@article {6957, title = {A small subset of fruitless subesophageal neurons modulate early courtship in Drosophila.}, journal = {PLoS One}, volume = {9}, year = {2014}, month = {2014 Apr 16}, pages = {e95472}, abstract = {

We show that a small subset of two to six subesophageal neurons, expressing the male products of the male courtship master regulator gene products fruitlessMale (fruM), are required in the early stages of the Drosophila melanogaster male courtship behavioral program. Loss of fruM expression or inhibition of synaptic transmission in these fruM(+) neurons results in delayed courtship initiation and a failure to progress to copulation primarily under visually-deficient conditions. We identify a fruM-dependent sexually dimorphic arborization in the tritocerebrum made by two of these neurons. Furthermore, these SOG neurons extend descending projections to the thorax and abdominal ganglia. These anatomical and functional characteristics place these neurons in the position to integrate gustatory and higher-order signals in order to properly initiate and progress through early courtship.

}, issn = {1932-6203}, doi = {10.1371/journal.pone.0095472}, author = {Tran, David H and Meissner, Geoffrey W and French, Rachael L and Baker, Bruce S} } @article {5484, title = {A Drosophila model for fetal alcohol syndrome disorders: role for the insulin pathway.}, journal = {Disease Models \& Mechanisms}, volume = {4}, year = {2011}, month = {2011 May}, pages = {335-46}, abstract = {

Prenatal exposure to ethanol in humans results in a wide range of developmental abnormalities, including growth deficiency, developmental delay, reduced brain size, permanent neurobehavioral abnormalities and fetal death. Here we describe the use of Drosophila melanogaster as a model for exploring the effects of ethanol exposure on development and behavior. We show that developmental ethanol exposure causes reduced viability, developmental delay and reduced adult body size. We find that flies reared on ethanol-containing food have smaller brains and imaginal discs, which is due to reduced cell division rather than increased apoptosis. Additionally, we show that, as in mammals, flies reared on ethanol have altered responses to ethanol vapor exposure as adults, including increased locomotor activation, resistance to the sedating effects of the drug and reduced tolerance development upon repeated ethanol exposure. We have found that the developmental and behavioral defects are largely due to the effects of ethanol on insulin signaling; specifically, a reduction in Drosophila insulin-like peptide (Dilp) and insulin receptor expression. Transgenic expression of Dilp proteins in the larval brain suppressed both the developmental and behavioral abnormalities displayed by ethanol-reared adult flies. Our results thus establish Drosophila as a useful model system to uncover the complex etiology of fetal alcohol syndrome.

}, keywords = {Adaptation, Animal, Animals, Apoptosis, Behavior, Brain, Cell Proliferation, Disease Models, Drosophila melanogaster, Drosophila Proteins, Ethanol, Eye, Female, Fetal Alcohol Syndrome, Humans, Insulin, Larva, Physiological, Pregnancy, Receptor, Signal Transduction, Survival Analysis}, issn = {1754-8411}, doi = {10.1242/dmm.006411}, author = {McClure, Kimberly D and French, Rachael L and Heberlein, Ulrike} } @article {5485, title = {Glycogen synthase kinase-3/Shaggy mediates ethanol-induced excitotoxic cell death of Drosophila olfactory neurons.}, journal = {Proceedings of the National Academy of Sciences of the United States of America}, volume = {106}, year = {2009}, month = {2009 Dec 8}, pages = {20924-9}, abstract = {

It has long been known that heavy alcohol consumption leads to neuropathology and neuronal death. While the response of neurons to an ethanol insult is strongly influenced by genetic background, the underlying mechanisms are poorly understood. Here, we show that even a single intoxicating exposure to ethanol causes non-cell-autonomous apoptotic death specifically of Drosophila olfactory neurons, which is accompanied by a loss of a behavioral response to the smell of ethanol and a blackening of the third antennal segment. The Drosophila homolog of glycogen synthase kinase-3 (GSK-3)beta, Shaggy, is required for ethanol-induced apoptosis. Consistent with this requirement, the GSK-3beta inhibitor lithium protects against the neurotoxic effects of ethanol, indicating the possibility for pharmacological intervention in cases of alcohol-induced neurodegeneration. Ethanol-induced death of olfactory neurons requires both their neural activity and functional NMDA receptors. This system will allow the investigation of the genetic and molecular basis of ethanol-induced apoptosis in general and provide an understanding of the molecular role of GSK-3beta in programmed cell death.

}, keywords = {Amino Acid, Animals, Cell Death, Drosophila melanogaster, Drosophila Proteins, Electricity, Ethanol, Gene Silencing, Glycogen Synthase Kinase 3, Lithium, N-Methyl-D-Aspartate, Neurotoxins, Olfactory Receptor Neurons, Receptors, Sequence Homology, Volatilization}, issn = {1091-6490}, doi = {10.1073/pnas.0910813106}, author = {French, Rachael L and Heberlein, Ulrike} }