The Role of E93 in Fat Body Remodeling in Drosophila melanogaster

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dc.contributorFink, Rachel
dc.contributorRice, Marian
dc.contributor.advisorWoodard, Craig
dc.contributor.authorLam, Wai Yan
dc.date.accessioned2012-05-15T17:54:39Z
dc.date.available2012-05-15T17:54:39Z
dc.date.gradyear2012en_US
dc.date.issued2012-05-15
dc.description.abstractIn Drosophila melanogaster, pulses of the steroid hormone ecdysone direct each of the major developmental transitions during the life cycle. During metamorphosis, increases in ecdysone direct destruction of obsolete larval tissue and the remodeling of other larval tissues. In particular, the larval fat body remodels by tissue dissociation, resulting in the redistribution of fat cells throughout the body of the pupa. During the larval stages, fat cells occur in single-cell layers of polygonal, white, translucent cells that are tightly associated. Following ecdysone signaling, morphological changes in the fat body result in the rounding and complete detachment of cells into independent and spherical cells from the tissue mass. The expression of E93 is induced as a primary response to ecdysone following expression of βftz-f1. E93 has been shown to display stage-specific expression in the larval salivary glands that foreshadows the onset of programmed cell death. In wild-type animals, E93 is expressed in the fat body at 12 hours after puparium formation (APF), coinciding with the last stage of fat body remodeling, detachment, during which individual fat cells are redistributed into the head capsule and body cavity. E93 is known to regulate various tissue specific developmental changes such as programmed cell death of larval salivary glands and the midgut. Given E93’s role in triggering the death of larval tissue, it is interesting that it does not trigger the death of fat tissue. However, considering the numerous roles E93 takes on during development, it is possible that E93 might also be involved in influencing fat body remodeling. Microscopy work utilizing light microscopy, fluorescence microscopy, transmission electron microscopy, scanning electron microscopy, and confocal microscopy reveals phenotypic differences between the wild-type and E93 mutant fat body after 12 hours APF. While wild-type fat body dissociates into individual and spherical fat cells, E93 mutant fat body is frequently found as aggregates of undetached fat cells and some individual, dissociated fat cells. I hypothesize that E93 may play a role in facilitating the detachment phase of fat tissue remodeling and that its absence would hinder proper fat body remodeling.en_US
dc.description.sponsorshipBiological Sciencesen_US
dc.identifier.urihttp://hdl.handle.net/10166/1009
dc.language.isoen_USen_US
dc.rightsAttribution 3.0 United States*
dc.rights.restrictedrestricted
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.subjectDrosophila melanogasteren_US
dc.subjectfat body remodelingen_US
dc.subjectE93en_US
dc.subjectprogrammed cell deathen_US
dc.subjectautophagyen_US
dc.subjectfat bodyen_US
dc.titleThe Role of E93 in Fat Body Remodeling in Drosophila melanogasteren_US
dc.typeThesis
mhc.degreeUndergraduateen_US
mhc.institutionMount Holyoke College

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