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. 2012 May 15;26(10):1070–1085. doi: 10.1101/gad.188003.112

Figure 1.

Figure 1.

NMJ defects of sphk-1 mutants. (A) Locomotion, measured by body bends per minute, of young adult wild type (26.6 ± 1.0), sphk-1(ok1097) mutants (20.7 ± 1.6), and sphk-1 mutants expressing sphk-1 cDNA under the sphk-1 promoter (sphk-1 rescue, 28.7 ± 0.8). Asterisks indicate values that differ significantly from wild type, and pound signs indicate differences between groups, as indicated (significance determined by ANOVA and Tukey post-hoc tests; [ns] not significant; n = 30). (B) Rates of worm paralysis of the indicated strains upon exposure to the ACh esterase inhibitor aldicarb (1.5 mM). (C) Rates of worm paralysis of the indicated strains upon exposure to the cholinergic agonist levamisole (200 μM). (D) Coexpression of a sphk-1 promoter fragment driving nuclear-localized GFP (P.sphk-1-GFP-NLS) and a cholinergic neuron reporter (P.acr-2-mCherry) in ventral cord motor neurons of young adults. Arrows indicate expression in cholinergic neurons, and the arrowhead indicates expression in GABAergic neurons. Bar, 20 μm. (E) Rates of paralysis on aldicarb (1.5 mM) of the indicated strains. Neuronal and muscle rescues denote transgenic sphk-1 mutants expressing full-length sphk-1 cDNA under a pan-neuronal promoter (P.snb-1) or body wall muscle promoter (P.myo-3), respectively. (F) Rates of worm paralysis upon exposure to aldicarb (0.5 mM) after pretreatment with SKI (50 μM) for 2 h. Error bars are ±SEM.