Clinical studies demonstrated that a lipid droplet (LD) biogenesis gene SEIPIN contributes to congenital generalized lipodystrophy, a disorder characterized by the absence of adipose tissue and muscular dystrophy. Dysfunction of SEIPIN1 affects both adipocyte development and lipid storage in non-adipose tissues. However, how SEIPIN1 dysfunction affects lipid biosynthesis, metabolism, and utilization in building the lipid-rich organelles that lead to the disease progression remains largely unknown. My lab will use a broad array of molecular, cellular, genetic, biochemical, and behavioral techniques to identify and explore putative suppressors of the Seipin mutants, and characterize their contributions to lipid metabolism, transfer, and LD formation. These newly identified suppressing factors may lead to the new direction of LD biology, and shed light on future therapies for lipodystrophies
