Maxence Nachury: A transporting view of the primary cilium

JCB • VOLUME 191 • NUMBER 3 • 2010 436 R ecent years have seen an explosion of interest in the primary cilium. This long-neglected organelle was widely considered to be an evolutionary dead end before its critical function in cell signaling began to be uncovered. The microtubule-based membrane protrusion is now thought of as a cellular antenna, receiving extracellular signals and transmitting them to the rest of the cell. Defects in cilia function cause a variety of diseases, collectively known as ciliopathies. Maxence Nachury admits that he hadn’t even heard of the primary cilium until a few years ago when he was a postdoc with Peter Jackson at Stanford University and Genentech. Before that, Nachury had studied both nuclear transport and mitotic spindle assembly as a PhD student with Karsten Weis and Rebecca Heald at UC Berkeley (1, 2). But the mysterious primary cilium grabbed Nachury’s attention when he realized that mutations in a number of different ciliary proteins caused the pleiotropic human disorder Bardet-Biedl syndrome (BBS). Despite his initial unfamiliarity with the subject, Nachury soon demonstrated that seven of these proteins form a conserved complex called the BBSome that transports membrane proteins to the cilium (3). Nachury then identifi ed an additional BBSome subunit required for both cilia formation and microtubule acetylation (4). Now with his own lab at Stanford University, Nachury recently showed that the BBSome acts as a membrane coat to traffi c signaling receptors into the cilium (5). In a recent interview, Nachury discussed the BBSome’s function and the cilium’s contribution to human disease.