<i>aha-1</i> and <i>ahr-1</i> are required cell-autonomously for BDU-PLM contact.

<p>(A–B) The contact between BDU and PLM is defective in <i>aha-1(xd4)</i> animals compared to wild type. Scale bars represent 10 µm. (C) The gene structure of <i>aha-1</i>. The molecular lesions in <i>xd4</i> and <i>ok1396</i> are labeled. The rescue activity of various <i>aha-1</i> constructs is indicated. (D–E) PLM and BDU neurite lengths are indistinguishable from wild type in <i>aha-1(xd4)</i> or <i>ahr-1(ju145)</i> mutants. (F) Quantification of BDU-PLM contact defects in mutants of the PAS-bHLH family. The severity of BDU-PLM contact defects is not enhanced in <i>aha-1(xd4) ahr-1(ia3)</i> double mutants compared to <i>aha-1(xd4)</i> or <i>ahr-1(ia3)</i> single mutants. (G) The <i>aha-1</i> mutant phenotype is partially rescued by expressing the <i>aha-1</i> gene in BDU (P<i>unc-53</i>::AHA-1) or PLM (P<i>mec-7</i>::AHA-1) cells and fully rescued by expressing it in both BDU and PLM (P<i>unc-53</i>::AHA-1 and P<i>mec-7</i>::AHA-1) cells. Error bars in (D–G) represent the SEM. NS, not significant. ** p<0.01.