Abstract
Rapid accumulation of reactive oxygen intermediates (e.g., H2O2) is a striking early event in the hypersensitive response including programmed cell death. Signalling pathways leading to these responses, however, remaine to be dissolved. To elucudate the signaling pathways, eleven rice lesion mimic mutants spl (spl1~11) with spontaneous cell death on their leaves, were investigated using suspension-cultured cell. Three of the mutants (spl2, spl7, spl11) were found to accumulate higher amount of H2O2 than the wild type, when treated with elicitor, indicating that these mutations are involved in accumulation of H2O2. Calyculin A (CA), an inhibitor of protein phosphatase, enhanced production of H2O2 in spl7 but not in the wild type, spl2 and spl11. Moreover, CA-enhanced H2O2 production in spl7 was reduced by addition of a Ca2+ chelator EGTA. These results imply that spl7 participates in regulation of H2O2 production at a protein dephosphorylate- and Ca2+ - dependent step.
