@article {2494, title = {A role for juvenile hormone in the prepupal development of Drosophila melanogaster.}, journal = {Development}, volume = {137}, year = {2010}, month = {2010 Apr}, pages = {1117-26}, abstract = {

To elucidate the role of juvenile hormone (JH) in metamorphosis of Drosophila melanogaster, the corpora allata cells, which produce JH, were killed using the cell death gene grim. These allatectomized (CAX) larvae were smaller at pupariation and died at head eversion. They showed premature ecdysone receptor B1 (EcR-B1) in the photoreceptors and in the optic lobe, downregulation of proliferation in the optic lobe, and separation of R7 from R8 in the medulla during the prepupal period. All of these effects of allatectomy were reversed by feeding third instar larvae on a diet containing the JH mimic (JHM) pyriproxifen or by application of JH III or JHM at the onset of wandering. Eye and optic lobe development in the Methoprene-tolerant (Met)-null mutant mimicked that of CAX prepupae, but the mutant formed viable adults, which had marked abnormalities in the organization of their optic lobe neuropils. Feeding Met(27) larvae on the JHM diet did not rescue the premature EcR-B1 expression or the downregulation of proliferation but did partially rescue the premature separation of R7, suggesting that other pathways besides Met might be involved in mediating the response to JH. Selective expression of Met RNAi in the photoreceptors caused their premature expression of EcR-B1 and the separation of R7 and R8, but driving Met RNAi in lamina neurons led only to the precocious appearance of EcR-B1 in the lamina. Thus, the lack of JH and its receptor Met causes a heterochronic shift in the development of the visual system that is likely to result from some cells {\textquoteright}misinterpreting{\textquoteright} the ecdysteroid peaks that drive metamorphosis.

}, keywords = {Animals, Basic Helix-Loop-Helix Transcription Factors, Biological, Corpora Allata, Diet, Drosophila melanogaster, Drosophila Proteins, Invertebrate, Juvenile Hormones, Larva, Metamorphosis, Neurons, Nonmammalian, Optic Lobe, Photoreceptor Cells, Pyridines, Receptors, Recombinant Fusion Proteins, RNA Interference, Steroid}, issn = {1477-9129}, doi = {10.1242/dev.037218}, author = {Riddiford, Lynn M and Truman, James W and Mirth, Christen K and Shen, Yu-Chi} } @article {2496, title = {The ecdysone receptor controls the post-critical weight switch to nutrition-independent differentiation in Drosophila wing imaginal discs.}, journal = {Development}, volume = {136}, year = {2009}, month = {2009 Jul}, pages = {2345-53}, abstract = {

In holometabolous insects, a species-specific size, known as critical weight, needs to be reached for metamorphosis to be initiated in the absence of further nutritional input. Previously, we found that reaching critical weight depends on the insulin-dependent growth of the prothoracic glands (PGs) in Drosophila larvae. Because the PGs produce the molting hormone ecdysone, we hypothesized that ecdysone signaling switches the larva to a nutrition-independent mode of development post-critical weight. Wing discs from pre-critical weight larvae [5 hours after third instar ecdysis (AL3E)] fed on sucrose alone showed suppressed Wingless (WG), Cut (CT) and Senseless (SENS) expression. Post-critical weight, a sucrose-only diet no longer suppressed the expression of these proteins. Feeding larvae that exhibit enhanced insulin signaling in their PGs at 5 hours AL3E on sucrose alone produced wing discs with precocious WG, CT and SENS expression. In addition, knocking down the Ecdysone receptor (EcR) selectively in the discs also promoted premature WG, CUT and SENS expression in the wing discs of sucrose-fed pre-critical weight larvae. EcR is involved in gene activation when ecdysone is present, and gene repression in its absence. Thus, knocking down EcR derepresses genes that are normally repressed by unliganded EcR, thereby allowing wing patterning to progress. In addition, knocking down EcR in the wing discs caused precocious expression of the ecdysone-responsive gene broad. These results suggest that post-critical weight, EcR signaling switches wing discs to a nutrition-independent mode of development via derepression.

}, keywords = {Animals, Body Patterning, Cell Differentiation, Developmental, Drosophila, Drosophila Proteins, Gene Expression Regulation, Genes, Genetically Modified, Homeodomain Proteins, Insect, Insulin, Nuclear Proteins, Receptors, Signal Transduction, Steroid, Sucrose, Transcription Factors, Wing, Wnt1 Protein}, issn = {0950-1991}, doi = {10.1242/dev.032672}, author = {Mirth, Christen K and Truman, James W and Riddiford, Lynn M} } @article {6525, title = {Developmental model of static allometry in holometabolous insects.}, journal = {Proceedings of the Royal Society B: Biological Sciences}, volume = {275}, year = {2008}, month = {2008 Aug 22}, pages = {1875-85}, abstract = {

The regulation of static allometry is a fundamental developmental process, yet little is understood of the mechanisms that ensure organs scale correctly across a range of body sizes. Recent studies have revealed the physiological and genetic mechanisms that control nutritional variation in the final body and organ size in holometabolous insects. The implications these mechanisms have for the regulation of static allometry is, however, unknown. Here, we formulate a mathematical description of the nutritional control of body and organ size in Drosophila melanogaster and use it to explore how the developmental regulators of size influence static allometry. The model suggests that the slope of nutritional static allometries, the {\textquoteright}allometric coefficient{\textquoteright}, is controlled by the relative sensitivity of an organ{\textquoteright}s growth rate to changes in nutrition, and the relative duration of development when nutrition affects an organ{\textquoteright}s final size. The model also predicts that, in order to maintain correct scaling, sensitivity to changes in nutrition varies among organs, and within organs through time. We present experimental data that support these predictions. By revealing how specific physiological and genetic regulators of size influence allometry, the model serves to identify developmental processes upon which evolution may act to alter scaling relationships.

}, keywords = {Animal Nutritional Physiological Phenomena, Animals, Biological, Biometry, Body Size, Drosophila, Metamorphosis, Models, Organ Size}, issn = {0962-8452}, doi = {10.1098/rspb.2008.0227}, author = {Shingleton, Alexander W and Mirth, Christen K and Bates, Peter W} }