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Previous studies have demonstrated the striking mutational effects of the  Drosophila  planar cell polarity gene  prickle (pk)  on larval motor axon microtubule-mediated vesicular transport and on adult epileptic behavior associated with neuronal circuit hyperexcitability. Mutant alleles of the  prickle - prickle  ( pk pk) and  prickle - spiny-legs  ( pk sple) isoforms (hereafter referred to as  pk  and  sple  alleles, respectively) exhibit differential phenotypes. While both  pk  and  sple  affect larval motor axon transport, only  sple  confers motor circuit and behavior hyperexcitability. However, mutations in the two isoforms apparently counteract to ameliorate adult motor circuit and behavioral hyperexcitability in heteroallelic  pk pk /pk sple  flies. We have further investigated the consequences of altered axonal transport in the development and function of the larval neuromuscular junction (NMJ). We uncovered robust dominant phenotypes in both  pk  and  sple  alleles, including synaptic terminal overgrowth (as revealed by anti-HRP and -Dlg immunostaining) and poor vesicle release synchronicity (as indicated by synaptic bouton focal recording). However, we observed recessive alteration of synaptic transmission only in  pk/pk  larvae, i.e. increased excitatory junctional potential (EJP) amplitude in  pk/pk  but not in  pk /+ or  sple / sple . Interestingly, for motor terminal excitability sustained by presynaptic Ca 2+  channels, both  pk  and  sple  exerted strong effects to produce prolonged depolarization. Notably, only  sple  acted dominantly whereas  pk /+ appeared normal, but was able to suppress the  sple  phenotypes, i.e.  pk/sple  appeared normal. Our observations contrast the differential roles of the  pk  and  sple  isoforms and highlight their distinct, variable phenotypic expression in the various structural and functional aspects of the larval NMJ.

journal of neurogenetics

Abnormal larval neuromuscular junction morphology and physiology in  Drosophila  prickle isoform mutants with known axonal transport defects and adult seizure behavior