Elucidating the role of ascorbic acid in flowering and pathogen defense in Arabidopsis thaliana

L-ascorbic acid (AA) protects plants against abiotic stress. Previous studies suggested that this antioxidant is also involved in the control of flowering and enhanced disease resistance. This study aimed to elucidate the mechanisms through which AA deficiency promotes flowering and pathogen resistance.;To decipher how AA influences flowering time, four AA-deficient Arabidopsis thaliana mutants vtc1-1, vtc2-1, vtc3-1 and vtc4-1 were grown under short and long days, respectively. These mutants flowered and senesced before the wild type irrespective of the photoperiod, a response that cannot simply be attributed to slightly elevated oxidative stress in the mutants. Genetic analyses demonstrated that various photoperiodic and autonomous flowering pathway mutants are epistatic to the vtc1-1 mutant. Our genetic transcript analyses suggest that AA acts upstream of the photoperiodic and autonomous pathways. However, a specific pathway in which AA acts could not be pinpointed. This suggests that AA plays a more general role in adjusting flowering time depending on environmental conditions.;The AA-deficient Arabidopsis vtc1-1 mutant was previously shown to exhibit increased resistance to the virulent bacterium 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, the four AA-deficient vtc1-1, vtc2-1, vtc3-1, and vtc4-1 mutants were studied. Double mutants with a defect in the AA-biosynthetic gene VTC1 and the SA signaling pathway genes PAD4, EDS5, and NPR1, respectively, were generated and studied. All vtc mutants were more resistant to P. syringae than the wild type. With the exception of vtc4-1, this correlated with constitutively upregulated H2O 2, SA and mRNA levels of PR genes. Double mutants exhibited decreased SA levels and enhanced susceptibility to P. syringae compared to the wild type, suggesting that vtc1-1 requires functional PAD4, EDS5 and NPR1 for SA biosynthesis and pathogen resistance. This work suggests that AA deficiency causes constitutive priming through a buildup of H2O2 that stimulates SA accumulation conferring enhanced disease resistance in vtc1-1, vtc2-1, and vtc3-1, whereas vtc4-1 might activate defense responses after infection