Ary Fig. 2E ). Reduction of Tao activity employing TaoRNAi resulted in striking dendritic overgrowth and concomitant enhance in postD-Phenylalanine Endogenous Metabolite synaptic 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 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 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 (Supplementary Fig. 2G ). We compared loss of Tao-induced synaptic and dendritic growth alterations in A08n neurons with overexpression of constitutively active Ras (UAS-Ras85DV12) or Rac1 (UASRac1V12), which have been previously shown to promote 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 growth. Even so, a potentially causal relationship among Tao-dependent and Ras-dependent development needs further investigation. Nonetheless, A08n neurons displayed a comparable enhance 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, additionally resulting in lowered postsynaptic site densities. Collectively, these data show that Tao kinase function in A08n neurons negatively co-regulates dendritic growth and postsynaptic numbers, hence limiting synaptic input for the C4da neuron presynaptic domain. Loss of Tao promotes ectopic growth throughout development. We then analyzed the effect of loss of Tao kinase function on C4da 08n neuron synaptic markers for the duration of 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 continuously Alprenolol Biological Activity elevated right after loss of Tao and, remarkably, kept growing at 120 h AEL (Fig. 4b). Regularly, C4da 08n neuron synapse numbers have been drastically elevated at 48 and 72 h, and specifically at 120 h AEL (Fig. 4c). These experiments recommend that Tao function is necessary all through improvement 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 enhance in option presynaptic inputs of A08n neurons (Fig. 4e). These final results are consistent with all the observed dendritic overgrowth phenotype with A08n dendrites invading adjacent neuropil domains upon loss of Tao (see Supplementary Fig. 2E, F). We next examined the developmental profile of ectopic postsynaptic puncta of A08n neurons, which were not localized inside the C4da neuron presynaptic domain upon loss of Tao function. We thus analyzed the number of postsynaptic Drep2-GFP puncta that overlapped together with the C2daC3da presynaptic domain labeled by anti-Fa.