Open AccessSignal transduction in systemic acquired resistance.
Author(s) -
John Ryals,
Kay A. Lawton,
Terrence P. Delaney,
Leslie Friedrich,
Helmut Keßmann,
Urs Neuenschwander,
Scott Uknes,
Bernard Vernooij,
Kristianna B. Weymann
Publication year - 1995
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.92.10.4202
Subject(s) - systemic acquired resistance , salicylic acid , signal transduction , pathogen , biology , microbiology and biotechnology , signal (programming language) , plant disease resistance , second messenger system , catalase , genetics , enzyme , gene , biochemistry , arabidopsis , computer science , mutant , programming language
Systemic acquired resistance (SAR) is an important component of plant defense against pathogen infection. Accumulation of salicylic acid (SA) is required for the induction of SAR. However, SA is apparently not the translocated signal but is involved in transducing the signal in target tissues. Interestingly, SA accumulation is not required for production and release of the systemic signal. In addition to playing a pivotal role in SAR signal transduction, SA is important in modulating plant susceptibility to pathogen infection and genetic resistance to disease. It has been proposed that SA inhibition of catalase results in H2O2 accumulation and that therefore H2O2 serves as a second messenger in SAR signaling. We find no accumulation of H2O2 in tissues expressing SAR; thus the role of H2O2 in SAR signaling is questionable.
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