UV-induced DNA damage promotes resistance to the biotrophic pathogen Hyaloperonospora parasitica in Arabidopsis

Kunz, Bernard A., Dando, Paige K., Grice, Desma M., Mohr, Peter G., Schenk, Peer M. and Cahill, David M. 2008, UV-induced DNA damage promotes resistance to the biotrophic pathogen Hyaloperonospora parasitica in Arabidopsis, Plant physiology, vol. 148, no. 2, pp. 1021-1031.

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Title UV-induced DNA damage promotes resistance to the biotrophic pathogen Hyaloperonospora parasitica in Arabidopsis
Author(s) Kunz, Bernard A.
Dando, Paige K.
Grice, Desma M.
Mohr, Peter G.
Schenk, Peer M.
Cahill, David M.
Journal name Plant physiology
Volume number 148
Issue number 2
Start page 1021
End page 1031
Total pages 11
Publisher American Society of Plant Physiologists
Place of publication Bethesda, Md, United States
Publication date 2008-10
ISSN 0032-0889
1532-2548
Summary 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 (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 7 d after UV exposure. Limiting repair of UV photoproducts by postirradiation incubation in the dark, or mutational inactivation of cyclobutane pyrimidine dimer photolyase, (6-4) photoproduct photolyase, or nucleotide excision repair increased the magnitude of UV-induced pathogen resistance. In the absence of treatment with 254-nm UV, plant nucleotide excision repair mutants also defective for cyclobutane pyrimidine dimer or (6-4) photoproduct photolyase displayed resistance to H. parasitica, partially attributable to short wavelength UV-B (280–320 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 Arabidopsis proteins to activate an immune response.
Language eng
Field of Research 060704 Plant Pathology
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2008, American Society of Plant Biologists
Persistent URL http://hdl.handle.net/10536/DRO/DU:30017500

Document type: Journal Article
Collection: School of Life and Environmental Sciences
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