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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
Author(s) -
Grant Murray,
Brown Ian,
Adams Sally,
Knight Marc,
Ainslie Alastair,
Mansfield John
Publication year - 2000
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1046/j.1365-313x.2000.00804.x
Subject(s) - cytosol , calcium , hypersensitive response , aequorin , gene , calcium channel blocker , biology , chemistry , biochemistry , microbiology and biotechnology , enzyme , plant disease resistance , organic chemistry
Summary Early events occurring during the hypersensitive resistance response (HR) were examined using the avrRpm1 / RPM1 gene‐for‐gene interaction in Arabidopsis challenged by Pseudomonas syringae pv. tomato . Increases in cytosolic Ca 2+ were measured in whole leaves using aequorin‐mediated bioluminescence. During the HR a sustained increase in Ca 2+ was observed which was dependent on the presence of both a functional RPM1 gene product and delivery of the cognate avirulence gene product AvrRpm1. The sequence‐unrelated avirulence gene avrB , which also interacts with RPM1 , generated a significantly later but similarly prolonged increase in cytosolic Ca 2+ . Accumulation of H 2 O 2 at reaction sites, as revealed by electron microscopy, occurred within the same time frame as the changes in cytosolic Ca 2+ . The NADPH oxidase inhibitor diphenylene iodonium chloride did not affect the calcium signature, but did block H 2 O 2 accumulation and the HR. By contrast, the calcium‐channel blocker LaCl 3 suppressed the increase in cytosolic Ca 2+ as well as H 2 O 2 accumulation and the HR, placing calcium elevation upstream of the oxidative burst.