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Developmental and neurogenetic studies on the peptidergic nerve system in Drosophila

by Choi, Youn-Jeong.

Abstract (Summary)
Neuropeptides in insects act as neurotransmitters and neuromodulators in the central nervous system (CNS) and as regulatory hormones released to the circulation. To gain insight into the mechanisms of tissue-specific Corazonin (Crz) regulation and functions in Drosophila, I cloned Crz-encoding genes from different species, and performed the phylogenetic analysis of Crz-encoding genes as well as Crz primary structures. To compare Crz expression patterns among different species, I performed in situ hybridization and immunohistochemistry to detect Crz expression in the CNS. Although Crz gene sequences reveal a great deal of diversity, Crz expression patterns are conserved among different species. In the larval CNS, Crz expression is observed in 4 pairs of cells in the cerebral lobes as well as in 8 pairs of bilateral cells in the ventral nerve cord (vCrz). During larval-to-pupal metamorphosis, vCrz neurons die of programmed cell death (PCD) while brain neurons in the pars lateralis undergo significant remodeling to form adult-specific structures. Neurites stemming from the remodeled Crz neurons project to the corpora cardiaca, a neurohemal organ, suggesting Crz’s endocrine function. The finding that somata of Crz neurons are located in the proximity of nerve terminal emanating from Pdf-expressing clock pacemaker neurons suggests that Crz neurons have a functional connection to the circardian clock. To determine neuronal cell death mechanisms, I utilize two different peptidergic neurons as model systems: vCrz and CCAP neurons. The vCrz neurons die within 6 hours after puparium formation while subsets of crustacean cardioactive peptide (CCAP) iv neurons die shortly after adult eclosion. The loss of Crz and CCAP signals was prevented by ectopic expression of the baculovirus apoptotic inhibitor, p35, indicating caspasedependent PCD. The vCrz cell death is triggered by ecdysone signaling mediated via EcR-B1 and EcR-B2. The vCrz PCD is prevented in a rpr-null mutant, however, targeted knockdown of diap1 does not accelerate PCD, suggesting that vCrz cell death occurs via a diap1-independent rpr activation. The vCrz cell death was delayed in dronc and dark mutants, suggesting apoptosome formation during the death program. By comparison, CCAP cell death was induced by both rpr and hid, and required dronc. The vCrz PCD was delayed but CCAP PCD was not affected by dcp-1-null mutation, supporting the presence of differential caspase machinery between the two different peptidergic neurons. v
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School:The University of Tennessee at Chattanooga

School Location:USA - Tennessee

Source Type:Master's Thesis

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