Vice Chancellor’s Award in Excellence for Research, Texas A&M University, 2018
National Science Foundation Career Award, 2013
American Society of Plant Biologists Early Career Award, 2008
Postdoc – Molecular Biology; Harvard Medical School, USA; 2008
Ph.D. – Plant Pathology; Kansas State University; USA; 2003
M.S. – Genetics; Chinese Academy of Sciences, China; 1998
B.S – Plant Genetics & Breeding; China Agricultural University, China; 1993
Lacking specialized immune cells and adaptive immunity, plants have developed the sophisticated innate immune system to defend pathogen attacks. Our primary research interest is to elucidate the activation and signaling mechanisms of host immunity upon pathogen infections with an integrated genetic, biochemical and cellular approach using Arabidopsis as a tractable model system. Plant immunity is inextricably linked with plant development and environmental stresses. We are also interested in understanding the signaling crosstalk that orchestrates plant responses to different extrinsic and intrinsic signals. Ultimately, knowledge gained from studying model plants will be applied to improve crop plants for resistance against different biotic and abiotic stresses.
Plants have evolved two tiers of immune receptors to detect infections: cell surface-resident pattern recognition receptors (PRRs) sensing microbial signatures and intracellular nucleotide-binding domain leucine-rich repeat (NLR) proteins recognizing pathogen effectors. We have carried out a series of sensitive and high-throughput genetic screens with Arabidopsis luciferase reporter lines for components governing differential and overlapping responses triggered upon PRR or NLR activation. From these screens, we have uncovered an unconventional phosphorylation cascade on RNA polymerase II in orchestrating immune gene transcription and demonstrated an essential function of protein poly(ADP-ribosylation) posttranslational modification in plant PRR-mediated immunity. We also revealed that malectin-like domain receptor-like kinases function as a molecular link between PRR and NLR protein complexes in regulating two-tiered plant immune system.
Defects or over-activation of immune receptors have been linked to detrimental effects often leading to cell death. However, the mechanisms underlying cell death control are poorly understood. The classical suppressor screen is not feasible for many essential genes due to the lethality of mutants. We have developed an innovative RNAi-based screen for suppressors of cell death caused by mutations in key immune regulators. This unbiased and highly efficient screen is based on an easy experimental procedure of Agrobacterium-mediated virus-induced gene silencing (VIGS) and a collection of indexed Arabidopsis knockout lines. With this approach, we have identified the components in the protein glycosylation pathway and endoplasmic reticulum (ER) quality control in the regulation of cell death by the shared PRR coreceptor BAK1.