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 particularly 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 to the medial triangular-shaped C4da axon Hygrolidin Autophagy projections. Conversely, hyperactivation of Tao kinase in A08n neurons resulted inside a lowered 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 (4-Fluorophenoxyacetic acid References Supplementary Fig. 2G ). We compared loss of Tao-induced synaptic and dendritic growth adjustments in A08n neurons with overexpression of constitutively active Ras (UAS-Ras85DV12) or Rac1 (UASRac1V12), which have been 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 in a Ras-like manner to coordinate dendritic and synaptic development. Nonetheless, a potentially causal partnership amongst Tao-dependent and Ras-dependent development needs further investigation. Nonetheless, A08n neurons displayed a comparable improve of postsynapses and dendritic volume with unchanged density in both situations (Supplementary Fig. 3D). In contrast, expression of constitutive active Rac1 led to a strongly altered dendritic field with loss of volume and postsynapses, in addition resulting in lowered postsynaptic website densities. Collectively, these information show that Tao kinase function in A08n neurons negatively co-regulates dendritic development and postsynaptic numbers, hence limiting synaptic input towards the C4da neuron presynaptic domain. Loss of Tao promotes ectopic development throughout development. We then analyzed the effect of loss of Tao kinase function on C4da 08n neuron synaptic markers in the course of larval improvement. TaoRNAi in A08n neurons didn’t strongly impact C4da presynapse numbers in comparison 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 growing at 120 h AEL (Fig. 4b). Regularly, C4da 08n neuron synapse numbers were 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 portion also C4da 08n neuron synapses. Loss of Tao function increased the synapsepresynapse ratio in C4da neurons at most time points suggesting an general shift in C4da neuron connectivity towards A08n neurons (Fig. 4d). In contrast, synapsepostsynapse ratios in A08n have been decreased at 72 and 96 h AEL indicating a relative boost in option presynaptic inputs of A08n neurons (Fig. 4e). These final results are constant with all 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 inside the C4da neuron presynaptic domain upon loss of Tao function. We therefore analyzed the amount of postsynaptic Drep2-GFP puncta that overlapped with the C2daC3da presynaptic domain labeled by anti-Fa.