Journal: PLoS Genetics

Article Title: Loss-of-function of the ciliopathy protein Cc2d2a disorganizes the vesicle fusion machinery at the periciliary membrane and indirectly affects Rab8-trafficking in zebrafish photoreceptors

doi: 10.1371/journal.pgen.1007150

Figure Lengend Snippet: Rab8 coats opsin-carrier-vesicles and targets them to the periciliary membrane, where their fusion is mediated by the Exocyst and by SNAREs including SNAP25 and Syntaxin 3 (and by an as yet undefined v-SNARE). CC2D2A at the transition zone is required for correct localization of SNAP25 to the periciliary membrane and provides a docking point for incoming vesicles through its interaction with NINL, which also binds the dynein motor and the Rab8 effector MICAL3. Thus, CC2D2A plays a role in concentrating all components required for correct vesicle fusion at the periciliary membrane.

Article Snippet: Primary antibodies were rabbit anti-Syntaxin3 (1:400, Alomone labs, ANR-005), rabbit anti-SNAP25 (1:1000, StressGen Biotechnologies, VAP-SV002), mouse monoclonal anti-Rab8a (1:100, Novus Biologicals, clone 3G1), rabbit anti-Cacna1fa (1:5000, a gift from Michael Taylor, University of Wisconsin [ ]), rabbit anti-blue opsin (1:250, gift from David Hyde) and rabbit anti green opsin (1:400, gift from David Hyde, University of Notre Dame).

Techniques: Membrane, Docking Assay