Abstract
Defects in protein trafficking within the cell body and cilia are thought to underlie the human disease Bardet-Biedl syndrome (BBS). In this issue, Nachury et al. (2007) reveal that a large complex of proteins implicated in BBS cooperates with Rabin8-the GTP exchange factor for the small GTPase Rab8-to promote cilia formation and presumably movement of membrane proteins from the cell into the cilium.
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