Endocytosis genes facilitate protein and membrane transport in C. elegans sensory cilia.
Endocytosis genes facilitate protein and membrane transport in C. elegans sensory cilia.
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DOI：
10.1016/j.cub.2012.01.060
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发表时间：
2012-03-20
期刊：
影响因子：
9.2
通讯作者：
Blacque, Oliver E.
中科院分区：
文献类型：
--
作者：
Kaplan, Oktay I.;Doroquez, David B.;Cevik, Sebiha;Bowie, Rachel V.;Clarke, Lara;Sanders, Anna A. W. M.;Kida, Katarzyna;Rappoport, Joshua Z.;Sengupta, Piali;Blacque, Oliver E.
Multiple intracellular transport pathways drive the formation, maintenance and function of cilia, a compartmentalised organelle associated with motility, chemo-/mechano-/photo-sensation, and developmental signaling. These pathways include cilium-based intraflagellar transport (IFT) and poorly understood membrane trafficking events. Defects in ciliary transport contribute to the aetiology of human ciliary disease such as Bardet-Biedl syndrome (BBS). In this study, we employ the genetically tractable nematode Caenorhabditis elegans to investigate if endocytosis genes function in cilium formation and/or the transport of ciliary membrane or ciliary proteins. Here we show that localisation of the clathrin light chain, AP-2 clathrin adaptor, dynamin and RAB-5 endocytic proteins overlaps with a morphologically discrete periciliary membrane compartment associated with sensory cilia. In addition, ciliary transmembrane proteins such as G protein-coupled receptors concentrate at periciliary membranes. Disruption of endocytic gene function causes expansion of ciliary and/or periciliary membranes as well as defects in the ciliary targeting and/or transport dynamics of ciliary transmembrane and IFT proteins. Finally, genetic analyses reveal that the ciliary membrane expansions in dynamin and AP-2 mutants require bbs-8 and rab-8 function, and that sensory signaling and endocytic genes may function in a common pathway to regulate ciliary membrane volume. These data implicate C. elegans endocytosis proteins localized at the ciliary base in regulating ciliary and periciliary membrane volume, and suggest that membrane retrieval from these compartments is counter-balanced by BBS-8 and RAB-8-mediated membrane delivery.
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