Figure 1. A new deletion allele of
wdfy-3 causes mild axon termination defects and suppresses axon termination defects caused by an
fsn-1 null allele:(A) Schematic of the predicted protein products for wildtype
wdfy-3,
wdfy-3(
ok912) and
wdfy-3(
cue30). The
wdfy-3(
ok912) allele consists of a small deletion (marked by red bracket), insertion of GAGACA and resulting frameshift. Therefore, the BEACH, WD repeats, and FYVE-type domains are predicted to be non-functional in the protein product of the
wdfy-3(
ok912) mutant. The newly created
wdfy-3(
cue30) removes the first 33 of 36 exons and is predicted to be a null allele. Red arrows mark the cut sites of Cas9, with the base pair number relative to the start codon indicated above the cut site. (B) Quantification of PLM axon overextension defects in wildtype (wt),
wdfy-3(
ok912) and
wdfy-3(
cue30) animals. The null
wdfy-3(
cue30) animals showed increased penetrance of PLM axon overextension defects relative to wildtype and
wdfy-3(
ok912). (C) PLM axon overextension defects caused by the
fsn-1(
gk429) null mutation are suppressed by the
wdfy-3(
cue30) and
wdfy-3(
ok912) mutations. Axons were visualized with the muIs32 transgene that encodes Pmec-7::gfp. Between 150 and 400 axons were observed in L4 stage hermaphrodites per genotype. Asterisks indicate statistically significant difference, Z-test for proportions (*p<0.01; ***p<0.0001). Error bars represent the standard error of the proportion.