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sma-10 is a critical regulator of SMA-6 trafficking.

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posted on 2017-07-13, 17:46 authored by Ryan J. Gleason, Mehul Vora, Ying Li, Nanci S. Kane, Kelvin Liao, Richard W. Padgett

(A) Loss of sma-10 leads to decreased colocalization of SMA-6 within late endosomes. (B) Loss of sma-10 leads to increased colocalization of SMA-6 within MVBs. (C) Mutants of cup-5, a necessary component of the lysosome, result in accumulation of cargos destined for the lysosome. cup-5 RNAi shows accumulation of SMA-6::GFP in a sma-10 mutant. (D) Body size rescue experiments in C. elegans. The C-terminal cytoplasmic tail of SMA-10 is not required for body size determination in C. elegans. Plasmid constructs expressing full length sma-10 [sma-10(+),red] and sma-10 lacking the cytoplasmic tail [sma-10(Δcyto),blue] from a hypodermal-specific promoter were injected into the sma-10(wk88) mutant background. At least 30 transformed animals were assayed for body size at L4 + 24 hr for each genotype. As observed, full length sma-10 (red) as well as sma-10 lacking the cytoplasmic tail (blue) fully rescue the small body size of sma-10(wk88) indicating that the cytoplasmic tail is not required for the rescue of the body size defects. Bar graphs represent Mean ± S.E.M. A One-way ANOVA was performed for the series. *** indicates p < 0.0001 as compared to the wild-type. A minimum of 15 animals per line were assayed for body size.