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First published online August 7, 2009
doi: 10.1242/10.1242/dev.038174

1 Ecole Polytechnique Fédérale de Lausanne (EPFL) SV ISREC,
Station 19, CH-1015 Lausanne, Switzerland.
2 University of Hohenheim, Institute of Zoology, D-70593 Stuttgart,
Germany.
Author for correspondence
(daniel.constam{at}epfl.ch)
Accepted 11 June 2009
Polycystic diseases and left-right (LR) axis malformations are frequently linked to cilia defects. Renal cysts also arise in mice and frogs lacking Bicaudal C (BicC), a conserved RNA-binding protein containing K-homology (KH) domains and a sterile alpha motif (SAM). However, a role for BicC in cilia function has not been demonstrated. Here, we report that targeted inactivation of BicC randomizes left-right (LR) asymmetry by disrupting the planar alignment of motile cilia required for cilia-driven fluid flow. Furthermore, depending on its SAM domain, BicC can uncouple Dvl2 signaling from the canonical Wnt pathway, which has been implicated in antagonizing planar cell polarity (PCP). The SAM domain concentrates BicC in cytoplasmic structures harboring RNA-processing bodies (P-bodies) and Dvl2. These results suggest a model whereby BicC links the orientation of cilia with PCP, possibly by regulating RNA silencing in P-bodies.
Key words: Polycystic kidney disease, PCP, Flow, Nodal, SAM domain, K-homology
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