
Differential Induction of Tobacco MAP Kinases by the Defense Signals Nitric Oxide, Salicylic Acid, Ethylene, and Jasmonic Acid
Author(s) -
Dhirendra Kumar,
Daniel F. Klessig
Publication year - 2000
Publication title -
molecular plant-microbe interactions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.565
H-Index - 153
eISSN - 1943-7706
pISSN - 0894-0282
DOI - 10.1094/mpmi.2000.13.3.347
Subject(s) - jasmonic acid , salicylic acid , kinase , nitric oxide , protein kinase a , systemic acquired resistance , microbiology and biotechnology , mitogen activated protein kinase , biochemistry , signal transduction , npr1 , chemistry , biology , medicine , arabidopsis , gene , mutant , heart failure , organic chemistry , natriuretic peptide
In tobacco, two mitogen-activated protein (MAP) kinases, designated salicylic acid (SA)-induced protein kinase (SIPK) and wounding-induced protein kinase (WIPK) are activated in a disease resistance-specific manner following pathogen infection or elicitor treatment. To investigate whether nitric oxide (NO), SA, ethylene, or jasmonic acid (JA) are involved in this phenomenon, the ability of these defense signals to activate these kinases was assessed. Both NO and SA activated SIPK; however, they did not activate WIPK. Additional analyses with transgenic NahG tobacco revealed that SA is required for the NO-mediated induction of SIPK. Neither JA nor ethylene activated SIPK or WIPK. Thus, SIPK may function downstream of SA in the NO signaling pathway for defense responses, while the signals responsible for resistance-associated WIPK activation have yet to be determined.