Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.715631
Title: Regulation of apoptosis-induced proliferation and non-apoptotic cell death in Drosophila
Author: Li, MingLi
Awarding Body: University of Birmingham
Current Institution: University of Birmingham
Date of Award: 2017
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Abstract:
Apoptosis-induced Proliferation (AiP) refers to an evolutionary conserved process that stress-induced apoptotic cells stimulate neighbouring cells to undergo extra proliferation to compensate for the loss of apoptotic cells. It is therefore involved in tissue regeneration in multi-cellular organisms. I found that dAtg1 (Drosophila autophagy-related gene 1), a gene best known in activating autophagy, is required for AiP. dAtg1 is transcriptionally induced by the JNK pathway, a stress response signalling pathway, during AiP and it regulates AiP by acting upstream of growth signals e.g. Wg/Wnt. Surprisingly, other Atg genes involved in autophagy are not required for AiP. Therefore, dAtg1 regulates AiP independent of its canonical roles in mediating autophagy. In parallel, I investigated the non-apoptotic cell death induced by Eiger (Egr), the Drosophila tumour necrosis factors (TNFs). In mammals, TNF induces apoptosis and, when apoptosis is blocked, necrosis. In Drosophila, the type of cell death induced by Egr remains elusive. I found that expression of egr in the developing Drosophila eye primarily induces apoptosis through the canonical apoptosis pathway. Intriguingly, when apoptosis is blocked by inactivation of effector caspases DrICE and Dcp-1, Egr induces necrosis instead. Therefore, mechanisms underlying TNF-induced cell death are more conserved in Drosophila than previously thought.
Supervisor: Not available Sponsor: University of Birmingham ; China Scholarship Council
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.715631  DOI: Not available
Keywords: QH301 Biology
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