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KIF16B/Rab14 molecular motor complex is critical for early embryonic development by transporting FGF receptor

Hitoshi Ueno1, Xiao Huang, Yosuke Tanaka

  • 1Department of Cell Biology and Anatomy, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.

Developmental Cell
|January 18, 2011
PubMed

Insights

The kinesin-3 motor KIF16B protein is crucial for transporting fibroblast growth factor receptors (FGFRs) during early embryonic development. Its absence disrupts cell development and leads to embryonic death.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Molecular Biology

Background:

  • Kinesin-mediated membrane trafficking is essential for cellular function but its role in development is unclear.
  • Fibroblast growth factor receptor (FGFR) signaling is vital for embryonic development.

Purpose of the Study:

  • To investigate the role of the kinesin-3 motor KIF16B in early embryonic development.
  • To elucidate the mechanism of KIF16B in the transport of fibroblast growth factor receptors (FGFRs).

Main Methods:

  • Utilized Kif16b knockout mouse models.
  • Investigated KIF16B-Rab14 interaction on FGFR-containing vesicles.
  • Employed a dominant-negative Rab14-GDP overexpression strategy.

Main Results:

  • Kif16b knockout embryos exhibited defects in epiblast and primitive endoderm development, leading to peri-implantation lethality.
  • KIF16B directly binds Rab14-GTP on FGFR vesicles for transport.
  • Rab14-GDP overexpression mimicked KIF16B or FGFR2 deficiency, impairing FGFR transport, FGF signaling, and development.

Conclusions:

  • The KIF16B/Rab14 complex is essential for the biosynthetic transport of FGFRs from the Golgi to endosomes.
  • This microtubule-based membrane trafficking pathway is critical for FGF signaling, basement membrane assembly, and early embryonic development.

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