Fig. 2

Neuronal expression of human PLS3 restores normal locomotion in smn-1(cb131) animals. a Locomotion rates of smn-1(cb131) animals decreased after a 20-s blue light stimulation of ChR2 in cholinergic neurons, in the presence of retinal. Introduction of somatic expression of human Plastin 3 (PLS3) restored normal locomotion rates immediately post-exhaustion. Two different PLS3 transgenes were used. Low copy is a homozygous single-copy insertion of [dpy-30p::PLS3], rtSi27 on chromosome II; high copy is an integrated multi-copy transgene incorporating the same transgene as low copy, rtIs59. Ubiquitous overexpression of the C. elegans ortholog of PLS3 (plst-1) was equally effective rtEx850. ANOVA F(2.9, 13.5) = 3.33, p < 0.05. b Neuronal expression of PLS3 rtEx852 [unc-119p::PLS3] rescued the post-exhaustion locomotion defects of smn-1(cb131) animals; expression in muscles rtEx851 [myo-3p::PLS3] did not. ANOVA F(1.56, 10.28) = 4.25, p < 0.05. c Overexpression of human PLS3 at high copy levels using rtIs59 increased basal locomotion rates in a wild-type background compared to controls. d smn-1(cb131) mutant animals were resistant to the cholinesterase inhibitor aldicarb, based on slower time to paralysis. Introduction of ubiquitously expressed human PLS3 restored sensitivity to normal levels. Note that C. elegans plst-1 was intact in all genotypes reported here and control animals contained the transgene rtSi28 [dpy-30p::empty] to account for insertion site and/or multi-copy promoter effects. In all assays, n ≥ 30 animals per determination, combined from 3 independent trials. Scorers were blinded to the genotypes of animals during the collection and analysis of data for the locomotion and aldicarb sensitivity assays. Student’s t test, Mann-Whitney U test (a–c), or log rank test (d): *p < 0.05, **p < 0.01. SEM indicated