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Fig. 3 | BMC Biology

Fig. 3

From: Genetic modifiers ameliorate endocytic and neuromuscular defects in a model of spinal muscular atrophy

Fig. 3

Identification of sym-2 as a suppressor of PLS3oe and smn-1 locomotion defects. a To find proteins in a putative SMN/PLS3 complex, we focused on candidates that independently pulled down in previous work [45] with both Drosophila Fimbrin and Drosophila Smn (left and right circles of Venn diagram, details in the “Methods” section). Candidates that had a corresponding C. elegans loss of function allele available in 2011 are listed and were examined. Only sym-2 loss of function suppressed PLS3oe and smn-1 defects in all three assays (right) used to screen these candidates. b Overexpression of human PLS3 increased basal locomotion rates compared to control animals. PLS3 was overexpressed from rtIs59, an integrated multi-copy transgene ubiquitously driving expression using the dpy-30 promoter. Decreased function of the C. elegans hnRNP F/H ortholog, sym-2, did not change locomotion rates in a wild-type background, but sym-2 perturbation suppressed increased locomotion in PLS3oe animals. ANOVA F(7962, 663) = 175.96, p < 0.05. c sym-2 perturbation suppressed locomotion defects in smn-1(cb131) animals immediately following ChR2 exhaustion. All animals in c carried oxIs364[unc-17p::ChR2]; ANOVA F(0.84, 0.55) = 17.51, p < 0.05. In all assays, n ≥ 30 animals per determination were used, combined from 3 independent trials. Scorers were blinded to the genotype of animals during the collection of data and data analysis. Student’s t test: **p < 0.01. SEM indicated

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