|Ph.D., 2001, Albert Einstein College of Medicine|
|Office:||University of Massachusetts Medical School
364 Plantation Street
Worcester, MA 01605
Autophagy is a highly conserved lysosome-mediated degradation process involving the formation of a double-membrane autophagosome. We previously used C. elegans to identify a set of metazoan-specific epg genes which act at steps unique to autophagy in multicellular organisms, including the formation of contacts between the ER and the isolation membrane (autophagosome precursor), and autophagosome maturation. Our lab focuses on understanding the molecular function of these autophagy genes using C.elegans and mammalian cell lines. We also use genetically modified mice to study the physiological function of these genes and to explore potential therapeutic targets for diseases related to these genes.
Current projects are focusing on the molecular mechanism underlying the establishment and disassembly of ER-isolation membrane contacts, the role of ER-associated degradation (ERAD) in oscillation of autophagic flux, and the function of autophagy genes in non-autophagy processes.
Highly motivated postdocs are encouraged to apply. Please contact Hong Zhang for additional details.