© 2004 Oxford University Press
Induction of PR-1 Accumulation Accompanied by Runaway Cell Death in the lsd1 Mutant of Arabidopsis is Dependent on Glutathione Levels but Independent of the Redox State of Glutathione
1 Research Institute for Biological Sciences, Okayama (RIBS Okayama), 7549-1 Yoshikawa, Kayou-cho, Okayama, 716-1241 Japan
2 Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST), Japan
The lesions simulating disease (lsd) mutants of Arabidopsis spontaneously develop hypersensitive-response-like lesions in the absence of pathogens. To address the function of the redox regulator glutathione in disease resistance, we examined the relationship between endogenous glutathione and PR-1 accumulation using one of these mutants, lsd1, as a disease resistance model. Lesion formation on lsd1 was suppressed by weak light and initiated by the subsequent transition to normal light. The application of buthionine sulfoximine, a specific inhibitor of glutathione biosynthesis, suppressed conditionally induced runaway cell death and expression of the PR-1 gene, suggesting that glutathione regulates the conditional cell death and PR-1 gene expression. The application of reduced (GSH) or oxidized (GSSG) glutathione to lsd1 upregulated the level of total glutathione ([GSH]+[GSSG]) accompanied by hastened accumulation of PR-1, and the basal level of total glutathione in lsd1 was higher than that in wild-type plants. The glutathione redox state defined as [GSH]/([GSH]+[GSSG]) decreased following the conditional transition, but the suppression of this decrease by the application of GSH did not inhibit the accumulation of PR-1. Taken together, conditional PR-1 accumulation in lsd1 is regulated not by the redox state but by the endogenous level of glutathione.
3 Corresponding author: E-mail, ogawa_k{at}bc4.so-net.ne.jp; Fax, +81-866-56-9454.
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