| Innate immunity refers to the ability of eukaryotic organisms to detect the presence of potentially harmful microbes through recognition of highly conserved surface molecules, referred to as pathogen-associated molecular patterns (PAMPs), and to activate defense responses to prevent infection. Like mammals and insects, plants can perceive microbial PAMPs and activate defenses. Microbial pathogens such as bacteria cause significant agricultural losses each year and chemical treatments aimed at abating these losses represent a substantial input cost for agriculture and are damaging to the environment. Therefore, new strategies to control crop losses due to pathogens without the use of chemicals will be highly desirable.; My research has contributed to our knowledge of both innate immunity in plants, and the mechanisms used by pathogenic bacteria to overcome innate immune responses. I performed genome-wide microarray analyses in collaboration with Dr. Roger Thilmony to determine global gene expression changes associated with the activation of innate immunity in Arabidopsis thaliana. This study provided the first look at the gene expression changes induced by perception of PAMPs present on live bacteria.; My work also contributed to the discovery of bacterium-induced stomatal closure as a novel component of innate immunity in plants. This research was performed in collaboration with Dr. Maeli Melotto and revealed that the guard cells of stomata, pores on the surface of the plant leaf, can sense bacterial PAMPs and close stomata to restrict entry of bacteria into the leaf tissue. Prior to this discovery, stomata were generally regarded as passive ports of bacterial entry. We found that bacterium-induced closure of stomata required the plant hormone abscisic acid (ABA) and an intact ABA signaling pathway. Additionally, we discovered that the phytotoxin COR is required for Pst DC3000 to open stomata, explaining the primary virulence function of COR.; The TTSS and effector proteins injected into the plant cells are crucial for the bacteria to overcome defenses and cause disease. I investigated the function of a single TTSS effector, the protein tyrosine phosphatase HopD2, by creating transgenic Arabidopsis lines expressing HopD2 or the catalytically-inactive HopD2C378S. I found that HopD2 blocks defense responses associated with PAMP-induced innate immunity, but not the HR. This activity was dependent on an intact phosphatase catalytic site and, interestingly, HopD2C378S had a dominant-negative effect on the function of the wild-type HopD2. Global gene expression profiling revealed that HopD2 does not affect gene expression levels in Arabidopsis , suggesting that HopD2 acts at a late stage, downstream or independent of PAMP-induced signaling and gene expression changes, to block activation of innate immunity. |
