title: Increased sensitivity to salt stress in an ascorbate-deficient Arabidopsis mutant.
abstract: The Arabidopsis thaliana ascorbate-deficient vtc-1 mutant has only 30% ascorbate contents of the wild type (WT). This ascorbate-deficient mutant was used here to study the physiological roles of ascorbate under salt stress in vivo. Salt stress resulted in a more significant decrease in CO2 assimilatory capacity in the vtc-1 mutant than in the WT. Photosystem II function in the Arabidopsis vtc-1 mutant also showed an increased sensitivity to salt stress. Oxidative stress, indicated by the hydrogen peroxide content, increased more dramatically in the vtc-1 mutant than in the WT under salt stress. To clarify the reason for the increased oxidative stress in the vtc-1 mutant, the contents of small antioxidant compounds and the activities of several antioxidant enzymes in the ascorbate-glutathione cycle were measured. Despite an elevated glutathione pool in the vtc-1 mutant, the ascorbate contents and the reduced form of ascorbate decreased very rapidly under salt stress. These results showed that the activities of MDAR and DHAR were lower in the vtc-1 mutant than in the WT under salt stress. Thus, low intrinsic ascorbate and an impaired ascorbate-glutathione cycle in the vtc-1 mutant under salt stress probably induced a dramatic decrease in the reduced form of ascorbate, which resulted in both enhanced ROS contents and decreased NPQ in the vtc-1 mutant.
authors.affiliation: Cold and Arid Regions Environmental and Engineering Research Institute, Chinese Academy of Sciences, Lanzhou, 730000, China.
authors.forename: Chenghong
authors.initials: C
authors.lastname: Huang
authors.forename: Wenliang
authors.initials: W
authors.lastname: He
authors.forename: Jinkui
authors.initials: J
authors.lastname: Guo
authors.forename: Xuexiang
authors.initials: X
authors.lastname: Chang
authors.forename: Peixi
authors.initials: P
authors.lastname: Su
authors.forename: Lixin
authors.initials: L
authors.lastname: Zhang
mesh_terms: D000975:Antioxidants / Q000378:metabolism; D017360:Arabidopsis / Q000187:drug effects / Q000201:enzymology* / Q000235:genetics; D029681:Arabidopsis Proteins / Q000235:genetics / Q000378:metabolism; D001205:Ascorbic Acid / Q000502:physiology*; D002245:Carbon Dioxide / Q000378:metabolism; D002734:Chlorophyll / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D050505:Mutant Proteins / Q000378:metabolism; D009713:Nucleotidyltransferases / Q000235:genetics / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology; D045322:Photosynthetic Reaction Center Complex Proteins / Q000378:metabolism; D045332:Photosystem II Protein Complex / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D012965:Sodium Chloride / Q000494:pharmacology*; D014867:Water / Q000378:metabolism
chemical_list: D000975:Antioxidants; D029681:Arabidopsis Proteins; D050505:Mutant Proteins; D045322:Photosynthetic Reaction Center Complex Proteins; D045332:Photosystem II Protein Complex; D017382:Reactive Oxygen Species; D014867:Water; D002734:Chlorophyll; D002245:Carbon Dioxide; D012965:Sodium Chloride; D006861:Hydrogen Peroxide; D009713:Nucleotidyltransferases; C026917:mannose 1-phosphate guanylyltransferase; D005978:Glutathione; D001205:Ascorbic Acid