Roles of salicylic acid, jasmonic acid, and ethylene in cpr-induced resistance in arabidopsis.

Published

Journal Article

Disease resistance in Arabidopsis is regulated by multiple signal transduction pathways in which salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) function as key signaling molecules. Epistasis analyses were performed between mutants that disrupt these pathways (npr1, eds5, ein2, and jar1) and mutants that constitutively activate these pathways (cpr1, cpr5, and cpr6), allowing exploration of the relationship between the SA- and JA/ET-mediated resistance responses. Two important findings were made. First, the constitutive disease resistance exhibited by cpr1, cpr5, and cpr6 is completely suppressed by the SA-deficient eds5 mutant but is only partially affected by the SA-insensitive npr1 mutant. Moreover, eds5 suppresses the SA-accumulating phenotype of the cpr mutants, whereas npr1 enhances it. These data indicate the existence of an SA-mediated, NPR1-independent resistance response. Second, the ET-insensitive mutation ein2 and the JA-insensitive mutation jar1 suppress the NPR1-independent resistance response exhibited by cpr5 and cpr6. Furthermore, ein2 potentiates SA accumulation in cpr5 and cpr5 npr1 while dampening SA accumulation in cpr6 and cpr6 npr1. These latter results indicate that cpr5 and cpr6 regulate resistance through distinct pathways and that SA-mediated, NPR1-independent resistance works in combination with components of the JA/ET-mediated response pathways.

Full Text

Duke Authors

Cited Authors

  • Clarke, JD; Volko, SM; Ledford, H; Ausubel, FM; Dong, X

Published Date

  • November 2000

Published In

Volume / Issue

  • 12 / 11

Start / End Page

  • 2175 - 2190

PubMed ID

  • 11090217

Pubmed Central ID

  • 11090217

Electronic International Standard Serial Number (EISSN)

  • 1532-298X

International Standard Serial Number (ISSN)

  • 1040-4651

Digital Object Identifier (DOI)

  • 10.1105/tpc.12.11.2175

Language

  • eng