To determine which α subunit(s) might be important, we examined clones lacking multiple edematous wings (mew), which encodes αPS1 and inflated (if), which encodes αPS2.

mew, if double mutant clones showed similar reductions in length and branching as mys clones, indicating that one, or both, of these genes is important for dendrite morphogenesis ( Figures 1C, 1E, and 1F). We examined roles for individual α subunits by transgenic RNAi-based knock down ( Dietzl et al., 2007) and found that depletion of mew, but not if, transcripts in class I neurons using 221-Gal4 led to a defect in dendritic arborization similar to that caused by RNAi of mys ( Figures 1I–1J). Consistent with these results, we did not observe a dendrite branching or length phenotype in if MARCM clones (p > 0.05; data not shown). Thus, PS1 (αPS1βPS) selleck chemicals probably plays a primary role in dendritic morphogenesis, although these data do not exclude a possible neuronal role for PS2 (αPS2βPS). Finally, consistent BMS-354825 nmr with a role for integrin-mediated adhesion in dendritic arborization, a mutation in rhea, which encodes a Drosophila talin essential for integrin function ( Brown et al., 2002), caused defects that were similar to those caused by mys mutations in class I neurons ( Figures 1D, 1G, and 1H). Together, these results reveal a cell-autonomous requirement for integrins in da neuron dendritic elaboration and/or

dendritic branch maintenance, likely reflecting a requirement for adhesive interactions between dendrites and the ECM. We next used MARCM to examine the requirements for integrins in dendritogenesis of the complex class IV neuron, ddaC. Like class I neurons, ddaC mys clones showed a decrease in

dendritic branch points ( Figures 1K–1M). Class IV dendrites also normally show robust self-repulsion between branches with only occasional crossing errors ( Figure 1K). We found that mys ddaC clones showed increased self-crossings and thus appeared to be defective in this repulsive Cell press response ( Figures 1L and 1N; Figure S1A available online). By contrast, sister dendrite crossing as a proportion of total branch number or total length was not significantly affected in class I mys clones (both p > 0.05, Wilcoxon rank-sum test). Excessive dendrite self-crossing observed in class IV neurons suggested that integrin-mediated dendrite-ECM interactions promote dendritic self-avoidance. We next examined expression patterns of integrins in the peripheral body wall at third instar larval stages. Immunolabeling with anti-βPS, αPS1, and αPS2 integrin revealed localization in puncta on the basal surface of the epidermis, and enrichment alongside dendrites (Figures S1B–S1F). Expression across the epidermis prevented unambiguous assessment of expression in da neuron dendrites; however, examination of arbors growing over mys epidermal clones that were devoid of βPS integrin provided support for dendritic localization ( Figures S1C–S1D′).