Overexpression of CuZnSOD and APX enhance salt stress tolerance in sweet potato

Copyright © 2016 Elsevier Masson SAS. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Plant physiology and biochemistry : PPB. - 1991. - 109(2016) vom: 13. Dez., Seite 20-27
1. Verfasser: Yan, Hui (VerfasserIn)
Weitere Verfasser: Li, Qiang, Park, Sung-Chul, Wang, Xin, Liu, Ya-Ju, Zhang, Yun-Gang, Tang, Wei, Kou, Meng, Ma, Dai-Fu
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2016
Zugriff auf das übergeordnete Werk:Plant physiology and biochemistry : PPB
Schlagworte:Journal Article APX CuZnSOD Salt stress Sweet potato Transgenic plants Reactive Oxygen Species Sodium Chloride 451W47IQ8X Ascorbate Peroxidases mehr... EC 1.11.1.11 Superoxide Dismutase EC 1.15.1.1
Beschreibung
Zusammenfassung:Copyright © 2016 Elsevier Masson SAS. All rights reserved.
Abiotic stresses cause accumulation of reactive oxygen species (ROS) in plants, CuZnSOD and APX are first line defenses against ROS caused by oxidative stress. In this study, CuZnSOD and APX were transferred into salt sensitive sweet potato (cv. Xushu 55-2) under control of stress inducible SWPA2 promoter and tolerance to salt stress was evaluated. When 100 mM NaCl was used to treat stem cuttings, transgenic plants showed enhanced tolerance compared to wild type (WT) plants. Rooting was significantly retarded in WT plants whereas all transgenic plants had significantly enhanced root growth under salt stress. Integration of SOD gene was confirmed by southern blot analysis, and the copy number ranged from 1 to 3. The expression levels of CuZnSOD and APX in transgenic plants were significantly increased up to 13.3 and 7.8 folds to WT under salinity conditions, respectively. SOD and APX activity and ROS staining showed enzyme activities of transgenic plants were increased under salt stress. These results show that CuZnSOD and APX have important roles in enhancing the salt tolerance of sweet potato
Beschreibung:Date Completed 10.04.2017
Date Revised 30.09.2020
published: Print-Electronic
Citation Status MEDLINE
ISSN:1873-2690
DOI:10.1016/j.plaphy.2016.09.003