Associate Professor, Pharmacology
- PhD, , University of California, San Francisco
P.O. Box 800735
1340 Jefferson Park Ave., Pinn Hall, Room 5213
Charlottesville, VA 22908
Genetics, Immunology, Metabolism, Molecular Biology, Molecular Pharmacology, Neuroendocrinology, Physiology, Translational Science
Molecular mechanisms linking innate immune and insulin signaling to control cell growth and metabolism
Infection in the juvenile stage disrupts growth and metabolism, often with long-lasting effects. In young children and in fruit fly larvae, infections disrupt production of homologous hormones: insulin-like growth factor 1 (IGF1) and Drosophila insulin-like peptide 6 (Dilp6), leading to reduced whole-animal growth. Infections also dramatically alter carbohydrate and lipid metabolism. In humans, a life-long effect of early childhood infections is increased risk of metabolic syndrome.
Our lab uses genetic approaches in flies and in mice to identify molecular mechanisms linking infection and innate immune signaling with disrupted growth and metabolism. We are working to identify transcriptional mechanisms that lead to decreased IGF1 and Dilp6 production in response to infection.
Our lab also identified that innate immune signaling induces phospholipid synthesis in a key immune organ, the fruit fly larval fat body, that is required for successfully combatting infection. We are working to identify components of the Toll signaling pathway that link infection with changes in cellular lipid metabolism.
A third major focus of the lab is to identify endocrine mechanisms that allow animals to adapt to distinct environmental challenges, whether due to infection or nutrient stress. Here we are working to determine roles of two highly related homologs, Dilp2, secreted by fourteen insulin-producing cells in the Drosophila larval brain, and Dilp6, secreted by the larval fat body, in regulating growth and metabolism.