Wednesday, August 23, 2017

Drosophila as a model for understanding genetic links to our responses to environmental toxins

A Drosophila model for toxicogenomics: Genetic variation in susceptibility to heavy metal exposure.
Shanshan Zhou, Sarah E. Luoma, Genevieve E. St. Armour, Esha Thakkar, Trudy F. C. Mackay, Robert R. H. Anholt

In PLoS Genetics 2017

From the author summary: "Although physiological effects of environmental toxins are well documented, we know little about the genetic factors that determine individual variation in susceptibility to toxins. Such information is difficult to obtain in human populations due to heterogeneity in genetic background and environmental exposure, and the diversity of symptoms and time lag with which they appear after toxic exposure. Here, we show that the fruit fly, Drosophila, can serve as a powerful genetic model system to elucidate the genetic underpinnings that contribute to individual variation in resistance to toxicity, using lead and cadmium exposure as an experimental paradigm. ... Thus, we demonstrate that based on evolutionary conservation of fundamental biological processes, we can use Drosophila as a powerful translational model for toxicogenomics studies."

Monday, August 14, 2017

Fly study of 14 candidate ADHD genes

Rohde PD, Madsen LS, Neumann Arvidson SM, Loeschcke V, Demontis D, Kristensen TN. Testing candidate genes for attention-deficit/hyperactivity disorder in fruit flies using a high throughput assay for complex behavior. Fly (Austin). 2016 Jan 2;10(1):25-34. PMID: 26954609; PMCID: PMC4934711.

From the abstract: "... Here we use a high-throughput locomotor activity assay to test the response on activity behavior of gene disruption in Drosophila melanogaster. The aim was to investigate the impact of disruption of 14 candidate genes for human attention-deficit/hyperactivity disorder (ADHD) on fly behavior. By obtaining a range of correlated measures describing the space of variables for behavioral activity we show, that some mutants display similar phenotypic responses, and furthermore, that the genes disrupted in those mutants had common molecular functions; namely processes related to cGMP activity, cation channels and serotonin receptors. ... Results provide additional support for the investigated genes being risk candidate genes for ADHD in humans."