The RPM1 plant disease resistance gene facilitates a rapid and sustained increase in cytosolic calcium that is necessary for the oxidative burst and hypersensitive cell death

Early events occurring during the hypersensitive resistance response (HR) w ere examined using the avrRpm1/RPM1 gene-for-gene interaction in Arabidopsi s challenged by Pseudomonas syringae pv. tomato. Increases in cytosolic Ca2 + were measured in whole leaves using aequorin-mediated bioluminescence. Du ring the HR a sustained increase in Ca2+ was observed which was dependent o n the presence of both a functional RPM1 gene product and delivery of the c ognate avirulence gene product AvrRpm1. The sequence-unrelated avirulence g ene avrB, which also interacts with RPM1, generated a significantly later b ut similarly prolonged increase in cytosolic Ca2+. Accumulation of H2O2 at reaction sites, as revealed by electron microscopy, occurred within the sam e time frame as the changes in cytosolic Ca2+. The NADPH oxidase inhibitor diphenylene iodonium chloride did not affect the calcium signature, but did block H2O2 accumulation and the HR. By contrast, the calcium-channel block er LaCl3 suppressed the increase in cytosolic Ca2+ as well as H2O2 accumula tion and the HR, placing calcium elevation upstream of the oxidative burst.