Caenorhabditis elegans require a GPCR to recognize and rapidly escape from toxin-producing Streptomyces at their head or tail.

Synthetic PPARγ ligands push and cobind with natural endogenous ligands, instead of compete and displace, which synergistically affects the structure and function of PPARγ.

Inhibition of C. elegans FLD-1 or Human TLCD1/2 prevents saturated fat lipotoxicity by allowing increased levels of membrane phospholipids that contain fluidizing long-chain polyunsaturated fatty acids.

Silencing the acyl-coA synthethase ACSL1 protects against saturated fat lipotoxicity by preventing the degradation of polyunsaturated fatty acids, allowing them to be incorporated into phospholipids and improves membrane fluidity.

A revertible Leigh Syndrome French Canadian Type (LSFC) disease model recapitulates the clinical phenotypes which can be rescued using a liver-specific genetic model therapy.

A novel pheromone/receptor neuron pair mediates attraction between Drosophila larvae, and evolved differences in pheromone signaling underlie changes in social behavior between drosophilid species.

A genome scale model of Brugia malayi metabolism illustrates a dynamic reliance on energy production pathways across its life cycle and identifies new drugs with experimentally supported anti-parasitic properties.

Normal adipogenesis requires de novo DNA methyltransferase 3A (DNMT3A) for proper differentiation and suppression of an age-associated pathogenic inflammatory program.

A pathogen effector mimics starvation-induced autophagy by subverting host endomembrane trafficking to stimulate biogenesis of autophagosomes around pathogen feeding sites, revealing how pathogens interlock distinct host compartments to facilitate infection.

Behavioral assays using Caenorhabditis elegans show that a learned pathogen avoidance following intestinal distention requires specific chemosensory neurons and TRPM channels in the intestine and excretory cell.