Table 2.

Double-mutant analysis between dpy-18(ok162) collagen/collagen-interacting protein mutants

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°C6
emb-9(hc90); dpy-18(ok162)15°C72<0.0001
emb-9(hc90)20°C14
emb-9(hc90); dpy-18(ok162)20°C61<0.0001
let-2(b246)15°C5
let-2(b246); dpy-18(ok162)15°C95n.s.
let-2(b246)20°C11
let-2(b246); dpy-18(ok162)20°C69<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.