Fig. 3: Intestinal and neuronal asah-1 expression has opposing effects on axonal development and health.
From: An intestinal sphingolipid confers intergenerational neuroprotection
a, Expression of asah-1 cDNA driven by the heterologous intestinal promoter (ges-1), but not the hypodermal (dpy-7) or muscle (myo-3) promoters, resulted in reduced PLM axon breaks in mec-17(ok2109); lon-2(e678) animals. b, PLM axon breaks were reduced in mec-17(ok2109); lon-2(e678) animals derived from Pges-1::asah-1 transgenic animals independently of inheritance of the transgene. The mec-17(ok2109); lon-2(e678) animals were either injected with Pges-1::asah-1 (transgenic lines nos. 1 and 2) or uninjected (−). c,d, Overexpression of asah-1 in the nervous system (rab-3 promoter) caused developmental axon outgrowth defects in the mechanosensory neurons of wild-type animals expressing the Pmec-4::gfp transgene (zdIs5). c, Proportion of PLM axon outgrowth defects in Pmec-4::gfp- and Pmec-4::gfp; Prab-3::asah-1-expressing L1 larvae. d, Schematic (top) and fluorescence micrographs (bottom) of ALM (left/right) and PLM (left/right) axons in wild-type (left) and Prab-3::asah-1-expressing animals (right). The typical axon outgrowth defect observed is marked in red. Left lateral view, anterior to the left. Scale bars, 25 μm. a–c, n = 305, 72, 80, 75, 72, 98 and 97 (a); n = 126, 147, 149, 123 and 124 (b); and n = 62 and 95 (c) hermaphrodite animals per condition (left to right). P values were determined using an ANOVA (a) or unpaired Student’s t-test (b,c). Error bars indicate the s.e.m. ****P ≤ 0.0001; ***P ≤ 0.001; **P ≤ 0.01; *P ≤ 0.05; and NS, not significant. Source data are provided.
