Ary Fig. 2E ). Reduction of Tao activity applying TaoRNAi resulted in striking dendritic overgrowth and concomitant enhance in postsynaptic puncta of A08n neurons. Immunostaining with an anti-Fas3 antibody, which specifically labels C2da, C3da, and C4da sensory axons, revealed that A08n dendrites and postsynapses extended into 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 in a decreased dendritic field and fewer postsynapses. Neither perturbation impacted the amount 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 development changes in A08n neurons with Glycodeoxycholic Acid manufacturer overexpression of constitutively active Ras (UAS-Ras85DV12) or Rac1 (UASRac1V12), which were previously shown to market 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 inside a Ras-like manner to coordinate dendritic and synaptic development. Nonetheless, a potentially causal connection in between Tao-dependent and Ras-dependent development demands further investigation. Nonetheless, A08n neurons displayed a comparable improve of postsynapses and dendritic volume with unchanged Uridine 5′-monophosphate disodium salt site density in each instances (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 internet site densities. Collectively, these information show that Tao kinase function in A08n neurons negatively co-regulates dendritic development and postsynaptic numbers, as a result limiting synaptic input to the C4da neuron presynaptic domain. Loss of Tao promotes ectopic growth all through improvement. We then analyzed the effect of loss of Tao kinase function on C4da 08n neuron synaptic markers through larval development. TaoRNAi in A08n neurons did not strongly influence C4da presynapse numbers when compared with controls except at 72 h AEL (Fig. 4a, Supplementary Fig. 4A ). In contrast, A08n postsynaptic numbers remained constantly elevated immediately after loss of Tao and, remarkably, kept increasing at 120 h AEL (Fig. 4b). Consistently, C4da 08n neuron synapse numbers have been substantially elevated at 48 and 72 h, and especially at 120 h AEL (Fig. 4c). These experiments recommend that Tao function is necessary all through development to restrict A08n postsynaptic numbers and in element also C4da 08n neuron synapses. Loss of Tao function improved 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 had been decreased at 72 and 96 h AEL indicating a relative improve in option presynaptic inputs of A08n neurons (Fig. 4e). These final results are constant using 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 were not localized within the C4da neuron presynaptic domain upon loss of Tao function. We hence analyzed the amount of postsynaptic Drep2-GFP puncta that overlapped using the C2daC3da presynaptic domain labeled by anti-Fa.