nejire (nej), the Drosophila homolog of CREB Binding Protein, has been studied as a regulator of embryonic pattern formation and of circadian rhythms in adult Drosophila, however its potential role in dendritic development remains largely unexplored. In a genetic screen for transcriptional regulators of dendritic development in complex arbor neurons, we identified nej as a novel regulator of dendritic development. Here, we investigate the role of nej as an essential regulator of dendritic growth and branching complexity using dendritic arborization (da) sensory neurons of the Drosophila larva. Loss-of-function studies implicate nej in regulating dendritic growth and proximal-distal branch order distribution as disruptions lead to a reduction in dendritic field coverage and a shift from distal terminal branching complexity to more proximal dendritic tufting in class IV (CIV) da neurons. Conversely, nej overexpression in CIV neurons leads to severe disruption in higher order dendritic growth and branching whereby nearly all branches above second order are absent. To identify putative functional domains required for nej-mediated arbor development, domain-specific deletion constructs were expressed in CIV neurons revealing that deletion of the N-terminal region (ΔNZK) leads to defects that largely phenocopy those observed with nej knockdown, whereas deletion of the C-terminal region (ΔQ) generates phenotypic defects consistent with overexpression of full-length nej, albeit even more severe. To gain further insight into nej-mediated signal transduction in dendritic development, we have investigated putative nej interacting molecules. These analyses reveal a regulatory relationship between nej and dar1, a transcription factor known to affect dendritic growth by regulation of the microtubule severing protein Spastin. dar1 overexpression produces a phenotype that is strikingly similar to that of nej knockdown and changes in nej expression cause shifts in the subcellular localization of Dar1 in CIV neurons. We also demonstrate a potential relationship between nej and shaggy (GSK3), which is known to affect microtubule dynamics in axons, as the expression of a kinase-dead shaggy results in CIV dendritic morphology that is phenotypically nearly identical to that caused by expression of the nej ΔNZK construct. Furthermore, our analyses suggest potential links to the NF-κB pathway, as relish overexpression phenocopies nej knockdown and relish knockdown causes a reduction in branching complexity that is phenotypically consistent with nej overexpression. Collectively, these analyses extend our understanding of molecular mechanisms of transcription factor activity at a class-specific level and how this regulation contributes to specification of distinct neuronal morphologies that underlie the establishment of complex neural networks.