Overexpression of the sweetpotato peroxidase geneswpa4enhances tolerance to methyl viologen-mediated oxidative stress and dehydration inArabidopsis thaliana
- Authors
- Kim, Yun-Hee; Hong, Jeum Kyu; Kim, Ho Soo; Kwak, Sang-Soo
- Issue Date
- Mar-2021
- Publisher
- SPRINGER INDIA
- Keywords
- Dehydration; Oxidative stress; Peroxidase; Reactive oxygen species; Sweetpotato; Transgenic arabidopsis
- Citation
- JOURNAL OF PLANT BIOCHEMISTRY AND BIOTECHNOLOGY, v.30, no.1, pp.215 - 220
- Indexed
- SCIE
SCOPUS
- Journal Title
- JOURNAL OF PLANT BIOCHEMISTRY AND BIOTECHNOLOGY
- Volume
- 30
- Number
- 1
- Start Page
- 215
- End Page
- 220
- URI
- https://scholarworks.bwise.kr/gnu/handle/sw.gnu/3989
- DOI
- 10.1007/s13562-020-00588-3
- ISSN
- 0971-7811
- Abstract
- We previously reported that transgenicArabidopsis thalianaplants overexpressing the sweet potato peroxidase geneswpa4under the control of the cauliflower mosaic virus (CaMV)35 spromoter showed increased levels of reactive oxygen species (ROS) and nitric oxide (NO), and higher expression of ROS and NO related genes than control plants. Here, we investigated the effect ofswpa4overexpression on the abiotic and biotic stress tolerance levels ofArabidopsisplants. Methyl viologen (MV) treatment-induced oxidative stress caused visible damage to the seedlings and rosette leaves of allArabidopsisplants, although the symptoms were more severe in control plants than in transgenic lines. Additionally, survival rates and ion leakage showed a slight decline in transgenic lines but a more severe decline in control plants after MV treatment. Transgenic plants also showed enhanced tolerance to drought stress. Dehydration treatment, followed by rehydration, resulted in a greater change in the relative water content and lipid peroxidation of control plants than in that of transgenic lines. However, transgenic plants did not show enhanced resistance to biotic stresses such as bacterial and fungal pathogens. These results indicate that transgenicArabidopsisplants can efficiently regulate defense levels during oxidative stress via the overexpression ofswpa4.
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