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Abscisic Acid Deficiency Antagonizes High-Temperature Inhibition of Disease Resistance through Enhancing Nuclear Accumulation of Resistance Proteins SNC1 and RPS4 in Arabidopsis

文献类型： 外文期刊

作者： Mang, Hyung-Gon 1 ; Qian, Weiqiang 1 ; Zhu, Ying 1 ; Qian, Jun 1 ; Kang, Hong-Gu 3 ; Klessig, Daniel F. 3 ; Hua, Jian 1 ;

作者机构： 1.Cornell Univ, Dept Plant Biol, Ithaca, NY 14853 USA

2.Zhejiang Acad Agr Sci, State Key Lab Breeding Base Zhejiang Sustainable, Hangzhou 310021, Zhejiang, Peoples R China

3.Cornell Univ, Boyce Thompson Inst Plant Res, Ithaca, NY 14853 USA

4.SW Texas State Univ, Dept Biol, San Marcos, TX 78666 USA

期刊名称：PLANT CELL （ 影响因子：11.277； 五年影响因子：12.061 ）

ISSN： 1040-4651

年卷期： 2012 年 24 卷 3 期

页码：

收录情况： SCI

摘要： Plant defense responses to pathogens are influenced by abiotic factors, including temperature. Elevated temperatures often inhibit the activities of disease resistance proteins and the defense responses they mediate. A mutant screen with an Arabidopsis thaliana temperature-sensitive autoimmune mutant bonzai1 revealed that the abscisic acid (ABA)-deficient mutant aba2 enhances resistance mediated by the resistance (R) gene SUPPRESSOR OF npr1-1 CONSTITUTIVE1 (SNC1) at high temperature. ABA deficiency promoted nuclear accumulation of SNC1, which was essential for it to function at low and high temperatures. Furthermore, the effect of ABA deficiency on SNC1 protein accumulation is independent of salicylic acid, whose effects are often antagonized by ABA. ABA deficiency also promotes the activity and nuclear localization of R protein RESISTANCE TO PSEUDOMONAS SYRINGAE4 at higher temperature, suggesting that the effect of ABA on R protein localization and nuclear activity is rather broad. By contrast, mutations that confer ABA insensitivity did not promote defense responses at high temperature, suggesting either tissue specificity of ABA signaling or a role of ABA in defense regulation independent of the core ABA signaling machinery. Taken together, this study reveals a new intersection between ABA and disease resistance through R protein localization and provides further evidence of antagonism between abiotic and biotic responses.

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