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First published online October 21, 2005; 10.1104/pp.105.067686

Plant Physiology 139:1291-1303 (2005)
© 2005 American Society of Plant Biologists

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ENVIRONMENTAL STRESS AND ADAPTATION TO STRESS

Ascorbic Acid Deficiency Activates Cell Death and Disease Resistance Responses in Arabidopsis1

Valeria Pavet, Enrique Olmos2, Guy Kiddle, Shaheen Mowla, Sanjay Kumar3, John Antoniw, María E. Alvarez and Christine H. Foyer*

Centro de Investigaciones en Química Biológica de Córdoba/Consejo Nacional de Investigaciones Científicas y Técnicas, Departamento de Química Biológica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Ciudad Universitaria, Cordoba 5000, Argentina (V.P., M.E.A.); and Crop Performance and Improvement Division (E.O., G.K., S.M., S.K., C.H.F.) and Wheat Pathogenesis Program, Plant-Pathogen Interactions Division (J.A.), Rothamsted Research, Harpenden, Hertfordshire AL5 2JQ, United Kingdom

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.

1 This work was supported by the Biotechnology and Biological Sciences Research Council (C.F., G.K., and J.A.); grants from Agencia Nacional de Promoción Científica y Tecnológica (BID 1201/OC–AR PICT 01–10123) and Fundación Antorchas and Secretaria de Ciencia y Tecnologia/Universidad Nacional de Córdoba (to M.E.A.); the Department of Biotechnology, Government of India, for a Biotechnology Overseas Associateship Award (to S.K.); the Royal Society (U.K.) for a short-term fellowship (to S.M.); CONICET for a fellowship (to V.P.); and the Spanish Government for a Mobility Grant of Researcher, Ministerio de Educacion y Ciencia (PR2004–0361; to E.O.).

2 Present address: Centro de Edafologia y Biologia Aplicada del Segura/Consejo Superior de Investigaciones Científicas, Department of Plant Physiology, P.O. Box 164, 30080 Murcia, Spain.

3 Present address: Biotechnology Division, Institute of Himalayan Bioresource Technology, P.O. Box 6, Palampur–176 061 (HP), India.

The authors responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) are: Christine H. Foyer (christine.foyer{at}bbsrc.ac.uk) and María E. Alvarez (malena{at}mail.fcq.unc.edu.ar).

Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.105.067686.

* Corresponding author; e-mail christine.foyer{at}bbsrc.ac.uk; fax 0044–1582–763010.

Received June 28, 2005; returned for revision August 12, 2005; accepted August 12, 2005.




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