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Published on July 30, 2008; 10.1104/pp.108.125435

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Received June 26, 2008
Accepted July 28, 2008

UV Induced DNA Damage Promotes Resistance to the Biotrophic Pathogen Hyaloperonospora parasitica in Arabidopsis

Bernard A. Kunz , Paige K. Dando , Desma M. Grice , Peter G. Mohr , Peer M. Schenk , and David M. Cahill *

School of Life and Environmental Sciences, Deakin University, Geelong, Victoria, 3217, Australia; School of Integrative Biology, The University of Queensland, St. Lucia, Queensland, 4072, Australia

* Corresponding author; email: cahill{at}deakin.edu.au.

Plant innate immunity to pathogenic microorganisms is activated in response to recognition of extracellular or intracellular pathogen molecules by transmembrane receptors or resistance proteins, respectively. The defense signaling pathways share components with those involved in plant responses to UV radiation, which can induce expression of plant genes important for pathogen resistance. Such intriguing links suggest that UV treatment might activate resistance to pathogens in normally susceptible host plants. Here we demonstrate that pre-inoculative UV (254 nm) irradiation of Arabidopsis thaliana susceptible to infection by the biotrophic oomycete Hyaloperonospora parasitica, the causative agent of Downy Mildew, induces dose- and time-dependent resistance to the pathogen detectable up to seven days after UV exposure. Limiting repair of UV photoproducts by post-irradiation incubation in the dark, or mutational inactivation of cyclobutane pyrimidine dimer (CPDs) photolyase, (6-4) photoproduct (6-4PP) photolyase or nucleotide excision repair (NER) increased the magnitude of UV-induced pathogen resistance. In the absence of treatment with 254-nm UV, plant NER mutants also defective for CPD or 6-4PP photolyase displayed resistance to H. parasitica partially attributable to short wavelength UV-B (280 to 320 nm) radiation emitted by incubator lights. These results indicate UV irradiation can initiate the development of resistance to H. parasitica in plants normally susceptible to the pathogen, and point to a key role for UV-induced DNA damage. They also suggest UV treatment can circumvent the requirement for recognition of H. parasitica molecules by A. thaliana proteins to activate an immune response.






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