HSN guidance defect (%) | p value | ||
---|---|---|---|
dpy-18(ok162) | 98 | ||
ddr-1(ok874) | 6 | ||
ddr-1(ok874); dpy-18(ok162) | 78 | <0.0001 | |
ddr-2(ok574) | 23 | ||
ddr-2(ok574); dpy-18(ok162) | 87 | <0.0001 | |
nid-1(cg119) | 70 | ||
nid-1(cg119); dpy-18(ok162) | 87 | <0.0001 | |
cle-1(cg120) | 20 | ||
cle-1(cg120); dpy-18(ok162) | 76 | <0.0001 | |
emb-9(hc90) | 15°C | 6 | |
emb-9(hc90); dpy-18(ok162) | 15°C | 72 | <0.0001 |
emb-9(hc90) | 20°C | 14 | |
emb-9(hc90); dpy-18(ok162) | 20°C | 61 | <0.0001 |
let-2(b246) | 15°C | 5 | |
let-2(b246); dpy-18(ok162) | 15°C | 95 | n.s. |
let-2(b246) | 20°C | 11 | |
let-2(b246); dpy-18(ok162) | 20°C | 69 | <0.0001 |
VNC defects of HSN axons in dpy-18(ok162) animals are suppressed by mutations in genes encoding type IV and type XV/XVIII collagens (EMB-9, LET-2, and CLE-1) and in collagen-interacting proteins (DDR-1, DDR-2, and NID-1). Data are expressed as mean ± SD and statistical significance was assessed by ANOVA followed by Dunnett's multiple-comparison test. n > 50, ****p < 0.0001. n.s., Not significant.