Recognizing featured Plant Cell first authors: Kun Wang
Kun Wang, first author of Two Abscisic Acid Responsive Plastid Lipase Genes Involved in Jasmonic Acid Biosynthesis in Arabidopsis thaliana
Current Position: Postdoctoral Fellow, Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health
Education: PhD, Biochemistry and Molecular Biology, Michigan State University.
Non-scientific Interests: Sports, programming and jazz music
I received my PhD training in Dr. Christoph Benning’s lab at Michigan State University. For my thesis projects, I was trying to understand the functions and mechanisms of chloroplast membrane remodeling. I started characterizing a galactosyltransferase encoding gene in tomato and its role in membrane remodeling to protect tomatoes from salt and drought stresses. Later on, I shifted to work with Arabidopsis, and asked how the plant photosynthetic membranes are catabolized, a question that mirrors the study of membrane lipid biosynthesis. Given the dynamic nature of these membranes, we hypothesized that fine-tuned lipid catabolism might be as physiologically important as lipid anabolism. I primarily focused on the chloroplast localized lipases, which are responsible for the first step of membrane turnover by releasing the acyl groups from the membrane lipids. With a combination of biochemical and genetic approaches, I was excited to find that these plastid lipases actually participate in diverse physiological processes, including transporting fatty acids from thylakoid membranes for seed oil biosynthesis and linking the abiotic and biotic pathways. We believe these discoveries are just a tip of the iceberg of the numerous roles of lipases, as a large number of predicted lipase genes exist in the Arabidopsis genome, which beg to be characterized in the future. After my PhD, I moved to the Farese-Walther lab at Harvard Medical School to extend my training in lipid biology. I am now intrigued by the question of how abnormal metabolism and trafficking of membrane lipids contribute to human neurodegenerative diseases, like frontotemporal dementia.