Poster: Oxidative Stress

Abs # 115: The ascorbate-deficient Arabidopsis mutant vtc1 has altered responses to both high light and pathogens

Presenter:	Barth, Carina , cb244@cornell.edu
Authors	Barth, Carina  (A)   Moeder, Wolfgang  (A)   Klessig, Daniel F (A)   Conklin, Patricia L (B)
Affiliations:	(A): Boyce Thompson Institute for Plant Research (B): Department of Biological Sciences, State University of New York College at Cortland

The ozone-sensitive Arabidopsis mutant vtc1 is deficient in L-ascorbic acid due to a mutation in GDP-mannose pyrophosphorylase (Conklin et al. 1999, PNAS 96, 4198-203), an enzyme involved in the proposed ascorbate biosynthetic pathway (Wheeler et al. 1998, Nature 393, 365-9). In this study, the physiology of this ascorbate deficiency was investigated in response to abiotic (high light) and biotic (virulent pathogens) stress. Upon high-light exposure, a lower xanthophyll cycle activity which is accompanied by decreased non-photochemical quenching was observed in vtc1 compared to wild type. However, potential activities of photosystems I and II are similarly affected in both genotypes. Elevation of the endogenous ascorbate content by feeding with the direct precursor of ascorbate, L-galactono-1,4-lactone, restored xanthophyll cycle activity and non-photochemical quenching in vtc1, but the degree of photoinhibition was neither diminished in wild type nor in vtc1. We conclude that the ascorbate deficiency in vtc1 does not lead to pronounced oxidative stress generated by high light in the chloroplast. Infection of wild-type and vtc1 leaves with either virulent Pseudomonas syringae or Peronospora parasitica resulted in largely reduced bacterial and hyphal growth respectively in vtc1, indicating that vtc1 is more resistant to these pathogens. Moreover, induction of pathogenesis-related proteins PR1 and PR5 is significantly higher in vtc1 than in wild type when challenged with virulent Pseudomonas syringae, although PR proteins are not constitutively elevated in this mutant. Salicylic acid content is slightly increased in vtc1. We surmise that the pathogen resistance of vtc1 is at least partially due to a stronger, salicylic-acid dependent up-regulation of the defense response.