A gain-of-function mutation in Msl10 triggers cell death and wound-induced hyperaccumulation of jasmonic acid in Arabidopsis  

作　　者：Yan Zou Satya Chintamanani Ping He Hirotada Fukushige Liping Yu Meiyu Shao Lihuang Zhu David F.Hildebrand Xiaoyan Tang Jian-Min Zhou 

机构地区：[1]School of Life Science and Technology, Shanghai Tech University [2]Syngenta Biotechnology, Inc.Slater [3]Department of Biochemistry and Biophysics, Institute for Plant Genomics and Biotechnology, Texas A&M University [4]Department of Agronomy, Agricultural Sciences Center-Noth, University of Kentucky [5]State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences [6]School of Life Sciences, Capital Normal University

出　　处：《Journal of Integrative Plant Biology》2016年第6期600-609,共10页植物学报（英文版）

基　　金：supported by a grant from Chinese Ministry of Science and Technology (2003-AA210080)

摘　　要：Jasmonates（JAs） are rapidly induced after wounding and act as key regulators for wound induced signaling pathway. However, what perceives the wound signal and how that triggers JA biosynthesis remains poorly understood. To identify components involved in Arabidopsis wound and JA signaling pathway, we screened for mutants with abnormal expression of a luciferase reporter, which is under the control of a wound-responsive promoter of an ethylene response factor（ERF） transcription factor gene, RAP2.6（Related to APetala 2.6）.The rea1（RAP2.6 expresser in shoot apex） mutant constitutively expressed the RAP2.6-LUC reporter gene in young leaves.Along with the typical JA phenotypes including shorter petioles,loss of apical dominance, accumulation of anthocyanin pigments and constitutive expression of JA response gene, rea1 plants also displayed cell death and accumulated high levels of JA in response to wounding. The phenotype of rea1 mutant is caused by a gain-of-function mutation in the C-terminus of a mechanosensitive ion channel MscS-like 10（MSL10）. MSL10 is localized in the plasma membrane and is expressed predominantly in root tip, shoot apex and vascular tissues. These results suggest that MSL10 is involved in the wound-triggered early signal transduction pathway and possibly in regulating the positive feedback synthesis of JA.Jasmonates（JAs） are rapidly induced after wounding and act as key regulators for wound induced signaling pathway. However, what perceives the wound signal and how that triggers JA biosynthesis remains poorly understood. To identify components involved in Arabidopsis wound and JA signaling pathway, we screened for mutants with abnormal expression of a luciferase reporter, which is under the control of a wound-responsive promoter of an ethylene response factor（ERF） transcription factor gene, RAP2.6（Related to APetala 2.6）.The rea1（RAP2.6 expresser in shoot apex） mutant constitutively expressed the RAP2.6-LUC reporter gene in young leaves.Along with the typical JA phenotypes including shorter petioles,loss of apical dominance, accumulation of anthocyanin pigments and constitutive expression of JA response gene, rea1 plants also displayed cell death and accumulated high levels of JA in response to wounding. The phenotype of rea1 mutant is caused by a gain-of-function mutation in the C-terminus of a mechanosensitive ion channel MscS-like 10（MSL10）. MSL10 is localized in the plasma membrane and is expressed predominantly in root tip, shoot apex and vascular tissues. These results suggest that MSL10 is involved in the wound-triggered early signal transduction pathway and possibly in regulating the positive feedback synthesis of JA.

关 键 词：Arabidopsis cell death jasmonates mechanosensitive ion channel wound 

分 类 号：Q943.2[生物学—植物学]