Sensitization of defense responses and activation of programmed cell death by a pathogen-induced receptor-like protein kinase in Arabidopsis

被引:151
作者
Chen, KG
Du, LQ
Chen, ZX [1 ]
机构
[1] Univ Idaho, Dept Microbiol Mol Biol & Biochem, Moscow, ID 83844 USA
[2] Purdue Univ, Dept Bot & Plant Pathol, W Lafayette, IN 47907 USA
基金
美国国家科学基金会;
关键词
Arabidopsis; defense response; disease resistance; programmed cell death; receptor-like protein kinase;
D O I
10.1023/B:PLAN.0000009265.72567.58
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
During the search for potential target genes of WRKY DNA-binding transcription factors, we have previously identified four pathogen-induced Arabidopsis genes (CRK5, CRK6, CRK10 and CRK11) encoding receptor-like protein kinases (RLKs) containing novel cysteine-rich repeats in their extracellular domains. In the present study, we transformed Arabidopsis plants with the RLK genes under control of the constitutive CaMV 35S promoter or a steroid-inducible Gal4 promoter. Expression of CRK5, but not the three other RLK genes, resulted in significant alterations in defense responses and leaf growth in transgenic plants. In transgenic plants harboring the 35S:: CRK5 construct, significantly elevated and constitutive expression of CRK5 correlated with enhanced leaf growth and increased resistance to the bacterial pathogen Pseudomonas syringae. The enhanced disease resistance in the transgenic plants was associated with more rapidly induced expression of the PR1 gene after pathogen infection. In transgenic plants transformed with CRK5 under control of the steroid-inducible promoter, expression of the transgene was induced at relatively high levels after the steroid application and this induced expression of CRK5 triggered hypersensitive response-like cell death. Induced CRK5 expression also activated cell death in the npr1, ndr1 and eds1 mutants and in the transgenic nahG plants that fail to accumulate salicylic acid. Thus, the novel RLK is capable of activating multiple distinct defense responses depending on the manner and/or the levels of its over-expression in transgenic plants.
引用
收藏
页码:61 / 74
页数:14
相关论文
共 66 条
[11]  
CLARK SE, 1993, DEVELOPMENT, V119, P397
[12]   The CLAVATA1 gene encodes a putative receptor kinase that controls shoot and floral meristem size in Arabidopsis [J].
Clark, SE ;
Williams, RW ;
Meyerowitz, EM .
CELL, 1997, 89 (04) :575-585
[13]   VH1, a provascular cell-specific receptor kinase that influences leaf cell patterns in Arabidopsis [J].
Clay, NK ;
Nelson, T .
PLANT CELL, 2002, 14 (11) :2707-2722
[14]   Characterization of an Arabidopsis thaliana receptor-like protein kinase gene activated by oxidative stress and pathogen attack [J].
Czernic, P ;
Visser, B ;
Sun, WN ;
Savouré, A ;
Deslandes, L ;
Marco, Y ;
Van Montagu, M ;
Verbruggen, N .
PLANT JOURNAL, 1999, 18 (03) :321-327
[15]   A CENTRAL ROLE OF SALICYLIC-ACID IN PLANT-DISEASE RESISTANCE [J].
DELANEY, TP ;
UKNES, S ;
VERNOOIJ, B ;
FRIEDRICH, L ;
WEYMANN, K ;
NEGROTTO, D ;
GAFFNEY, T ;
GUTRELLA, M ;
KESSMANN, H ;
WARD, E ;
RYALS, J .
SCIENCE, 1994, 266 (5188) :1247-1250
[16]   ARABIDOPSIS MUTANTS SIMULATING DISEASE RESISTANCE RESPONSE [J].
DIETRICH, RA ;
DELANEY, TP ;
UKNES, SJ ;
WARD, ER ;
RYALS, JA ;
DANGL, JL .
CELL, 1994, 77 (04) :565-577
[17]   Harpin induces disease resistance in Arabidopsis through the systemic acquired resistance pathway mediated by salicylic acid and the NIM1 gene [J].
Dong, HS ;
Delaney, TP ;
Bauer, DW ;
Beer, SV .
PLANT JOURNAL, 1999, 20 (02) :207-215
[18]   Expression profiles of the Arabidopsis WRKY gene superfamily during plant defense response [J].
Dong, JX ;
Chen, CH ;
Chen, ZX .
PLANT MOLECULAR BIOLOGY, 2003, 51 (01) :21-37
[19]   Identification of genes encoding receptor-like protein kinases as possible targets of pathogen- and salicylic acid-induced WRKY DNA-binding proteins in Arabidopsis [J].
Du, LQ ;
Chen, ZX .
PLANT JOURNAL, 2000, 24 (06) :837-847
[20]   EDS1, an essential component of R gene-mediated disease resistance in Arabidopsis has homology to eukaryotic lipases [J].
Falk, A ;
Feys, BJ ;
Frost, LN ;
Jones, JDG ;
Daniels, MJ ;
Parker, JE .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (06) :3292-3297