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• W2124918753 abstract "The planar cell polarity (PCP) effector Fuz had not been studied in mice. Due to disrupted ciliogenesis, Fuz mutant mice show neural tube and skeletal defects. Fuz regulates trafficking of membrane cargoes to cilia through its interaction with a GTPase of the Rab family. The planar cell polarity (PCP) signalling pathway is essential for embryonic development because it governs diverse cellular behaviours, and 'core PCP' proteins, such as Dishevelled and Frizzled, have been extensively characterized1,2,3,4. By contrast, the 'PCP effector' proteins, such as Intu and Fuz, remain largely unstudied5,6. These proteins are essential for PCP signalling, but they have never been investigated in mammals and their cell biological activities remain entirely unknown. We report here that Fuz mutant mice show neural tube defects, skeletal dysmorphologies and Hedgehog signalling defects stemming from disrupted ciliogenesis. Using bioinformatics and imaging of an in vivo mucociliary epithelium, we established a central role for Fuz in membrane trafficking, showing that Fuz is essential for trafficking of cargo to basal bodies and to the apical tips of cilia. Fuz is also essential for exocytosis in secretory cells. Finally, we identified a Rab-related small GTPase as a Fuz interaction partner that is also essential for ciliogenesis and secretion. These results are significant because they provide new insights into the mechanisms by which developmental regulatory systems such as PCP signalling interface with fundamental cellular systems such as the vesicle trafficking machinery." @default.
• W2124918753 created "2016-06-24" @default.
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• W2124918753 date "2009-09-20" @default.
• W2124918753 modified "2023-10-13" @default.
• W2124918753 title "The planar cell polarity effector Fuz is essential for targeted membrane trafficking, ciliogenesis and mouse embryonic development" @default.
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• W2124918753 doi "https://doi.org/10.1038/ncb1966" @default.
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• W2124918753 hasPublicationYear "2009" @default.
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