The role of Myoglianin in Drosophila metamorphosis
- Author(s): Alvarez, Maribel;
- Advisor(s): Arora, Kavita;
- et al.
Signaling by the Transforming Growth Factor-Beta; (TGF-Beta) superfamily is essential for many cellular processes and is required throughout the life of many organisms. TGF-Beta; signaling triggers distinct developmental programs and cellular processes, thus disruption of the pathway is associated with defects in development and growth of the organism. Signaling specificity is achieved through the use of distinct pathway components and combinatorial action with other cell signaling pathways. The main goal of my thesis project was to understand the roles of two ligands of the TGF-Beta; superfamily, Maverick (Mav) and Myoglianin (Myo), and their mechanism of action in Drosophila. We first characterized several mutant alleles for mav and myo that were previously generated in the lab. Next, we investigated the role of mav at the neuromuscular junction (NMJ). Loss-of-function analysis suggests that mav has no affect on growth of the NMJ. However, ectopic expression of mav in glial cells does have an affect on the NMJ, suggesting that while not essential, NMJ growth may be sensitive to changes in levels of Mav. Phenotypic analysis of mutations in myo that encodes an activin ligand, revealed a wide range of metamorphosis phenotypes reminiscent of loss of the steroid hormone ecdysone. We investigated the role of myo in several tissues that undergo specific changes during metamorphosis. We determined that myo is selectively required for expression of the ecdysone receptor EcR-B1 isoform in a diverse group of neurons in the central nervous system, but not in other EcR-B1 expressing tissues, for example gut, fat body and salivary glands. Therefore one of the roles of Myo is to regulate the ability of specific cells to respond to ecdysone. Importantly, we found that salivary gland destruction in response to ecdysone signaling is dependent on activin signaling, but this occurs through regulation of EcR-B1 in specific cells in the brain, rather than in the salivary gland itself. Our data argue for a model in which ecdysone signaling utilizes both direct and indirect inputs to coordinate salivary gland destruction during pupal metamorphosis. The work presented here provides insights into the requirement of Myo/activin signaling in regulation and coordination of steroid dependent biological processes in animals.