The cytoskeleton is a defining component of eukaryotic cells including neurons and constitutes the foundation of their inner architecture. Despite many significant advances, it is not yet clear how genetically encoded growth rules are dynamically expressed through the local molecular interactions of cytoskeletal components driving dendritic arborization. Cell-type specific dendritic morphologies emerge via complex growth mechanisms modulated by intrinsic signaling involving transcription factors that mediate neuronal identity, as well as functional and morphological properties of the neuron subtype. Thus, in pursuit of identifying a convergent nodal point of combinatorial transcription factor regulation and modulation of the actin and microtubule cytoskeletons in Drosophila dendritic arborization (da) sensory neurons, we found that Formin3 (Form3) is a target of both Cut and Knot, two key transcription factors known for their modulatory role of cytoskeletal components. To investigate the role(s) of form3 in dendritic development, we conducted in vivo neurogenetic analyses of loss-of-function mutants, together with Form3 overexpression analyses and immunohistochemistry (IHC) studies of Form3 localization. Intriguingly, among the six Drosophila Formins, only disruptions in form3 function elicit strong defects on dendritic development, whereas disruption of the other five fly Formins had mild or no effect on class IV (CIV) dendrite morphogenesis. We demonstrate that Form3 is differentially expressed in da neuron subclasses and functions cell-autonomously in CIV neurons to stabilize distal higher order branching along the proximal-distal axis of dendritic arbors. Furthermore, live confocal imaging of cytoskeletal multi-fluor reporters and fixed tissue IHC analyses reveal that form3 mutation leads to collapse of the microtubule (MT) cytoskeleton. Biochemical analyses indicate Form3 directly interacts with MTs via the FH1/FH2 domains. Form3 is predicted to interact with two ATAT1 alpha-tubulin N-acetyltransferases suggesting it may promote MT stabilization via acetylation. Analyses of acetylated dendritic MTs supports this hypothesis as defects in form3 lead to reductions, whereas overexpression promotes increases in MT acetylation. Neurologically, INF2 (the human ortholog of form3) mutations have been demonstrated to be causative for dominant intermediate Charcot-Marie-Tooth (CMT) disease E. CMT sensory neuropathies lead to distal sensory loss resulting in a reduced ability to sense heat, cold, and pain. Intriguingly, disruption of Form3 function in CIV nociceptive neurons results in a severe impairment in nocifensive behavior in response to noxious heat suggesting that INF2 and form3 may share a primordial function in regulating nociception.