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dc.contributorBacon, Sarah
dc.contributorRobinson, Margaret
dc.contributor.advisorWoodard, Craig
dc.contributor.authorAlexander, Grace
dc.date.accessioned2021-05-14T17:18:12Z
dc.date.available2021-05-14T17:18:12Z
dc.identifier.urihttps://ida.mtholyoke.edu/handle/10166/6294
dc.description.abstractThe larval fat bodies of Drosophila melanogaster are responsible for storing energy from the larval feeding stages for use during pupal development. In most larval tissues, programmed cell death (PCD) is triggered by two pulses of the steroid hormone 20-hydroxyecdysone (ecdysone), delivered at the end of the third larval instar stage and at 12 hours after puparium formation, respectively. Ecdysone signaling induces the transcription of the death activator genes, rpr, hid, and grim, which interact with the E3-ubiquitin ligase Diap1 to give rise to PCD. Diap1 has been found to promote the degradation of the PCD initiator caspase Dronc, thus acting as an inhibitor of unwanted cell death. Upon ecdysone-induced transcription, the death activator genes promote the auto-ubiquitination of Diap1, removing its inhibitory effect and triggering caspase activation. Studies have shown that Dronc plays an essential role in the promotion of PCD, with its loss of function being associated with a decrease in necessary PCD. Unlike other larval tissues, larval fat bodies are noted for their resistance to PCD, dissociating from a tissue to free, individual fat cells rather than undergoing PCD. This study follows upon previously conducted research, hypothesizing that up-regulation of Dronc and down-regulation of Diap1 promotes PCD in Drosophila melanogaster, and predicting that the PCD-resistant larval fat bodies will display up-regulation of Diap1 and down-regulation of Dronc. This study plans to compare the relative levels of Diap1 and Dronc in PCD-resistant larval fat bodies to those in the larval salivary glands, a PCD-susceptible larval tissue. Preliminary results indicate that this experiment can be done and that all primers and equipment are working as intended. Next steps include the analysis of cDNA synthesized from larval fat bodies and larval salivary glands collected from pupae at 12 hours after puparium formation via qRT-PCR. Understanding of the role of these expression levels in the regulation of PCD has broader implications for research into cancer development, degenerative diseases, and treatments thereof.en_US
dc.description.sponsorshipBiological Sciencesen_US
dc.language.isoen_USen_US
dc.subjectDrosophila melanogasteren_US
dc.subjectDiap1en_US
dc.subjectDroncen_US
dc.subjectEcdysone signalingen_US
dc.subjectProgrammed cell deathen_US
dc.subjectApoptosisen_US
dc.subjectßFTZ-F1en_US
dc.subjectLarval fat bodiesen_US
dc.subjectLarval salivary glandsen_US
dc.subjectCanceren_US
dc.subjectNeurodegenerative diseaseen_US
dc.subjectDevelopmental biologyen_US
dc.subjectGeneticsen_US
dc.subjectSteroid hormonesen_US
dc.subject20-hydroxyecdysoneen_US
dc.subjectEcdysoneen_US
dc.subjectMetamorphosisen_US
dc.titleGenetic Analysis of Programmed Cell Deathen_US
dc.typeThesis
dc.date.gradyear2021en_US
mhc.institutionMount Holyoke College
mhc.degreeUndergraduateen_US
dc.rights.restrictedpublicen_US


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