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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 3. — unc-108 mutants have reduced locomotion and aldicarb sensitivity but not SV release at the NMJ. (A) The locomotory defects of unc-108 mutants are synthetically enhanced in unc-108; egl-3 double mutants to the level of unc-31/CAPS. Error bars = SEM (***, P < 0.005; Student's t test; all strains were compared with wild type; double mutants are compared with egl-3 and unc-31 single mutants). (B and C) Dominant unc-108 mutants are resistant to the ACh esterase inhibitor aldicarb (B), similar to rab-3, and exhibit a wild type–like sensitivity to the postsynaptic nicotinic receptor agonist levamisole (C). The weakly levamisole-resistant lev-10 mutant is shown as control. Error bars = SEM (n = 30). (D) The evoked release of SVs at the NMJ is similar between wild type and dominant unc-108 and ric-19 mutants. Error bars = SEM.