Abstract
We previously reported that depletion of OsPti1a caused lesion formation on leaves and induced a series of defense responses without pathogen in rice. OsPti1a is a tomato SlPti1 homolog which encodes a Ser/Thr kinase and negatively regulates R gene-mediated disease resistance. The phenotypes of ospti1a mutant were complemented by expression of mutant protein OsPti1aK96N, which is deficient in kinase activity, as well as by OsPti1aWT and SlPti1. Additionally, high expression of another SlPti1 homolog OsPti1b, whose endogenous expression level was very low and its kinase activity was undetectable in vitro, also complemented the ospti1a phenotypes, indicating that OsPti1a-mediated defense signaling requires over certain amount of OsPti1 protein rather than the kinase activity of it. The experiment with cultured-cell revealed that cell death induction in ospti1a mutant by H2O2 treatment was sensitive and enhanced compared with in wild type, suggesting that OsPti1a is required for negative regulation of H2O2-induced cell death.