Epithelial tubular organs are essential for viability of all higher organisms. Epithelial tube architecture is intimately linked to organ function as seen with the intricate tubular morphologies associated with each domain of the mammalian kidney. Learning how tube architecture is controlled at the molecular and cellular level is a key to understanding both developmental abnormalities as well as common human diseases linked to disruptions in tube morphology, such as polycystic kidney disease and atherosclerosis. To study how organs achieve their correct size, shape and position in the animal, we use the model system of the Drosophila trachea, an organ for which tube elongation is primarily mediated by changes in cell shape and arrangement. Tube elongation requires integration of information from multiple signaling pathways acting on and through basic components of the secretory machinery and epithelial junctions found at or near the apical/lumenal surface. What we do not understand is how these signaling pathways relay information from extracellular and intracellular cues to the machinery required to modulate apical membrane dynamics. In this study, we propose to learn how the downstream effectors of two key tracheal transcription factors - Trachealess and Ribbon - integrate cues emanating from both within and outside cells to invoke changes in the basic cellular machinery to alter tube dimensions. First, we focus on two new Trh/Rib candidate effectors - RhoGEF/CG33275 and FLMNA/Jbug - that are likely to act downstream of the planar cell polarity (PCP) signaling pathway, which has been shown by us and others to prevent tube over-elongation. Isoforms of both RhoGEFCG33275 and FLMNAJbug localize to the apical surface and RNAi knockdown and over expression of both genes affect tube morphology. Importantly, overexpression of either protein results in PCP-like phenotypes in adult tissues. Next, we follow up on our findings with the Trh target Mipp1 to link extracellular pools of inositol polyphosphates to filopodia formation and FGF-dependent migration, which drives tube elongation through cell rearrangement. Finally, we establish a genetic pipeline to screen shared Trh/Rib targets as an approach to circumnavigate the challenges posed by functional redundancy.