Identification and cloning of a negative regulator of systemic acquired resistance, SNlI1, through a screen for suppressors of npr1-1

被引：204

作者：

Li, X ^{[1
]}

Zhang, YL ^{[1
]}

Clarke, JD ^{[1
]}

Li, Y ^{[1
]}

Dong, XN ^{[1
]}

机构：

[1] Duke Univ, Dept Bot, Dev Cell & Mol Biol Grp, Durham, NC 27708 USA

来源：

CELL | 1999年 / 98卷 / 03期

基金：

美国国家科学基金会;

关键词：

D O I：

10.1016/S0092-8674(00)81962-5

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：

Systemic acquired resistance (SAR) is a plant immune response induced after a local infection by necrotizing pathogens. The Arabidopsis NPR1 gene is a positive regulator of SAR, essential for transducing the SAR signal salicylic acid (SA). Mutations in the NPR1 gene abolish the SA-induced expression of pathogenesis-related (PR) genes and resistance to pathogens. To identify additional regulators of SAR, we screened for suppressors of npr1-1. In the npr1-1 background, the sni1 (suppressor of npr1-1, inducible 1) mutant shows near wild-type levels of PR1 expression and resistance to pathogens after induction. Restoration of SAR in npr1-1 by the recessive sni1 mutation indicates that wild-type SNI1 may function as a negative regulator of SAR. We cloned the SNI1 gene and found that it encodes a leucine-rich nuclear protein.

引用

页码：329 / 339

页数：11

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