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. 2009 Sep 21;186(6):897–914. doi: 10.1083/jcb.200902096

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© 2009 Sumakovic et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 9. — ric-19 mutants show similar phenotypes to unc-108 mutants. (A) ric-19 mutants show movement defects, which can be rescued by neuronal expression of ric-19. Knockdown of RIC-19 in unc-108 has no additional affect on locomotion. (B) ric-19(ok833) mutants are resistant to the ACh esterase inhibitor aldicarb, similarly to unc-108(n501). Aldicarb resistance can be rescued by neuronal expression of ric-19 (n = 30). (C and D) ric-19 deletion or ric-19 RNAi decreases axonal NLP-21–YFP fluorescence (nuIs183) similar to unc-108 mutants. ric-19 RNAi in unc-108 mutants shows epistasis. Neuronal expression of RIC-19 rescues DCV defects of ric-19 mutants. (E) Western blot showing the efficiency of RIC-19 knockdown by RNAi in unc-108(n501) mutants. (F and G) ric-19 mutants secrete less NLP-21–derived YFP (nuIs183), as measured by coelomocyte fluorescence, which is in agreement with the reduced axonal YFP levels in DCVs. This defect can be rescued by neuronal ric-19 expression. (A, B, D, and G) Error bars = SEM (**, P < 0.01; ***, P < 0.005; Student's t test). Bars: (C) 10 µm; (F) 5 µm.