The Role of E93 in Fat Body Remodeling and Autophagy in Drosophila Melanogaster Third Instar Larvae

dc.contributor.advisorWoodard, Craig
dc.contributor.authorChibaya, Loretah
dc.date.accessioned2012-05-11T17:49:53Z
dc.date.available2012-05-11T17:49:53Z
dc.date.gradyear2012en_US
dc.date.issued2012-05-11
dc.description.abstractDuring metamorphosis in holometabolous insects such as the fruit fly, Drosophila melanogaster, obsolete larval tissues such as salivary glands undergo programmed cell death. In contrast, the larval fat body is retained and remodeled from sheets of attached, flat, polygonal cells to individual spherical, free-floating cells (Hoshizak, 2005; Nelliot et al., 2006; Cherbas et al, 2003). It has been established that fat body remodeling is regulated by the insect steroid hormone 20-Hydroxyecdysone (20E), which controls the process of metamorphosis. The early stages of metamorphosis in D. melanogaster include two high-titer 20E pulses, one at the end of the third instar larval stage and the other during the late prepupal stage, approximately 12 hours after puparium formation (APF; puparium formation = the beginning of metamorphosis). Fat body remodeling in wild type D. melanogaster occurs in the late prepupa in response to the prepupal 20E pulse. The late larval 20E pulse induces the transcription of primary response genes E74, E75 and BR-C, which are necessary for the initiation of metamorphosis. In the larval salivary gland, the 20E pulse in the late prepupa induces the transcription of the same set of early genes but also induces an additional gene, E93. During the period of low 20E titer, mid-prepupal genes are induced (Thummel, 1996). One such mid-prepupal gene encodes the competence factor ßftz-f1. ßftz-f1is a nuclear receptor that provides competence for early genes to be induced by 20E in late prepupae. ßftz-f1 directs the stage specific induction of E93 which is expressed in the fat body at 12 hours APF when fat body dissociation occurs (Baehrecke and Thummel, 1995). In this study, I proposed that the ectopic expression of ßftz-f1 in D. melanogaster third instar larvae during the first 20E pulse will trigger the premature expression of E93, resulting in premature fat body remodeling. My results to date have shown that ectopic expression of ßftz-f1 in third instar larva leads to premature expression of E93 and fat body remodeling. Transmission electron microscopy showed that autophagosomes are present in dissociating fat bodies suggesting that the fat body fuels the process of metamorphosis by releasing nutrients.en_US
dc.description.sponsorshipBiological Sciencesen_US
dc.identifier.urihttp://hdl.handle.net/10166/1003
dc.language.isoen_USen_US
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 United States*
dc.rights.restrictedrestricted
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/us/*
dc.subjectDrosophila melanogasteren_US
dc.subjectE93en_US
dc.titleThe Role of E93 in Fat Body Remodeling and Autophagy in Drosophila Melanogaster Third Instar Larvaeen_US
dc.typeThesis
mhc.degreeUndergraduateen_US
mhc.institutionMount Holyoke College

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