Classic myrosinase-dependent degradation of indole glucosinolate attenuates fumonisin B1-induced programmed cell death in Arabidopsis.
Classic myrosinase-dependent degradation of indole glucosinolate attenuates fumonisin B1-induced programmed cell death in Arabidopsis.
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吲哚芥子油苷的经典黑芥子酶依赖性降解可减弱拟南芥中伏马菌素 B1 诱导的程序性细胞死亡。
DOI：
10.1111/tpj.12778
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发表时间：
2015-03
期刊：
影响因子：
7.2
通讯作者：
Wang, Qiaomei
中科院分区：
文献类型：
--
作者：
Jia, Chengguo;Zhang, Liping;Gigolashvili, Tamara;Wang, Qiaomei
真菌毒素伏马菌素B1（FB 1）引起活性氧（ROS）的积累，然后导致拟南芥细胞程序性死亡（PCD）。在研究FB 1诱导的硫代葡萄糖苷生物合成的过程中，我们发现吲哚硫代葡萄糖苷（IGS）参与了FB 1诱导的PCD的减弱。用FB 1处理提高了与Camalexin和IGS的生物合成相关的基因的表达。脂肪族硫代葡萄糖苷（AGS）或camalexin生物合成缺陷的突变体在FB 1浸润后显示出与Col-0相似的病变;然而，cyp 79 B2 cyp 79 B3双突变体，缺乏IGS和camalexin的诱导，显示出更严重的病变。基于经典黑芥子酶β-硫代葡萄糖苷葡萄糖水解酶（TGG）缺陷型双突变体tgg 1 tgg 2，而非非典型黑芥子酶缺陷型突变体pen 2 -2，对FB 1比Col-0更敏感，并且TGG 1而非pen 2的表达升高与IGS减少相关的事实，我们得出结论：TGG依赖性IGS水解参与FB 1诱导的PCD。吲哚-3-乙腈（IAN）和吲哚-3-甲醇（I3 C），IGS的常见衍生物，用于喂养实验中，这挽救了严重的细胞死亡表型，这与减少ROS的积累以及增加抗氧化酶的活性和ROS清除能力。尽管吲哚-3-乙酸（IAA）参与限制FB 1诱导的PCD，喂养IAN和I3 C衰减FB 1诱导的PCD的IAA受体突变体TIR 1 -1就像在Col-0。综上所述，我们的研究结果表明，TGG催化的IGS分解产物通过其抗氧化行为减少ROS的积累，并以独立于IAA的方式减弱FB 1诱导的PCD。
The mycotoxin fumonisin B1 (FB1) causes the accumulation of reactive oxygen species (ROS) which then leads to programmed cell death (PCD) in Arabidopsis. In the process of studying FB1-induced biosynthesis of glucosinolates, we found that indole glucosinolate (IGS) is involved in attenuating FB1-induced PCD. Treatment with FB1 elevates the expression of genes related to the biosynthesis of camalexin and IGS. Mutants deficient in aliphatic glucosinolate (AGS) or camalexin biosynthesis display similar lesions to Col-0 upon FB1 infiltration; however, the cyp79B2 cyp79B3 double mutant, which lacks induction of both IGS and camalexin, displays more severe lesions. Based on the fact that the classic myrosinase β-thioglucoside glucohydrolase (TGG)-deficient double mutant tgg1 tgg2, rather than atypical myrosinase-deficient mutant pen2-2, is more sensitive to FB1 than Col-0, and the elevated expression of TGG1, but not of PEN2, correlates with the decrease in IGS, we conclude that TGG-dependent IGS hydrolysis is involved in FB1-induced PCD. Indole-3-acetonitrile (IAN) and indole-3-carbinol (I3C), the common derivatives of IGS, were used in feeding experiments, and this rescued the severe cell death phenotype, which is associated with reduced accumulation of ROS as well as increased activity of antioxidant enzymes and ROS-scavenging ability. Despite the involvement of indole-3-acetic acid (IAA) in restricting FB1-induced PCD, feeding of IAN and I3C attenuated FB1-induced PCD in the IAA receptor mutant tir1-1 just as in Col-0. Taken together, our results indicate that TGG-catalyzed breakdown products of IGS decrease the accumulation of ROS by their antioxidant behavior, and attenuate FB1 induced PCD in an IAA-independent way.
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