During development, flat epithelia give rise to tubular structures that exhibit a spectacular variety of shapes, sizes, and functions. Although tubes are essential for multi-cellular life, relatively little is known about the genetic and molecular mechanisms that create tubes. A tractable model for tubulogenesis in Drosophila, one that resembles primary neurulation in vertebrates, is the formation of dorsal appendages (DAs), eggshell structures that facilitate gas exchange for the embryo. DAs are secreted by cellular tubes that form during oogenesis in the egg chamber. An egg chamber consists of one oocyte and 15 germline nurse cells surrounded by a somatic follicular epithelium: columnar cells cover the oocyte and squamous “stretch” cells cover the nurse cells. Cues from these different cell types facilitate DA formation, which occurs when two dorsal patches of columnar cells fold into tubes and elongate by migrating over the stretch cells, all in the absence of cell division or cell death. Mutations in the genes encoding the SOX transcription factor, Bullwinkle (BWK), which functions in the germline, or non-receptor tyrosine kinases SHARK and SRC42A, which function in the stretch cells, lead to DA cell adhesion defects, aberrant cell migration, open tubes, and moose-antler-like DAs. Other components of the pathway are unknown. To discover new genes that regulate tubulogenesis downstream of bwk, we used mass spectrometry to identify differentially expressed proteins in the stretch cells of bwk vs. wild-type egg chambers. Members of a novel family of growth factors, Imaginal disc growth factors (IDGFs), were upregulated in the stretch cells of bwk egg chambers. IDGFs are catalytically inactive, chitinase-like proteins that have human orthologs and arose through gene duplication. Due to a conserved mutation that renders them inactive as chitinases, IDGFs have acquired new functions through evolution. Using stretch-cell specific overexpression, RNAi, and CRISPR/Cas9-mediated gene deletions, we found not only that IDGF upregulation is sufficient to cause DA defects, but that IDGF expression is also required normally at optimal levels for proper DA morphogenesis. Our data suggest that IDGFs may function redundantly in this context. Although previous studies demonstrate that IDGFs interact synergistically with insulin to modulate growth and polarization of cultured cells, our data suggest that the insulin signaling pathway is not the central mode of action for IDGFs in DA formation. Determining how these novel growth factors function will be a key to understanding the genetic and molecular basis of tubulogenesis.