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. 2011 May 12;108(22):9274–9279. doi: 10.1073/pnas.1011711108

Fig. 5.

Fig. 5.

Suppression of electrical activity by slo-1 gain-of-function mutations induces progressive touch receptor neuron defects. (Scale bar: 5 μm.) (A) Immunofluorescence images of ALM neurons in the wild-type, slo-1(ky389), slo-1(ky399), and slo-1(js118); Psnb-1::slo-1 animals at D3 and D7 of adulthood, with touch receptor neurons labeled by the 6–11B-1 antibody. ky389 and ky399 are gain-of-function mutations, and js118 is a recessive loss-of-function mutation. Acetylated tubulin was decreased and disorganized in the neuronal cell bodies in slo-1(ky389), slo-1(ky399), and slo-1(js118); Psnb-1::slo-1 mutants. Single arrows: bubble-like lesions; single arrowheads: discontinuity of the acetylated tubulin immunoreactivity; double arrows: ALM cell bodies; double arrowheads: branching from the nerve processes. (B) Quantification of ALM defects in wild type, slo-1(ky389), slo-1(ky399), and slo-1(js118); Psnb-1::slo-1 animals at D1, D3, and D7. Error bars are SEs of proportions. The number of cells scored is indicated. N/A, not available.