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Browsing by Subject "Prothoracic gland"

Now showing 1 - 3 of 3
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    Activin signaling promotes the competence of the prothoracic gland during Drosophila metamorphosis
    (2010-08) Gibbens, Ying Ye
    In insects, the timing of metamorphosis is modulated by a large titer of the steroid hormone ecdysone produced by the prothoracic gland. However, the molecular mechanisms that control production of the ecdysone titer are not completely understood. Here we show that blocking Activin signaling in Drosophila prothoracic gland causes developmental arrest prior to metamorphosis. This defect is due to the absence of the ecdysone titer, a likely consequence of reduced expression of the ecdysone biosynthetic enzymes. We further demonstrate that Activin signaling may regulate the competence of the prothoracic gland to respond to prothoracicotropic hormone and insulin, two hormonal signals that have been shown to trigger ecdysone synthesis. These findings suggest that Activin signaling is required for insect metamorphosis by providing competence that allows tissue- and stage-specific response to metamorphic stimuli.
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    Mechanisms of PTTH signaling and steroid hormone biosynthesis in Bombyx mori and Drosophila melanogaster.
    (2012-08) Herder, Rachel Jeanne
    Animals use steroid hormones to regulate the timing of development and growth. In insects, the developmental processes of hatching, molting, metamorphosis and eclosion are all regulated by a steroid hormone, 20-hydroxyecdysone (20E). Biosynthesis of ecdysone (E), the immediate precursor to 20E, is thought to be regulated, in part, by a small neuropeptide called prothoracicotropic hormone (PTTH ). PTTH is produced by neurons that innervate the prothoracic gland (PG) and signals to this tissue to up-regulate biosynthesis of E in insects, including Drosophila melanogaster (fruit fly) and Bombyx mori (silk worm). When PTTH signaling is disrupted, developmental timing is altered. This thesis focuses on further elucidating the role of PTTH signaling in development through three separate but related aims. First, to better understand the global effects of PTTH signaling on transcriptional regulation in the PG, we used Illumina Next Generation sequencing to compare the transcriptome of PTTH-stimulated and –unstimulated PGs. This was used as an unbiased approach to determine what genes are up and down regulated in response to PTTH stimulation. At the time of this thesis writing, the sequencing reactions have been completed, however, the bioinformatics analysis is still underway. Second, to better understand how PTTH acts to up-regulate gene expression, we analyzed regulatory elements in target genes using a promoter-bashing approach. Using this approach, we uncovered three minimal enhancer regions from phantom, spookier and disembodied, members of the Halloween family of E biosynthetic genes that are expressed in the PG. Additionally, we have discovered several small, highly conserved, sequence motifs that are necessary for reporter gene expression in the PG. Third, we examined a single PTTH-responsive gene, called Membrane Steroid Binding Protein (MSBP), with the goal of elucidating its role in ecdysone biosynthesis. We have confirmed that MSBP is expressed in ecdysone producing tissues and that MSBP expression changes in response to PTTH. However, MSBP-/- animals show no obvious phenotype, suggesting either redundancy or no requirement of MSBP in regulating developmental timing.
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    Regulation of developmental timing in Drosophila melanogaster: genetics versus environment
    (2019-07) Pan, Xueyang
    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.