Upadhyay, Ambuj2020-10-262020-10-262019-08https://hdl.handle.net/11299/216813University of Minnesota Ph.D. dissertation. August 2019. Major: Molecular, Cellular, Developmental Biology and Genetics. Advisor: Michael O'Connor. 1 computer file (PDF); viii, 188 pages.The mechanisms governing static allometry of organ size has long been enigmatic. A central hypothesis predicts that during animal growth, body size is perceived by organs via inter-organ signals, which directs organ growth to match body size. Ligands of the Transforming Growth Factor β (TGFβ) superfamily are prime candidates for mediating this coordination of organ-body size. In Drosophila, multiple ligands of the Activin-like subfamily (Myoglianin, Activin-β, and Dawdle) signal via the only type-I receptor Baboon (Babo). Similar to defects in insulin signaling, null mutants of babo result in small imaginal discs and small overall body size. This is in part due to metabolic defects caused by defects in Daw signaling. In this dissertation I report how Activin-β and Myoglianin regulate body size and organ growth respectively. In Chapter one, I review known mechanisms governing growth in Drosophila. In Chapter two, I show that Activin-β signaling via Babo in the muscles is required for muscle growth and proper body size, but not imaginal disc growth. Remarkably, it is the motoneurons in the central brain secretes Activin-β necessary for body size. In Chapter three, I show that Myoglianin regulates imaginal disc growth which express specific combination of receptors that make the cells sensitive to only one ligand. Additionally, it is the larval muscles secrete Myoglianin which regulates imaginal disc growth but not body size. In chapter four, I speculate as to how such inter-organ signaling mechanisms can ensure proper allometry within species, and suggest additional experiments that would test this emerging model.enActivin betadrosophilamyoglianinorgan growth and scalingTGF betawing disc growthThesis or Dissertation