Loss of Necrotic Spotted Lesions 1 associates with cell death and defense responses in Arabidopsis thaliana

被引:60
作者
Noutoshi, Yoshiteru
Kuromori, Takashi
Wada, Takuji
Hirayama, Takashi
Kamiya, Asako
Imura, Yuko
Yasuda, Michiko
Nakashita, Hideo
Shirasu, Ken
Shinozaki, Kazuo
机构
[1] RIKEN, Tsukuba Inst, Tsukuba, Ibaraki 3050074, Japan
[2] RIKEN, Yokohama Inst, Genom Sci Ctr, Tsurumi Ku, Yokohama, Kanagawa 2300045, Japan
[3] Yokohama City Univ, Int Grad Sch Arts & Sci, Tsurumi Ku, Yokohama, Kanagawa 230045, Japan
[4] Riken Inst Phys & Chem Res, Plant Funct Lab, Wako, Saitama 3510198, Japan
[5] John Innes Ctr Plant Sci Res, Sainsbury Lab, Norwich NR4 7UH, Norfolk, England
基金
日本科学技术振兴机构;
关键词
cell death; defense responses; salicylic acid; MACPF domain;
D O I
10.1007/s11103-006-9001-6
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
We isolated a lesion mimic mutant, n ecrotic potted lesions 1 (nsl1), from Ds-tagged Arabidopsis thaliana accession No-0. The nsl1 mutant exhibits a growth retardation phenotype and develops spotted necrotic lesions on its rosette and cauline leaves. These phenotypes occur in the absence of pathogens indicating that nsl1 mutants may constitutively express defense responses. Consistent with this idea, nsl1 accumulates high levels of callose and autofluorescent phenolic compounds localized to the necrotic lesions. Furthermore RNA gel blot analysis revealed that genes associated with disease resistance activation are upregulated in the nsl1 mutants and these plants contain elevated levels of salicylic acid (SA). Crossing nsl1 with an SA deficient mutant, eds16-1, revealed that the nsl1 lesions and growth retardation are dependent upon SA. The nsl1 phenotypes are not suppressed under either the rar1-10 or sgt1b-1 genetic background. NSL1 encodes a novel 612aa protein which contains a membrane-attack complex/perforin (MACPF) domain, which is conserved in bacteria, fungi, mammals and plants. The possible modes of action of NSL1 protein in negative regulation of cell death programs and defense responses are discussed.
引用
收藏
页码:29 / 42
页数:14
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