Developmental ethanol exposure causes central nervous system dysfunction and may slow the aging process in a Drosophila model of fetal alcohol spectrum disorder.

Alcohol is a known teratogen, and developmental exposure to ethanol results in fetal alcohol spectrum disorder (FASD). Children born with FASD can exhibit a range of symptoms including low birth weight, microcephaly, and neurobehavioral problems. Treatment of patients with FASD is estimated to cost 4 billion dollars per year in the United States alone, and 2 million dollars per affected individual's lifetime.

A Novel Gene Controlling the Timing of Courtship Initiation in Drosophila melanogaster.

Over the past 35 years, developmental geneticists have made impressive progress toward an understanding of how genes specify morphology and function, particularly as they relate to the specification of each physical component of an organism. In the last 20 years, male courtship behavior in Drosophila melanogaster has emerged as a robust model system for the study of genetic specification of behavior. Courtship behavior is both complex and innate, and a single gene, fruitless (fru), is both necessary and sufficient for all aspects of the courtship ritual.

Developmental ethanol exposure leads to dysregulation of lipid metabolism and oxidative stress in Drosophila.

Ethanol exposure during development causes an array of developmental abnormalities, both physiological and behavioral. In mammals, these abnormalities are collectively known as fetal alcohol effects (FAE) or fetal alcohol spectrum disorder (FASD). We have established a Drosophila melanogaster model of FASD and have previously shown that developmental ethanol exposure in flies leads to reduced expression of insulin-like peptides (dILPs) and their receptor.

A small subset of fruitless subesophageal neurons modulate early courtship in Drosophila.

We show that a small subset of two to six subesophageal neurons, expressing the male products of the male courtship master regulator gene products fruitless Male (fru M), are required in the early stages of the Drosophila melanogaster male courtship behavioral program. Loss of fru M expression or inhibition of synaptic transmission in these fru M(+) neurons results in delayed courtship initiation and a failure to progress to copulation primarily under visually-deficient conditions. We identify a fru M-dependent sexually dimorphic arborization in the tritocerebrum made by two of these neurons.

A Drosophila model for fetal alcohol syndrome disorders: role for the insulin pathway.

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.

Division of labor: subsets of dorsal-appendage-forming cells control the shape of the entire tube.

The function of an organ relies on its form, which in turn depends on the individual shapes of the cells that create it and the interactions between them. Despite remarkable progress in the field of developmental biology, how cells collaborate to make a tissue remains an unsolved mystery. To investigate the mechanisms that determine organ structure, we are studying the cells that form the dorsal appendages (DAs) of the Drosophila melanogaster eggshell.

Glycogen synthase kinase-3/Shaggy mediates ethanol-induced excitotoxic cell death of Drosophila olfactory neurons.

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 female sterile mutation twin peaks is a novel allele of tramtrack and reveals a requirement for Ttk69 in epithelial morphogenesis.

The Drosophila gene tramtrack (ttk) encodes two transcriptional repressors, Ttk69 and Ttk88, which are required for normal embryogenesis and imaginal disc development. Here, we characterize a novel female sterile allele of tramtrack called twin peaks (ttk(twk)) that, unlike othertramtrack alleles, has no effect on viability and produces no obvious morphological defects, except during oogenesis. Females homozygous for twin peaks produce small eggs with thin eggshells and short dorsal respiratory appendages.