, 2010). hpo-30 mutants display a striking asymmetric defect in which the majority of PVD lateral branches are restricted to the right side ( Figure 7H), and most of these fasciculate with motor neuron commissures ( Figure 7I). Thus, hpo-30 appears to function largely in commissure-independent stabilization of lateral branches. This analysis defines two mechanisms of dendrite stabilization, one that requires HPO-30 and is not associated with the commissures and a separate pathway that utilizes a different protein for fasciculation

with motor neuron commissures ( Smith et al., 2010). HPO-30 is also likely to support higher order PVD branching since the residual 2° branches in hpo-30 mutants do not result in recognizable menorahs with a full complement of 3° and 4° dendrites ( Figures 7 and 8). The frequent occurrence of overlapping PVD dendrites selleck compound in the hpo-30 mutant ( Figures 7A and 7H) is suggestive of an additional role in dendrite self-avoidance. Because HPO-30 is required

for PVD dendritic branching, we hypothesized that HPO-30 is also necessary for branching of the extra PVD-like cell, cAVM, in ahr-1 mutants. This idea was substantiated by the finding that cAVM lateral branches were largely eliminated in ahr-1;hpo-30 double mutants ( Figures 8C and 8D). To ask if AHR-1 regulates HPO-30, we visualized hpo-30::GFP in an ahr-1 mutant background and confirmed that hpo-30::GFP is ectopically expressed in cAVM ( Figure S7). These results indicate that AHR-1 blocks expression of HPO-30 to prevent touch neurons from adopting the lateral branching architecture of the PVD neuron ( Figure 6K). Reduced hpo-30::GFP expression in Galunisertib cAVM in an ahr-1;mec-3 double mutant confirmed that mec-3 function is necessary for ectopic hpo-30::GFP expression in cAVM in an ahr-1 mutant background Carnitine dehydrogenase (data not shown). This effect is also consistent with our finding that mec-3

promotes hpo-30::GFP expression in PVD ( Figure 7D). Thus, our results are indicative of a transcriptional mechanism in touch neurons ( Figure 6K) in which ahr-1 activates mec-3 while simultaneously blocking expression of hpo-30, a mec-3 target gene that promotes lateral branching. Having shown that hpo-30 function is required for the PVD-like dendritic morphology of cAVM ( Figure 8D), we next asked if hpo-30 expression was sufficient to induce lateral branching in wild-type light touch neurons. Normally, touch neurons adopt a simple, unbranched morphology ( Figures 1 and 8). Ectopic expression of HPO-30 in PLM with the mec-4 promoter, however, resulted in the appearance of aberrant lateral branches that are not observed in the wild-type ( Figure 8F). AVM and PVM did not show ectopic branches in this experiment, but their longitudinal processes are located in the ventral nerve cord ( Figure 1) and thus are not in contact with the epidermal region in which HPO-30 normally promotes PVD branching.