Ary Fig. 2E ). Reduction of Tao activity utilizing TaoRNAi resulted in striking dendritic overgrowth and concomitant increase 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 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 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 development (Supplementary Fig. 2G ). We Hexaflumuron custom synthesis compared loss of Tao-induced synaptic and dendritic growth modifications in A08n neurons with overexpression of constitutively active Ras (UAS-Ras85DV12) or Rac1 (UASRac1V12), which have been previously shown to market synaptic development at 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. Having said that, a potentially causal relationship amongst Tao-dependent and Ras-dependent development calls for additional investigation. Nonetheless, A08n neurons displayed a comparable improve of postsynapses and dendritic volume with unchanged density in both instances (Supplementary Fig. 3D). In contrast, expression of constitutive active Rac1 led to a strongly altered dendritic field with loss of volume and postsynapses, furthermore resulting in lowered postsynaptic internet site densities. Collectively, these data show that Tao kinase function in A08n neurons negatively co-regulates dendritic growth and postsynaptic numbers, thus limiting synaptic input for the C4da neuron presynaptic domain. Loss of Tao promotes ectopic growth throughout development. We then analyzed the influence of loss of Tao kinase function on C4da 08n neuron synaptic markers in the course of larval development. TaoRNAi in A08n neurons didn’t strongly affect 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 following loss of Tao and, remarkably, kept growing at 120 h AEL (Fig. 4b). Regularly, C4da 08n neuron synapse numbers were considerably elevated at 48 and 72 h, and especially at 120 h AEL (Fig. 4c). These experiments recommend that Tao function is needed all through development to restrict A08n postsynaptic numbers and in part 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 have been decreased at 72 and 96 h AEL indicating a relative boost in alternative presynaptic inputs of A08n neurons (Fig. 4e). These outcomes are consistent 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 Alpha Inhibitors targets domain upon loss of Tao function. We as a result analyzed the amount of postsynaptic Drep2-GFP puncta that overlapped with all the C2daC3da presynaptic domain labeled by anti-Fa.