"Plants encounter various biotic and abiotic stresses throughout their life cycles. Accordingly, plants have developed sophisticated defense strategies to cope with stresses. Among these, the plant hormone jasmonate (JA) bestows upon plants the ability to defend against attacks by a wide variety of herbivores as well as necrotrophic pathogens. Perception of pathogen or herbivore attacks promotes synthesis of jasmonoyl-L-isoleucine (JA-Ile), the bioactive form of JA, which binds to the COI1-JAZ receptor, triggering degradation of JAZ repressors and induction of transcriptional reprogramming associated with plant defense. Interestingly, some virulent pathogens have evolved strategies to manipulate JA signaling to facilitate their exploitation of plant hosts. For example, strains of the bacterial pathogen Pseudomonas syringae produce proteinaceous effectors as well as a JA-mimicking toxin, coronatine (COR), to activate JA signaling and promote disease susceptibility. In the first part of my dissertation research, I explored the possibility that targeted modification of the JA receptor could be a promising new approach to 'protect' the disease-vulnerable components of plants. Guided by the crystal structure of the COI-JAZ receptor and evolutionary clues, I succeeded in modifying the JA receptor to allow for sufficient endogenous JA signaling but greatly reduced sensitivity to COR. Transgenic Arabidopsis expressing this modified receptor not only are fertile and maintain a high level of insect defense, but also gain the ability to resist COR-producing pathogens P. syringae pv. tomato (Pst) DC3000 and P. s. pv. maculicola (Psm) ES4326. The second part of my dissertation research investigates pathogen-induced stomatal closure as an innate immune response. Studies have shown that stomatal closure plays a role in restricting bacterial invasion, whereas highly evolved pathogens produce virulence factors, such as COR in the case of P. syringae, to counteract stomatal defense. A previous genetic screen led to identification of six Arabidopsis scord (susceptibility to a COR-deficient mutant of Pst DC3000) mutants that are defective in bacterium-triggered stomatal closure. I attempted and succeeded in cloning two SCORD genes. SCORD6 encodes a GDP-D-mannose-4,6-dehydratase involved in the de novo synthesis of GDP-L-fucose and SCORD7 codes for the TRICHOME BIREFRINGENCE (TBR) protein, belonging to TBR-Like protein family, which is proposed to be involved in synthesis and/or modification of pectin or O-acetylation of xyloglucan and xylan. Both scord6 and scord7 are defective in pathogen-/salicylic acid (SA)-mediated stomatal closure but not in abscisic acid (ABA)-mediated stomatal closure. The identification of SCORD6 and SCORD7 genes highlights plant cell-wall-based regulation of stomatal defense and contributes to the general understanding of the multifaceted host defense mechanisms against pathogen infection in plants."--Pages ii-iii.
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