Ary Fig. 2E ). Reduction of Tao activity applying TaoRNAi resulted in striking dendritic overgrowth and concomitant increase in postNω-Propyl-L-arginine Epigenetics synaptic puncta of A08n neurons. Immunostaining with an anti-Fas3 antibody, which especially labels C2da, C3da, and C4da sensory axons, revealed that A08n dendrites and postsynapses extended in to the adjacent domains of C2da and C3da neurons, which align laterally for the medial triangular-shaped C4da axon projections. Conversely, hyperactivation of Tao kinase in A08n neurons resulted within a decreased dendritic field and fewer postsynapses. Neither perturbation impacted the number of A08n postsynapses per dendritic volume suggesting that Tao activity co-regulates dendritic and synaptic growth (Supplementary Fig. 2G ). We compared loss of Tao-induced synaptic and dendritic growth changes in A08n neurons with overexpression of constitutively active Ras (UAS-Ras85DV12) or Rac1 (UASRac1V12), which were previously shown to promote synaptic development in the fly NMJ36,37. Strikingly, RasV12 but not Rac1V12 overexpression phenocopied the loss of Tao (Supplementary Fig. 3A ) indicating that Tao acts within a Ras-like manner to coordinate dendritic and synaptic development. However, a potentially causal relationship between Tao-dependent and Ras-dependent development needs additional investigation. Nonetheless, A08n neurons displayed a comparable raise of postsynapses and dendritic volume with unchanged density in each circumstances (Supplementary Fig. 3D). In contrast, expression of constitutive active Rac1 led to a strongly altered dendritic field with loss of volume and postsynapses, on top of that resulting in lowered postsynaptic web-site densities. Collectively, these data show that Tao kinase function in A08n neurons negatively co-regulates dendritic development and postsynaptic numbers, thus limiting synaptic input to the C4da neuron presynaptic domain. Loss of Tao promotes ectopic development all through development. We then analyzed the effect of loss of Tao kinase function on C4da 08n neuron synaptic markers during larval improvement. TaoRNAi in A08n neurons did not strongly impact C4da presynapse numbers when compared with controls except at 72 h AEL (Fig. 4a, Supplementary Fig. 4A ). In contrast, A08n postsynaptic numbers remained continuously elevated immediately after loss of Tao and, remarkably, kept escalating at 120 h AEL (Fig. 4b). Regularly, C4da 08n neuron synapse numbers had been significantly elevated at 48 and 72 h, and specifically at 120 h AEL (Fig. 4c). These experiments recommend that Tao function is required all through development to restrict A08n postsynaptic numbers and in element also C4da 08n neuron synapses. Loss of Tao function enhanced the synapsepresynapse ratio in C4da neurons at most time points suggesting an all round shift in C4da neuron connectivity towards A08n neurons (Fig. 4d). In contrast, synapsepostsynapse ratios in A08n were decreased at 72 and 96 h AEL indicating a relative increase in option presynaptic inputs of A08n neurons (Fig. 4e). These final results are consistent with the observed dendritic overgrowth phenotype with A08n dendrites invading adjacent neuropil domains upon loss of Tao (see Supplementary Fig. 2E, F). We subsequent examined the developmental profile of ectopic postsynaptic puncta of A08n neurons, which weren’t localized within the C4da neuron presynaptic domain upon loss of Tao function. We as a result analyzed the number of postsynaptic Drep2-GFP puncta that overlapped together with the C2daC3da presynaptic domain labeled by anti-Fa.