Regulation of developmental timing in Drosophila melanogaster: genetics versus environment
2019-07
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Regulation of developmental timing in Drosophila melanogaster: genetics versus environment
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2019-07
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Abstract
Development of animals involves both an intrinsic program determined by genetics and an adaptive system reacting to environmental variants. In fruit fly Drosophila melanogaster, the juvenile-to-adult transition is largely governed by a neuroendocrine axis in which the PTTH-producing PG neurons and the larval endocrine organ prothoracic gland (PG) play the central role. However, the mechanism underlying the regulation of this neuroendocrine axis is not fully understood. In this thesis two discoveries are made on both the genetic control of the neuroendocrine axis and its response to nutritional stress. Firstly, the author demonstrates that autophagy acts as a nutritionally-regulated gating mechanism which helps ensure productive metamorphosis in Drosophila. Autophagy in the PG is specifically stimulated by nutrient restriction at the early, but not the late third instar larva stage, which inhibits precocious metamorphosis during nutrient restriction in undersized larvae. Induction of autophagy disrupts production of the steroid hormone ecdysone at the time of pupariation not by destruction of hormone biosynthetic capacity, but rather by limiting the availability of the steroid hormone precursor cholesterol in the endocrine cells via a lipophagy mechanism. These findings demonstrate an autophagy mechanism in PG cells that helps shape the nutritional checkpoints and guarantee a successful juvenile-to-adult transition in animals confronting nutritional stress. Secondly, the author shows that Jeb/Alk and Pvf/Pvr pathways function jointly with PTTH/Torso pathway in the PG neuron-PG neuroendocrine axis to control developmental timing in Drosophila. In the two pathways, Jeb and Pvf ligands are expressed in the PG neurons, which activate the Alk and Pvr receptors respectively in the PG. Suppression of the Jeb/Alk or Pvf/Pvr pathway causes developmental timing delay in the larva, which is exacerbated when combined with mutation of ptth. Activation of the pathways rescues the developmental delay caused by ptth mutation, indicating a compensatory effect. These data demonstrate that the Jeb/Alk and Pvf/Pvr pathways are among the previously proposed additional signals from the PG neuron-PG axis which function jointly with the PTTH/Torso pathway to control developmental timing.
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University of Minnesota Ph.D. dissertation. July 2019. Major: Molecular, Cellular, Developmental Biology and Genetics. Advisor: Michael O'Connor. 1 computer file (PDF); x, 175 pages + 6 supplementary video files
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Pan, Xueyang. (2019). Regulation of developmental timing in Drosophila melanogaster: genetics versus environment. Retrieved from the University Digital Conservancy, https://hdl.handle.net/11299/206635.
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