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.
|State||Published - Jul 13 2021|
Bibliographical noteFunding Information:
This work was supported by National Natural Science Foundation of China (grant 31871354 ), the Hundred Talents Program (Chinese Academy of Sciences), Startup Funding of Anhui Agricultural University , and the “Wanjiang Scholar” program .
© 2021 The Author(s)
- HO-mediated retrograde signal
- chloroplastic ROS
- salt stress
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology (all)