LESION SIMULATING DISEASE1 Interacts with Catalases to Regulate Hypersensitive Cell Death in Arabidopsis
LESION SIMULATING DISEASE1 Interacts with Catalases to Regulate Hypersensitive Cell Death in Arabidopsis
复制标题
拟南芥中的病变模拟疾病 1 与过氧化氢酶相互作用调节过敏性细胞死亡
DOI：
10.1104/pp.113.225805
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发表时间：
2013-10-01
期刊：
影响因子：
7.4
通讯作者：
Zuo, Jianru
中科院分区：
文献类型：
--
作者：
Li, Yansha;Chen, Lichao;Zuo, Jianru
LSD1是拟南芥细胞程序性死亡(PCD)的重要负调控因子。LSD1的功能缺失突变会导致由活性氧引发的失控细胞死亡。LSD1编码一种新的锌指蛋白，其生化活性未知。在这里，我们报道了通过亲和纯化和基于蛋白质组学的质谱学分析鉴定CATALASE 3(Cat3)是一种LSD1相互作用的蛋白质。拟南芥基因组包含三个同源的过氧化氢酶基因(CAT1、CAT2和Cat3)。酵母双杂交和免疫共沉淀分析表明，LSD1在体外和体内都能与这三种过氧化氢酶相互作用，这种相互作用需要LSD1的锌指。我们发现LSD1突变体的过氧化氢酶活性降低，说明过氧化氢酶活性部分依赖于LSD1。LSD1突变体对过氧化氢酶抑制剂3-氨基-1，2，4-三氮唑的敏感性高于野生型，这表明LSD1与过氧化氢酶之间的相互作用参与了过氧化物体中产生的活性氧的调节。遗传学研究表明，LSD1与过氧化氢酶基因相互作用，调节光依赖型失控细胞死亡和超敏型细胞死亡。此外，受LSD1和过氧化氢酶相互作用调节的PCD还需要水杨酸的积累。这些结果表明，LSD1-过氧化氢酶相互作用在拟南芥PCD的调控中起着重要作用。
LESION SIMULATING DISEASE1 (LSD1) is an important negative regulator of programmed cell death (PCD) in Arabidopsis (Arabidopsis thaliana). The loss-of-function mutations in LSD1 cause runaway cell death triggered by reactive oxygen species. LSD1 encodes a novel zinc finger protein with unknown biochemical activities. Here, we report the identification of CATALASE3 (CAT3) as an LSD1-interacting protein by affinity purification and mass spectrometry-based proteomic analysis. The Arabidopsis genome contains three homologous catalase genes (CAT1, CAT2, and CAT3). Yeast two-hybrid and coimmunoprecipitation analyses demonstrated that LSD1 interacted with all three catalases both in vitro and in vivo, and the interaction required the zinc fingers of LSD1. We found that the catalase enzymatic activity was reduced in the lsd1 mutant, indicating that the catalase enzyme activity was partially dependent on LSD1. Consistently, the lsd1 mutant was more sensitive to the catalase inhibitor 3-amino-1,2,4-triazole than the wild type, suggesting that the interaction between LSD1 and catalases is involved in the regulation of the reactive oxygen species generated in the peroxisome. Genetic studies revealed that LSD1 interacted with CATALASE genes to regulate light-dependent runaway cell death and hypersensitive-type cell death. Moreover, the accumulation of salicylic acid was required for PCD regulated by the interaction between LSD1 and catalases. These results suggest that the LSD1-catalase interaction plays an important role in regulating PCD in Arabidopsis.