Joshua D. Mast

This study shows that glial cells regulate sphingolipid levels to drive daily remodeling of circadian circuits in Drosophila.

This paper uses yeast models to study PMM2-CDG mutations, identifies compounds that suppress growth defects, and suggests pathogenicity mechanisms in human patients.

This study uses a Drosophila model of NGLY1 Deficiency to identify therapeutic compounds and gene modifiers that rescue developmental defects.

The paper describes genetic and transgenic reagents for several Drosophila species to facilitate genetic studies.