J Integr Plant Biol. ›› 2016, Vol. 58 ›› Issue (6): 600-609.DOI: 10.1111/jipb.12427

• Molecular Physiology • Previous Articles    

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

Yan Zou1†*, Satya Chintamanani2†, Ping He3, Hirotada Fukushige4, Liping Yu5, Meiyu Shao1, Lihuang Zhu5, David F. Hildebrand4, Xiaoyan Tang6 and Jian-Min Zhou5   

  1. 1School of Life Science and Technology, ShanghaiTech University, Shanghai, China
    2Syngenta Biotechnology, Inc. Slater, Iowa, USA
    3Department of Biochemistry and Biophysics, Institute for Plant Genomics and Biotechnology, Texas A&M University, Texas, USA
    4Department of Agronomy, Agricultural Sciences Center-Noth, University of Kentucky, Lexington, Kentucky, USA
    5State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China
    6School of Life Sciences, Capital Normal University, Beijing, China
  • Received:2015-08-04 Accepted:2015-09-09 Published:2015-09-10
  • About author:These authors contributed equally to the work.
    *Correspondence: E-mail: zouyan@shanghaitech.edu.cn


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.

Key words: Arabidopsis, cell death, jasmonates, mechanosensitive ion channel, wound

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