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

First Author  Ueno H Year  2011
Journal  Dev Cell Volume  20
Issue  1 Pages  60-71
PubMed ID  21238925 Mgi Jnum  J:168572
Mgi Id  MGI:4889011 Doi  10.1016/j.devcel.2010.11.008
Citation  Ueno H, et al. (2011) KIF16B/Rab14 molecular motor complex is critical for early embryonic development by transporting FGF receptor. Dev Cell 20(1):60-71
abstractText  Kinesin-mediated membrane trafficking is a fundamental cellular process, but its developmental relevance is little understood. Here we show that the kinesin-3 motor KIF16B/Rab14 complex acts in biosynthetic Golgi-to-endosome traffic of the fibroblast growth factor receptor (FGFR) during early embryonic development. Kif16b(-/-) mouse embryos failed in developing epiblast and primitive endoderm lineages and died in the peri-implantation stage, similar to previously reported FGFR2 knockout embryos. KIF16B associated directly with the Rab14-GTP adaptor on FGFR-containing vesicles and transported them toward the plasma membrane. To examine whether the nucleotide state of Rab14 serves as a switch for transport, we performed Rab14-GDP overexpression. This dominant negative approach reproduced the whole putative sequence of KIF16B or FGFR2 deficiency: impairment in FGFR transport, FGF signaling, basement membrane assembly by the primitive endoderm lineage, and epiblast development. These data provide one of the first pieces of genetic evidence that microtubule-based membrane trafficking directly promotes early development.
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