Salicylic acid induction-deficient mutants of Arabidopsis express PR-2 and PR-5 and accumulate high levels of camalexin after pathogen inoculation.

Details

Serval ID
serval:BIB_DD0945C8BA13
Type
Article: article from journal or magazin.
Collection
Publications
Title
Salicylic acid induction-deficient mutants of Arabidopsis express PR-2 and PR-5 and accumulate high levels of camalexin after pathogen inoculation.
Journal
Plant Cell
Author(s)
Nawrath C., Métraux J.P.
ISSN
1040-4651 (Print)
ISSN-L
1040-4651
Publication state
Published
Issued date
1999
Volume
11
Number
8
Pages
1393-1404
Language
english
Abstract
In Arabidopsis, systemic acquired resistance against pathogens has been associated with the accumulation of salicylic acid (SA) and the expression of the pathogenesis-related proteins PR-1, PR-2, and PR-5. We report here the isolation of two nonallelic mutants impaired in the pathway leading to SA biosynthesis. These SA induction-deficient (sid) mutants do not accumulate SA after pathogen inoculation and are more susceptible to both virulent and avirulent forms of Pseudomonas syringae and Peronospora parasitica. However, sid mutants are not as susceptible to these pathogens as are transgenic plants expressing the nahG gene encoding an SA hydroxylase that degrades SA to catechol. In contrast to NahG plants, only the expression of PR-1 is strongly reduced in sid mutants, whereas PR-2 and PR-5 are still expressed after pathogen attack. Furthermore, the accumulation of the phytoalexin camalexin is normal. These results indicate that SA-independent compensation pathways that do not operate in NahG plants are active in sid mutants. One of the mutants is allelic to eds5 (for enhanced disease susceptibility), whereas the other mutant has not been described previously.
Keywords
Alleles, Arabidopsis/genetics, Genes, Plant, Indoles/metabolism, Mutation, Oomycetes/pathogenicity, Plant Diseases/genetics, Plant Proteins/metabolism, Pseudomonas/pathogenicity, Salicylic Acid/metabolism, Thiazoles/metabolism
Pubmed
Web of science
Open Access
Yes
Create date
24/01/2008 19:49
Last modification date
20/08/2019 16:01
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