Ascorbic acid deficiency activates cell death and disease resistance responses in Arabidopsis thaliana

VALERIA PAVET; ENRIQUE OLMOS; GUY KIDDLE; SHAHEEN MOWLA; SANJAY KUMAR; JOHN ANTONIW,; MARIA E. ALVAREZ; CHRISTINE H. FOYER

AMER SOC PLANT BIOLOGISTS

Lugar: Rockville; Año: 2005 vol. 139 p. 1291 - 1291

rogrammed 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