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. 2021 Nov 24;17(11):e1009877. doi: 10.1371/journal.pgen.1009877

Fig 2. RAB-27’s synaptic vesicle tethering cofactors do not inhibit regeneration.

Fig 2

(A) Colocalization of transgenic GFP::RAB-27 and mCherry::RAB-3 at synapses of DD/VD neurons. (B) Relative axon length in control (oxIs12) animals, rab-3(js49), rbr-1(js232), rab-27(sa24), rab-3(js49); rab-7(sa24) mutants. Axons cut per genotype, L to R: 183, 37, 55, 196, 21, 69. Kolmogorov-Smirnov test was used. ns, not significant, * p < 0.05, *** p < 0.0005. (C) Relative axon length in control animals, rab-27(sa24) mutants, and animals expressing RAB-3 cDNA under an intestine-specific promoter, in control and rab-27 mutant backgrounds. Number of axons cut per genotype, L to R: 61, 55, 53, 50. Kolmogorov-Smirnov test was used. ns, not significant, * p < 0.05, ** p < 0.005. (D) Mutants in the aex pathway display a defect in the defecation motor program, visualized by a loss of waste expulsion (Exp) following posterior body contraction (pBoc). D1 adult animals were randomly selected and observed for 5 DMP cycles, and the ratio of Exp/pBoc was plotted. Intestinal (Pspl-1) but not GABA neuron-specific (Punc-47) expression of rab-27 cDNA was sufficient to rescue DMP in rab-27 mutant worms. Expression of rab-3 cDNA in the intestine of rab-27 mutant animals did not rescue DMP defects. pBoc cycles observed, L to R: 49, 119, 30, 49, 62, 54, 56, 40, 58. ns, not significant, * p < 0.05, ** p < 0.05, *** p < 0.0005, **** p < 0.0001, Fisher’s Exact Test. Error bars represent SEM.