title: Ascorbic acid deficiency in arabidopsis induces constitutive priming that is dependent on hydrogen peroxide, salicylic acid, and the NPR1 gene.
abstract: The ascorbic acid (AA)-deficient Arabidopsis thaliana vtc1-1 mutant exhibits increased resistance to the virulent bacterial pathogen Pseudomonas syringae. This response correlates with heightened levels of salicylic acid (SA), which induces antimicrobial pathogenesis-related (PR) proteins. To determine if SA-mediated, enhanced disease resistance is a general phenomenon of AA deficiency, to elucidate the signal that stimulates SA synthesis, and to identify the biosynthetic pathway through which SA accumulates, we studied the four AA-deficient vtc1-1, vtc2-1, vtc3-1, and vtc4-1 mutants. We also studied double mutants defective in the AA-biosynthetic gene VTC1 and the SA signaling pathway genes PAD4, EDS5, and NPR1, respectively. All vtc mutants were more resistant to P. syringae than the wild type. With the exception of vtc4-1, this correlated with constitutively upregulated H(2)O(2), SA, and messenger RNA levels of PR genes. Double mutants exhibited decreased SA levels and enhanced susceptibility to P. syringae compared with the wild type, suggesting that vtc1-1 requires functional PAD4, EDS5, and NPR1 for SA biosynthesis and pathogen resistance. We suggest that AA deficiency causes constitutive priming through a buildup of H(2)O(2) that stimulates SA accumulation, conferring enhanced disease resistance in vtc1-1, vtc2-1, and vtc3-1, whereas vtc4-1 might be sensitized to H(2)O(2) and SA production after infection.
authors.affiliation: Department Of Biology, West Virginia University, 53 Campus Drive, Morgantown, USA.
authors.forename: Madhumati
authors.initials: M
authors.lastname: Mukherjee
authors.forename: Katherine E
authors.initials: KE
authors.lastname: Larrimore
authors.forename: Naushin J
authors.initials: NJ
authors.lastname: Ahmed
authors.forename: Tyler S
authors.initials: TS
authors.lastname: Bedick
authors.forename: Nadia T
authors.initials: NT
authors.lastname: Barghouthi
authors.forename: M Brian
authors.initials: MB
authors.lastname: Traw
authors.forename: Carina
authors.initials: C
authors.lastname: Barth
mesh_terms: D017360:Arabidopsis / Q000235:genetics / Q000378:metabolism* / Q000382:microbiology; D029681:Arabidopsis Proteins / Q000235:genetics / Q000378:metabolism*; D001205:Ascorbic Acid / Q000378:metabolism*; D002265:Carboxylic Ester Hydrolases / Q000235:genetics / Q000378:metabolism; D018506:Gene Expression Regulation, Plant; D006861:Hydrogen Peroxide / Q000378:metabolism*; D007113:Immunity, Innate / Q000235:genetics; D026901:Membrane Transport Proteins / Q000235:genetics / Q000378:metabolism; D009154:Mutation; D010935:Plant Diseases / Q000235:genetics / Q000382:microbiology; D044224:Pseudomonas syringae / Q000472:pathogenicity; D020133:Reverse Transcriptase Polymerase Chain Reaction; D020156:Salicylic Acid / Q000378:metabolism*; D014774:Virulence
chemical_list: D029681:Arabidopsis Proteins; C455514:EDS5 protein, Arabidopsis; D026901:Membrane Transport Proteins; C105496:NPR1 protein, Arabidopsis; D006861:Hydrogen Peroxide; D002265:Carboxylic Ester Hydrolases; C400766:PAD4 protein, Arabidopsis; D020156:Salicylic Acid; D001205:Ascorbic Acid