3D ensured robust proliferation by controlling the translation of various p53 regulators, which maintain low p53 activity in the undifferentiated state. In this way, EIF3D-mediated translation contributes to tuning the homeostasis of the primed pluripotency networks, ensuring the maintenance of an undifferentiated state with high proliferative potential. This study provides further insights into the translation network in maintaining pluripotency.</jats:p>

収録刊行物

  • Science Advances

    Science Advances 11 (15), 2025-04-11

    American Association for the Advancement of Science (AAAS)

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