Abstract
We previously reported that all ten members of the SnRK2 protein kinase family encoded by the rice genome (SAPK1 through SAPK10) are rapidly activated by hyperosmotic stress and that some of them (SAPK8, 9 and 10) are activated also by ABA. Thr/Ser to Asp mutations were introduced to the region corresponding to the activation loop to create constitutively active mutants. Contrary to the expectation, all these mutant forms lost kinase activities but were still phosphorylated in response to hyperosmotic stress, indicating that it is not autophosphorylation but depends on the upstream protein kinase. Further analyses, which attempt to identify the putative upstream kinases and potential target substrates as well as pharmacological studies to gain insight into the upstream signaling components will be reported.
