Differential regulation of sleep by blue, green, and red light in .

Introduction: Exposure to blue-enriched light from electronic devices is an emergent disruptor of human sleep, especially at particular times of day. Further dissection of this phenomenon necessitates modeling in a tractable model organism.

Methods: Thus, we investigated the effects of light color on sleep in .

Optogenetic activation of SIFamide (SIFa) neurons induces a complex sleep-promoting effect in the fruit fly Drosophila melanogaster.

Sleep is a universal and extremely complicated function. Sleep is regulated by two systems-sleep homeostasis and circadian rhythms. In a wide range of species, neuropeptides have been found to play a crucial role in the communication and synchronization between different components of both systems.

Optogenetic activation of short neuropeptide F (sNPF) neurons induces sleep in Drosophila melanogaster.

Sleep abnormalities have widespread and costly public health consequences, yet we have only a rudimentary understanding of the events occurring at the cellular level in the brain that regulate sleep. Several key signaling molecules that regulate sleep across taxa come from the family of neuropeptide transmitters. For example, in Drosophila melanogaster, the neuropeptide Y (NPY)-related transmitter short neuropeptide F (sNPF) appears to promote sleep.

Accumulation, elimination, sequestration, and genetic variation of lead (Pb) loads within and between generations of Drosophila melanogaster.

We examined accumulation, sequestration, elimination, and genetic variation for lead (Pb) loads within and between generations of Drosophila melanogaster. Flies were reared in control or leaded medium at various doses and tested for their Pb loads at different stages of development (larvae, eclosion, newly-eclosed adults, and mature adults). Pb loads were tested using Inductively Coupled Plasma Mass Spectrometry (ICP-MS).

Drosophila melanogaster as a model for lead neurotoxicology and toxicogenomics research.

Drosophila melanogaster is an excellent model animal for studying the neurotoxicology of lead. It has been known since ancient Roman times that long-term exposure to low levels of lead results in behavioral abnormalities, such as what is now known as attention deficit hyperactivity disorder (ADHD). Because lead alters mechanisms that underlie developmental neuronal plasticity, chronic exposure of children, even at blood lead levels below the current CDC community action level (10 μg/dl), can result in reduced cognitive ability, increased likelihood of delinquency, behaviors associated with ADHD, changes in activity level, altered sensory function, delayed onset of sexual maturity in girls, and changes in immune function.

Pb2+: an endocrine disruptor in Drosophila?

Environmental exposure to Pb(2+) affects hormone-mediated responses in vertebrates. To help establish the fruit fly, Drosophila melanogaster, as a model system for studying such disruption, we describe effects of Pb(2+) on hormonally regulated traits. These include duration of development, longevity, females' willingness to mate, fecundity and adult locomotor activity.

Genetical toxicogenomics in Drosophila identifies master-modulatory loci that are regulated by developmental exposure to lead.

The genetics of gene expression in recombinant inbred lines (RILs) can be mapped as expression quantitative trait loci (eQTLs). So-called "genetical genomics" studies have identified locally acting eQTLs (cis-eQTLs) for genes that show differences in steady-state RNA levels. These studies have also identified distantly acting master-modulatory trans-eQTLs that regulate tens or hundreds of transcripts (hotspots or transbands).

Genetic aspects of behavioral neurotoxicology.

Considerable progress has been made over the past couple of decades concerning the molecular bases of neurobehavioral function and dysfunction. The field of neurobehavioral genetics is becoming mature. Genetic factors contributing to neurologic diseases such as Alzheimer's disease have been found and evidence for genetic factors contributing to other diseases such as schizophrenia and autism are likely.

Variations at a quantitative trait locus (QTL) affect development of behavior in lead-exposed Drosophila melanogaster.

We developed Drosophila melanogaster as a model to study correlated behavioral, neuronal and genetic effects of the neurotoxin lead, known to affect cognitive and behavioral development in children. We showed that, as in vertebrates, lead affects both synaptic development and complex behaviors (courtship, fecundity, locomotor activity) in Drosophila. By assessing differential behavioral responses to developmental lead exposure among recombinant inbred Drosophila lines (RI), derived from parental lines Oregon R and Russian 2b, we have now identified a genotype by environment interaction (GEI) for a behavioral trait affected by lead.