Receptor kinases (RKs) play an important role in the mechanisms witch which organisms perceive and respond to environmental signals; regulating growth and development in both animals and plants. The long-term goal of the proposed project is to elicit the signal transaction cascade regulated by RKs. This information will enhance our understanding of cellular transformation and carcinogenesis in animals and lead to the development of environmentally safe strategies for disease control in plants. The short-term goal of the proposed project is to establish the causal connection between pathogen induced activation of the rice receptor-like kinase, XA21, and the downstream defense responses. Based on information from receptor tyrosine kinases in animal systems, we hypothesize that the catalytic domain of XA21 plays a key role in XA21-mediated signal transduction and that specific residues as binding sites for intracellular proteins. These proteins may then directly or indirectly transduce various defense responses. We also hypothesize that the pathogen may secrete factors into the host cell that influence the signal transduction pathway. In partial support of these hypotheses, we have found that the intracellular domain can autophosphorylate itself in vitro, that a pathogen GTP-binding protein and a rice catalase interact specifically with the XA21 in plants undergoing a resistance response. To test these hypotheses, we propose to carry out the following objectives: 1. Confirm the essential role of phosphorylation in XA21-mediated disease resistance. 2. Identify and characterize rice proteins that interact with the Xa21- kinase. 3. Characterize the defense response and defense-related gene expression in the XA21-mediated defense pathway. 4. Determine the biological significance of the xoo/GBP interaction. Accomplishments of the proposed objectives will, for the first time, lead to the establishment of the causal connection between a plant receptor kinase and the associated downstream response.
Showing the most recent 10 out of 28 publications