1. Academic Validation
  2. EGY3 mediates chloroplastic ROS homeostasis and promotes retrograde signaling in response to salt stress in Arabidopsis

EGY3 mediates chloroplastic ROS homeostasis and promotes retrograde signaling in response to salt stress in Arabidopsis

  • Cell Rep. 2021 Jul 13;36(2):109384. doi: 10.1016/j.celrep.2021.109384.
Yong Zhuang 1 Ming Wei 2 Chengcheng Ling 3 Yangxuan Liu 2 Abdul Karim Amin 3 Penghui Li 2 Pengwei Li 3 Xufan Hu 3 Huaxu Bao 3 Heqiang Huo 4 Jan Smalle 5 Songhu Wang 6
Affiliations

Affiliations

  • 1 School of Horticulture, Anhui Agricultural University, Hefei 230036, China; CAS Center for Excellence in Molecular Plant Sciences, Chengdu Institute of Biology, Chinese Academy of Sciences, Chengdu 610041, China.
  • 2 CAS Center for Excellence in Molecular Plant Sciences, Chengdu Institute of Biology, Chinese Academy of Sciences, Chengdu 610041, China.
  • 3 School of Horticulture, Anhui Agricultural University, Hefei 230036, China.
  • 4 Mid-Florida Research and Education Center, University of Florida, Institute of Food and Agricultural Sciences, Apopka, FL 32703, USA.
  • 5 Plant Physiology, Biochemistry and Molecular Biology Program, Department of Plant and Soil Sciences, College of Agriculture, University of Kentucky, Lexington, KY 40546, USA.
  • 6 School of Horticulture, Anhui Agricultural University, Hefei 230036, China; CAS Center for Excellence in Molecular Plant Sciences, Chengdu Institute of Biology, Chinese Academy of Sciences, Chengdu 610041, China. Electronic address: [email protected].
Abstract

The chloroplast is the main organelle for stress-induced production of Reactive Oxygen Species (ROS). However, how chloroplastic ROS homeostasis is maintained under salt stress is largely unknown. We show that EGY3, a gene encoding a chloroplast-localized protein, is induced by salt and oxidative stresses. The loss of EGY3 function causes stress hypersensitivity while EGY3 overexpression increases the tolerance to both salt and chloroplastic oxidative stresses. EGY3 interacts with chloroplastic Cu/Zn-SOD2 (CSD2) and promotes CSD2 stability under stress conditions. In egy3-1 mutant Plants, the stress-induced CSD2 degradation limits H2O2 production in chloroplasts and impairs H2O2-mediated retrograde signaling, as indicated by the decreased expression of retrograde-signal-responsive genes required for stress tolerance. Both exogenous application of H2O2 (or APX inhibitor) and CSD2 overexpression can rescue the salt-stress hypersensitivity of egy3-1 mutants. Our findings reveal that EGY3 enhances the tolerance to salt stress by promoting the CSD2 stability and H2O2-mediated chloroplastic retrograde signaling.

Keywords

Cu/Zn-SOD2; H(2)O(2)-mediated retrograde signal; chloroplastic ROS; salt stress.

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