Control of vertebrate intraflagellar transport by the planar cell polarity effector Fuz

被引:42
作者
Brooks, Eric R. [1 ,2 ]
Wallingford, John B. [1 ,2 ,3 ]
机构
[1] Univ Texas Austin, Sect Mol Cell & Dev Biol, Austin, TX 78712 USA
[2] Univ Texas Austin, Inst Cellular & Mol Biol, Austin, TX 78712 USA
[3] Univ Texas Austin, Howard Hughes Med Inst, Austin, TX 78712 USA
基金
美国国家卫生研究院;
关键词
HEDGEHOG SIGNAL-TRANSDUCTION; FLAGELLAR LENGTH CONTROL; CHLAMYDOMONAS-FLAGELLA; KIDNEY-DISEASE; IFT PARTICLES; CILIA; PROTEIN; CILIOGENESIS; MOUSE; DEFECTS;
D O I
10.1083/jcb.201204072
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cilia play key roles in development and homeostasis, and defects in cilia structure or function lead to an array of human diseases. Ciliogenesis is accomplished by the intraflagellar transport (IFT) system, a set of proteins governing bidirectional transport of cargoes within ciliary axonemes. In this paper, we present a novel platform for in vivo analysis of vertebrate IFT dynamics. Using this platform, we show that the planar cell polarity (PCP) effector Fuz was required for normal IFT dynamics in vertebrate cilia, the first evidence directly linking PCP to the core machinery of ciliogenesis. Further, we show that Fuz played a specific role in trafficking of retrograde, but not anterograde, IFT proteins. These data place Fuz in the small group of known IFT effectors outside the core machinery and, additionally, identify Fuz as a novel cytoplasmic effector that differentiates between the retrograde and anterograde IFT complexes.
引用
收藏
页码:37 / 45
页数:9
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