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Titolo:
Roles of salicylic acid, jasmonic acid, and ethylene in cpr-induced resistance in Arabidopsis
Autore:
Clarke, JD; Volko, SM; Ledford, H; Ausubel, FM; Dong, XN;
Indirizzi:
Duke Univ, Dept Biol, Dev Cell & Mol Biol Grp, Durham, NC 27708 USA Duke Univ Durham NC USA 27708 v Cell & Mol Biol Grp, Durham, NC 27708 USA Harvard Univ, Sch Med, Dept Genet, Boston, MA 02114 USA Harvard Univ Boston MA USA 02114 ch Med, Dept Genet, Boston, MA 02114 USA Massachusetts Gen Hosp, Dept Biol Mol, Boston, MA 02114 USA Massachusetts Gen Hosp Boston MA USA 02114 Biol Mol, Boston, MA 02114 USA
Titolo Testata:
PLANT CELL
fascicolo: 11, volume: 12, anno: 2000,
pagine: 2175 - 2190
SICI:
1040-4651(200011)12:11<2175:ROSAJA>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
SYSTEMIC ACQUIRED-RESISTANCE; PLANT-DISEASE-RESISTANCE; TOBACCO MOSAIC-VIRUS; PATHOGENESIS-RELATED PROTEINS; SIGNAL-TRANSDUCTION PATHWAY; DEPENDENT DEFENSE-RESPONSE; RACE-SPECIFIC ELICITORS; FOR-GENE CONCEPT; CELL-DEATH; SUSCEPTIBILITY MUTANTS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Life Sciences
Citazioni:
87
Recensione:
Indirizzi per estratti:
Indirizzo: Dong, XN Duke Univ, Dept Biol, Dev Cell & Mol Biol Grp, Durham, NC 27708 USA Duke Univ Durham NC USA 27708 Mol Biol Grp, Durham, NC 27708 USA
Citazione:
J.D. Clarke et al., "Roles of salicylic acid, jasmonic acid, and ethylene in cpr-induced resistance in Arabidopsis", PL CELL, 12(11), 2000, pp. 2175-2190

Abstract

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 dataindicate 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 combinationwith components of the JA/ET-mediated response pathways.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/08/20 alle ore 14:44:18