Plants are constantly challenged by pathogens and pests. Billions of dollars are lost each year due to plant diseases, which have posed tremendous economic challenges worldwide. Understanding how plants defend themselves against invaders is key in developing strategies to improve disease-resistance traits in economically important plants. The main research goal in my laboratory is to use the model plant Arabidopsis thaliana to understand mechanisms of plant disease resistance. In particular, we are interested in identifying plant genes that are important for defense, characterizing the function of these genes in the regulation of defense and/or other biological processes, and ultimately manipulating the function of these genes to increase disease resistance in crop plants. Currently we have two main research projects in the lab.
1. Elucidating salicylic acid signaling networks: The small phenolic compound salicylic acid (SA) is critical for plant defense against a broad spectrum of pathogens, including viral, bacterial, and fungal pathogens. SA also cross talks other signaling pathways, including those mediated by jasmonic acid and reactive oxygen species, and is involved in plant development besides stress response. Given the importance of SA in cellular function, it is necessary to uncover additional genes that contribute to SA signaling and understand how these genes function to form complicated signaling networks to influence plant development and defense responses. We have a powerful genetic tool, acd6-1 whose small size shows a strong correlation with the severity of defense and cell death phenotypes (Figure 1). Thus acd6-1 can be conveniently used in throughput genetic screens to identify genes with impaired defense and to study genetic interactions of defense mutants. We have identified many Arabidopsis mutants through acd6-1 suppressor (sup) screen. So far we cloned five disrupted SUP genes, investigated the function of three genes, and examined the genetic interactions of many defense genes in the acd6-1 background. Currently we focus on investigating the function of one such SUP gene that links plant defense with flowering time control (Figure 2).
2. Investigate molecular basis underlying the interplay between plant innate immunity and the circadian clock: The circadian clock is the internal time-measuring machinery critical for growth and development of many organisms and their responses to environmental stimuli. Although the molecular composition of the circadian clock differs greatly between plants and other organisms, the basic principle of clock function, which is the ability to self-sustain, is conserved. Like in other organisms, the circadian clock in plants consists of core clock components, which form complicated interlocking transcription-translation feedback loops (TTFLs) that are subject to both transcriptional and posttranscriptional regulation (Figure 3). Like other organisms, plants have evolved timed defense by incorporating external and internal time cues, therefore being able to anticipate likely attacks from invaders at different times of a day and to poise defense responses for rapid deployment when encountering a real attack (Figure 4). Recent work from several laboratories including my laboratory has established a direct role for the circadian clock in regulating plant defense against pathogen and pest challenges. In particular, my group was the first to show that defense activation by pathogen attacks could reciprocally affect clock activity, revealing the crosstalk between the circadian clock and plant innate immunity. The molecular basis underlying such crosstalk is unclear and a better understanding of this topic could provide much needed information on the temporal control of plant innate immunity. My group is actively pursuing this exciting research. Our research has revealed that while they work together to influence the precision of the circadian clock, many clock genes likely employ distinct mechanisms to regulate plant defense. In addition, the host circadian clock can be modulated by activation of defense signaling as well as by pathogen-derived molecules.