Fig. 6: UA and S1P promote PLM axon transport and microtubule stability.
From: An intestinal sphingolipid confers intergenerational neuroprotection
a,b, Continuous exposure to UA or S1P reduces inappropriate posterior accumulation of UNC-104::GFP (kinesin; a) and mCherry::RAB-3 (pre-synaptic guanosine triphosphatase; b) in the PLM axons of mec-17(ok2109) animals. Scale bars, 25 μm. c,d, Continuous exposure to UA or S1P reduces colchicine-induced PLM axon breaks in mec-17(ok2109); lon-2(e678) (c) and wild-type (d) animals. Wild-type and mec-17(ok2109); lon-2(e678) animals were exposed to 200 µM and 100 µM colchicine, respectively. Two-day-old adult animals were scored. e, Continuous UA or S1P exposure reduces PLM axon breaks in lin-14(n355n679) lon-2(e678) animals. f, Continuous exposure to S1P, but not UA, reduces D-type motor neuron commissure defects in lin-14(n355n679) animals. g, Continuous exposure to UA or S1P reduces PVQ axon defects in ced-10(rp100) animals (g). a–g, Continuous exposure: P0 to L4 larva to F1 to adult; n = 245, 247, 103 and 99 (a); n = 107, 119, 96 and 94 (b); n = 112, 152, 146, 99, 101 and 102 (c); n = 76, 74, 96, 76, 75 and 67 (d); n = 149, 175, 138 and 144 (e); n = 109, 106, 97 and 107 (f); and n = 102, 117, 156 and 150 (g) hermaphrodite animals per condition (left to right). P values were determined using an ANOVA (c,d) or unpaired Student’s t-test (a,b,e–g). ****P ≤ 0.0001; ***P ≤ 0.001; **P ≤ 0.01; *P ≤ 0.05; and NS, not significant. Error bars indicate the s.e.m. Source data are provided.
