Arabidopsis UBC13 differentially regulates two programmed cell death pathways in responses to pathogen and low-temperature stress

First author: Lipu Wang; Affiliations: Capital Normal University (首都师范大学): Beijing, China

Corresponding author: Wei Xiao (萧伟)

UBC13 is required for Lys63‐linked polyubiquitination (多聚泛素化) and innate immune responses in mammals, but its functions in plant immunity remain to be defined. Here we used genetic and pathological methods to evaluate roles of Arabidopsis UBC13 in response to pathogens and environmental stresses. Loss of UBC13 failed to activate the expression of numerous cold‐ esponsive genes and resulted in hypersensitivity (超敏性) to low‐ emperature stress, indicating that UBC13 is involved in plant response to low‐ emperature stress. Furthermore, the ubc13 mutant displayed low‐ emperature‐induced and salicylic acid‐dependent lesion (病变) mimic phenotypes. Unlike typical lesion mimic mutants, ubc13 did not enhance disease resistance against virulent (致命的) bacterial and fungal pathogens, but diminished hypersensitive response and compromised effector‐ riggered immunity against avirulent (无致病力的) bacterial pathogens. UBC13 differently regulates two types of programmed cell death in response to low temperature and pathogen. The lesion mimic phenotype in the ubc13 mutant is partially dependent on SNC1. UBC13 interacts with an F‐ox protein CPR1 that regulates the homeostasis of SNC1. However, the SNC1 protein level was not altered in the ubc13 mutant, implying that UBC13 is not involved in CPR1‐ egulated SNC1 protein degradation. Taken together, our results revealed that UBC13 is a key regulator in plant response to low temperature and pathogens.

UBC13在动物中作用于Lys63连接的多聚泛素化及天然免疫响应，但在植物中是否参与了植物免疫仍然不清楚。本文利用遗传学和病理学的方法检测了拟南芥UBC13在病原物和环境胁迫响应中所扮演的作用。缺失UBC13基因能够使得许多冷胁迫相关基因的不能被激活表达，导致植物对低温具有超敏感性，说明植物中的UBC13参与了低温胁迫的响应。此外，ubc13突变体还显示出低温诱导的和水杨酸依赖型的病变模拟表型。与其它的病变模拟突变体不一样，ubc13突变体并不增强植物对致病性病毒和真菌病原物的抗性，然而减小了植物的超敏反应及对于无致病性细菌病原物的效应物诱导免疫。UBC13在响应低温和病原物时调控了两种不同类型的细胞程序性死亡。ubc13突变体中的病变模拟表型部分依赖于SNC1。UBC13可直接与F‐ox蛋白CPR1发生相互作用，调控SNC1的内稳态。然而，在ubc13突变体中SNC1的蛋白水平并未发生改变，说明UBC13并未参与CPR1调控的SNC1蛋白降解。综上，本文的研究结果显示UBC13在植物低温和病原菌响应中发挥关键调控作用。

通讯：萧伟（http://smkxxy.cnu.edu.cn/szll/zrjs/qrjhjs/4390.htm）

个人简介：1982，南京农业大学，学士；1984年，多伦多大学，硕士；1988年，萨斯喀彻温大学，博士；1990-1992年，哈佛大学，博士后。

研究方向：非常规泛素化的发现及其相关途径分子机制的探索。

doi: https://doi.org/10.1111/nph.15435

Journal: New Phytologist

First Published: 15 September, 2018

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