Gap junctions, or electrical synapses, mediate fast communication between neurons but the mechanisms that direct gap junction assembly between specific neurons or within specific subcellular compartments are poorly understood. Gap junction localization ultimately depends on kinesins, which walk along microtubule (MT) tracks to deliver gap junction components to their cellular destinations. We are investigating gap junction assembly in VA motor neurons in which the UNC-4 transcription factor and its corepressor UNC-37 regulate the neuron specificity and placement of electrical synapses. Gap junction trafficking is disrupted in
unc-4 mutants (Palumbos et al, worm meeting 2019). To investigate the mechanism of this effect, we utilized the MT plus-end marker, EBP-2::GFP, to monitor MT dynamics. We determined that the rate of MT polymerization and outgrowth length are reduced in
unc-37 mutant VA neurons. VAB-8, an atypical kinesin that binds MTs but lacks motor activity, is negatively regulated by UNC-4/UNC-37. We are now testing the hypothesis that ectopic expression of VAB-8 in
unc-4 mutant VA neurons disrupts gap junction trafficking by altering MT dynamics.