Steroid regulation of programmed cell death during Drosophila metamorphosis

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Publication Type dissertation
School or College School of Medicine
Department Human Genetics
Author Jiang, Changan
Contributor Bachrecke, Eric; Lamblin, Anne-Francoise; Steller, Hermann; Ip, Tony; Hultmark, Dan; Bienz,Mariann
Title Steroid regulation of programmed cell death during Drosophila metamorphosis
Date 1999-12
Description During Drosophila metamorphosis, pulses of the steroid hormone ecdysone trigger the histolysis of larval tissues in a stage-specific manner, but the mechanism of this developmental response remains unclear. In these studies, we show that histolysis of both the larval midgut and salivary glands is accompanied by increased nuclei permeability, DNA fragmentation and caspase activation, indicative of apoptotic cell death. Two Drosophila cell death activators, reaper (rpr) and head involution defective (hid), are induced by ecdysone in the larval midgut and salivary glands immediately preceding their histolysis, suggesting that the larval tissues are destroyed through the activation of the same apoptotic pathway that is employed during Drosophila embryogenesis. In addition, the cell death inhibitor diap2 is transiently induced in mid-prepupal salivary glands, but repressed in late prepupae, as rpr and hid are induced. These expression patterns suggest that ecdysone directs salivary gland cell death by simultaneously repressing diap2 and inducing rpr and hid. This hypothesis is supported by the results of our molecular genetic analysis which indicates that ecdysone triggers the switch in death gene expression through the ecdysone receptor and ecdysone-regulated transcription factors. Two ecdysone-inducible orphan nuclear receptors, E75A and E75B, are sufficient to repress diap2. In addition, ecdysone induces the Broad-Complex (BR-C) and E74A, which function together with the ecdysone receptor to induce rpr and hid. Our preliminary studies also show that two stress-activated transcription factors, AP-1 and NF-kappa-B, may function as stage-specific activators of rpr and hid in larval salivary glands. Based on these studies, we propose that the ecdysone receptor, ecdysone-induced transcription factors and the stress-response pathways cooperate to precisely regulate larval salivary gland cell death.
Type Text
Publisher University of Utah
Subject Physiology; Steroids
Subject MESH Drosophila; Insects; Cell Death
Dissertation Institution University of Utah
Dissertation Name PhD
Language eng
Relation is Version of Digital reproduction of "Steroid regulation of programmed cell death during Drosophila metamorphosis." Spencer S. Eccles Health Sciences Library. Print version of "Steroid regulation of programmed cell death during Drosophila metamorphosis." available at J. Willard Marriott Library Special Collection, QL3.5 1999 .J53.
Rights Management © Changan Jiang.
Format Medium application/pdf
Format Extent 2,726,528 bytes
Identifier undthes,5326
Source Original: University of Utah Spencer S. Eccles Health Sciences Library (no longer available).
Master File Extent 2,726,560 bytes
ARK ark:/87278/s67h1md2
Setname ir_etd
Date Created 2012-04-24
Date Modified 2021-05-06
ID 191232
Reference URL
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