title: Ascorbic acid deficiency activates cell death and disease resistance responses in Arabidopsis.
abstract: Programmed cell death, developmental senescence, and responses to pathogens are linked through complex genetic controls that are influenced by redox regulation. Here we show that the Arabidopsis (Arabidopsis thaliana) low vitamin C mutants, vtc1 and vtc2, which have between 10% and 25% of wild-type ascorbic acid, exhibit microlesions, express pathogenesis-related (PR) proteins, and have enhanced basal resistance against infections caused by Pseudomonas syringae. The mutants have a delayed senescence phenotype with smaller leaf cells than the wild type at maturity. The vtc leaves have more glutathione than the wild type, with higher ratios of reduced glutathione to glutathione disulfide. Expression of green fluorescence protein (GFP) fused to the nonexpressor of PR protein 1 (GFP-NPR1) was used to detect the presence of NPR1 in the nuclei of transformed plants. Fluorescence was observed in the nuclei of 6- to 8-week-old GFP-NPR1 vtc1 plants, but not in the nuclei of transformed GFP-NPR1 wild-type plants at any developmental stage. The absence of senescence-associated gene 12 (SAG12) mRNA at the time when constitutive cell death and basal resistance were detected confirms that elaboration of innate immune responses in vtc plants does not result from activation of early senescence. Moreover, H2O2-sensitive genes are not induced at the time of systemic acquired resistance execution. These results demonstrate that ascorbic acid abundance modifies the threshold for activation of plant innate defense responses via redox mechanisms that are independent of the natural senescence program.
authors.affiliation: Departamento de Química Biológica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Ciudad Universitaria, Cordoba 5000, Argentina.
authors.forename: Valeria
authors.initials: V
authors.lastname: Pavet
authors.forename: Enrique
authors.initials: E
authors.lastname: Olmos
authors.forename: Guy
authors.initials: G
authors.lastname: Kiddle
authors.forename: Shaheen
authors.initials: S
authors.lastname: Mowla
authors.forename: Sanjay
authors.initials: S
authors.lastname: Kumar
authors.forename: John
authors.initials: J
authors.lastname: Antoniw
authors.forename: María E
authors.initials: ME
authors.lastname: Alvarez
authors.forename: Christine H
authors.initials: CH
authors.lastname: Foyer
mesh_terms: D000975:Antioxidants / Q000378:metabolism; D017360:Arabidopsis / Q000033:anatomy & histology / Q000166:cytology* / Q000254:growth & development / Q000378:metabolism*; D029681:Arabidopsis Proteins / Q000378:metabolism; D001205:Ascorbic Acid / Q000378:metabolism* / Q000494:pharmacology; D016923:Cell Death / Q000187:drug effects; D002467:Cell Nucleus / Q000378:metabolism; D048429:Cell Size; D003546:Cysteine Endopeptidases / Q000378:metabolism; D018506:Gene Expression Regulation, Plant; D005798:Genes, Bacterial / Q000235:genetics; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D009154:Mutation / Q000235:genetics; D010084:Oxidation-Reduction; D010641:Phenotype; D010935:Plant Diseases / Q000382:microbiology*; D018515:Plant Leaves / Q000166:cytology / Q000254:growth & development / Q000378:metabolism / Q000382:microbiology; D021381:Protein Transport; D044224:Pseudomonas syringae / Q000235:genetics / Q000502:physiology
chemical_list: D000975:Antioxidants; D029681:Arabidopsis Proteins; C105496:NPR1 protein, Arabidopsis; C402082:SAG12 protein, Arabidopsis; D003546:Cysteine Endopeptidases; D005978:Glutathione; D001205:Ascorbic Acid; D019803:Glutathione Disulfide