Classic myrosinase‐dependent degradation of indole glucosinolate attenuates fumonisin B1‐induced programmed cell death in Arabidopsis. (March 2015)

• Record Type: Journal Article
• Authors: Zhao, Yanting; Wang, Jiansheng; Liu, Yuanyuan; Miao, Huiying; Cai, Congxi; Shao, Zhiyong; Guo, Rongfang; Sun, Bo; Jia, Chengguo; Zhang, Liping; Gigolashvili, Tamara; Wang, Qiaomei
• Is Part Of: Plant journal. Volume 81:Number 6(2015:Mar.)
• Page Start: 920
• Page End: 933
• Publication Date: 2015-03
• Subjects: Plant molecular biology -- Periodicals; Plant cells and tissues -- Periodicals; Botany -- Periodicals; 580
• DOI: 10.1111/tpj.12778
• Languages: English
• ISSNs: 0960-7412

Abstract

<abstract abstract-type="main" id="tpj12778-abs-0001"> <title>Summary</title> <p>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 <italic>cyp79B2 cyp79B3</italic> double mutant<italic>, </italic> 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 <italic>tgg1 tgg2</italic>, rather than atypical myrosinase‐deficient mutant <italic>pen2‐2</italic>, is more sensitive to FB1 than Col‐0, and the elevated expression of <italic>TGG1</italic>, but not of <italic>PEN2</italic>, 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 <italic>tir1‐1</italic> 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.</p> </abstract>