title: Catalase is a sink for H2O2 and is indispensable for stress defence in C3 plants.
abstract: Hydrogen peroxide (H2O2) has been implicated in many stress conditions. Control of H2O2 levels is complex and dissection of mechanisms generating and relieving H2O2 stress is difficult, particularly in intact plants. We have used transgenic tobacco with approximately 10% wild-type catalase activity to study the role of catalase and effects of H2O2 stress in plants. Catalase-deficient plants showed no visible disorders at low light, but in elevated light rapidly developed white necrotic lesions on the leaves. Lesion formation required photorespiratory activity since damage was prevented under elevated CO2. Accumulation of H2O2 was not detected during leaf necrosis. Alternative H2O2-scavenging mechanisms may have compensated for reduced catalase activity, as shown by increased ascorbate peroxidase and glutathione peroxidase levels. Leaf necrosis correlated with accumulation of oxidized glutathione and a 4-fold decrease in ascorbate, indicating that catalase is critical for maintaining the redox balance during oxidative stress. Such control may not be limited to peroxisomal H2O2 production. Catalase functions as a cellular sink for H2O2, as evidenced by complementation of catalase deficiency by exogenous catalase, and comparison of catalase-deficient and control leaf discs in removing external H2O2. Stress analysis revealed increased susceptibility of catalase-deficient plants to paraquat, salt and ozone, but not to chilling.
authors.affiliation: Department of Genetics, Flanders Interuniversity Institute for Biotechnology (VIB), Universiteit Gent, Belgium.
authors.forename: H
authors.initials: H
authors.lastname: Willekens
authors.forename: S
authors.initials: S
authors.lastname: Chamnongpol
authors.forename: M
authors.initials: M
authors.lastname: Davey
authors.forename: M
authors.initials: M
authors.lastname: Schraudner
authors.forename: C
authors.initials: C
authors.lastname: Langebartels
authors.forename: M
authors.initials: M
authors.lastname: Van Montagu
authors.forename: D
authors.initials: D
authors.lastname: Inzé
authors.forename: W
authors.initials: W
authors.lastname: Van Camp
mesh_terms: D060387:Ascorbate Peroxidases; D001205:Ascorbic Acid / Q000378:metabolism; D002245:Carbon Dioxide / Q000378:metabolism; D002374:Catalase / Q000235:genetics / Q000378:metabolism*; D002734:Chlorophyll / Q000378:metabolism; D003080:Cold Temperature; D005978:Glutathione / Q000031:analogs & derivatives / Q000378:metabolism; D019803:Glutathione Disulfide; D006861:Hydrogen Peroxide / Q000378:metabolism*; D008027:Light; D018384:Oxidative Stress; D010126:Ozone / Q000494:pharmacology; D010269:Paraquat / Q000494:pharmacology; D010544:Peroxidases / Q000378:metabolism; D010788:Photosynthesis; D018515:Plant Leaves / Q000033:anatomy & histology; D030821:Plants, Genetically Modified; D010947:Plants, Toxic; D017382:Reactive Oxygen Species / Q000378:metabolism; D012965:Sodium Chloride / Q000494:pharmacology; D014026:Nicotiana / Q000235:genetics / Q000378:metabolism*
chemical_list: D017382:Reactive Oxygen Species; D002734:Chlorophyll; D002245:Carbon Dioxide; D012965:Sodium Chloride; D010126:Ozone; D006861:Hydrogen Peroxide; D010544:Peroxidases; D060387:Ascorbate Peroxidases; D002374:Catalase; D005978:Glutathione; D010269:Paraquat; D001205:Ascorbic Acid; D019803:Glutathione Disulfide