Salicylic acid-mediated cell death in the Arabidopsis len3 mutant

被引:3
作者
Ishikawa, Atsushi [1 ]
Kimura, Yuri
Yasuda, Michiko
Nakashita, Hideo
Yoshida, Shigeo
机构
[1] Fukui Prefectural Univ, Dept Biosci, Fukui 9101195, Japan
[2] Saitama Univ, Grad Sch Sci & Engn, Saitamashi, Saitama 3388570, Japan
[3] RIKEN, Environm Mol Biol Lab, Wako, Saitama 3510198, Japan
[4] RIKEN, Plant Sci Ctr, Yokohama, Kanagawa 2300045, Japan
关键词
Arabidopsis; lesion; salicylic acid; cell death;
D O I
10.1271/bbb.50683
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
The Arabidopsis lesion initiation 3 (len3) mutant develops lesions on leaves without pathogen attack. len3 plants exhibit stunted growth, constitutively express pathogenesis-related (PR) genes, PR-1, PR-2, and PR-5, and accumulate elevated levels of salicylic acid (SA). Furthermore, len3 is a semidominant, male gametophytic lethal mutation with partial defects in female gametophytic development. To determine the signaling pathway activated in len3 plants, we crossed the len3 plants with nahG, npr1-1, and pad4-1 plants and analyzed the phenotypes of the double mutants. The len3-conferred phenotypes, including cell death and PR-1 expressions, were suppressed in the double mutants. Thus SA, NPR1, and PAD4 are required for the phenotypes. However, none of these double mutants could completely suppress the len3-conferred stunted growth. This result suggests that an SA-, NPR1-, and PAD4-independent pathway is also involved in the phenotype. Treatment with BTH (benzo(1,2,3)thiadiazole-7-carbothioic acid), an SA analog, induced cell death in len3 nahG plants but not in len3 npr1 or len3 pad4 plants, suggesting the involvement of the PAD4-dependent but SA-independent second signal pathway in cell death in len3 plants.
引用
收藏
页码:1447 / 1453
页数:7
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