Figure 2.

sax-1 and sax-2 morphological defects appear late in development and do not lead to severe behavioral defects. (A) sax-1 and sax-2 mutants generate chemotaxis responses to attractive odorants detected by the AWC sensory neurons. Wild-type animals are represented by black bars, sax-1(ky211) by striped bars, sax-1(ky491) by stippled bars, and sax-2(ky216) by white bars. Animals were tested for chemotaxis to three attractive odorants sensed by AWC: benzaldehyde (1:200 dilution in ethanol), isoamyl alcohol (1:100 dilution), and 2-butanone (1:1000 dilution). Chemotaxis assays were conducted as described (Bargmann et al., 1993). A chemotaxis index of 1 indicates complete attraction, whereas a chemotaxis index of 0 indicates no response. Error bars indicate the SE of the mean based on five to seven independent assays performed on ∼100 animals in each assay. (B) ASJ ectopic neurite defects increase in severity during larval and adult stages in sax-1 and sax-2 mutants. Animals were scored at each of the four larval stages (L1–L4) and as 1- or 3-d-old adults. Error bars indicate the SE of proportion; n = 47–246 animals scored for each data point. ASJ morphology was scored with the use of the tax-2Δ::gfp transgene. Asterisks indicate populations that were significantly more defective than animals at the previous developmental stage at p < 0.01 (χ² test). For ASJ neurons in sax-1(ky211) mutants, L3 differs from L2 at p = 0.007; young adult differs from L4 at p = 0.003; and old adult differs from young adult at p = 0.002. For ASJ neurons in sax-2(ky216) mutants, L3 differs from L2 at p < 0.001; young adult differs from L4 at p = 0.002; and old adult differs from young adult at p < 0.001. (C) AWC cell shape defects are apparent at all developmental stages. For AWC neurons in sax-2 mutants, L2 differs from L1 at p < 0.001.