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. 2016 Jul 11;113(30):E4377–E4386. doi: 10.1073/pnas.1600015113

Fig. 2.

Fig. 2.

Double mutant analysis using pharyngeal pumping suggests SV recycling defects. (A) C. elegans neuromuscular function is assessed as pharyngeal grinder (arrow) movement during feeding. (B–D) Complete loss of endophilin-A, synaptojanin, or syndapin (unc-57(ok310), unc-26(s1710), or sdpn-1(ok1667)) did not alter smn-1(ok355) pharyngeal pumping defects. (E and F) Complete loss of Munc-18 or synaptobrevin [unc-18(e234) or snb-1(md247)] exacerbated smn-1(ok355) pharyngeal pumping defects. Additive defects with SV exocytosis loss-of-function mutants suggested that SMN-1 depletion impairs the SV recycling pathway. Total number of animals tested listed for each genotype ± SEM; Mann–Whitney U test, two-tailed: *P < 0.05; **P < 0.01; ***P < 0.001; n.s., not significant.