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UV induces resistance in Arabidopsis Thaliana to the Oomycete Pathogen Hyaloperonospora Parasitica

Cahill, D., Kunz, B., Dando, P., Grice, D., Wade, B. and McKenzie, K. 2006, UV induces resistance in Arabidopsis Thaliana to the Oomycete Pathogen Hyaloperonospora Parasitica, in ComBio 2006 : Proceedings of the Australian Society for Biochemistry and Molecular Biology Combined Conference, Australian Society for Biochemistry and Molecular Biology Inc, Kent Town, S.Aust., pp. 52-52.

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Title UV induces resistance in Arabidopsis Thaliana to the Oomycete Pathogen Hyaloperonospora Parasitica
Author(s) Cahill, D.
Kunz, B.
Dando, P.
Grice, D.
Wade, B.
McKenzie, K.
Conference name Australian Society for Biochemistry and Molecular Biology Combined Conference (2006 : Brisbane, Qld.)
Conference location Brisbane, Qld.
Conference dates 24-28 Sep. 2006
Title of proceedings ComBio 2006 : Proceedings of the Australian Society for Biochemistry and Molecular Biology Combined Conference
Publication date 2006
Start page 52
End page 52
Publisher Australian Society for Biochemistry and Molecular Biology Inc
Place of publication Kent Town, S.Aust.
Summary Owing to their sessile nature, plants have evolved mechanisms to minimise the damaging effects of abiotic and biotic stresses. Attack by pathogenic fungi, viruses and bacterium is a major type of biotic stress. To resist infection, plants recognise invading pathogens and induce disease resistance through multiple signal transduction pathways. In addition, appropriate stimulation can cause plants to increase their resistance to future pathogen attack. We have found that exposure to non-lethal doses of UV-C (254 nm) renders a normally susceptible ecotype of Arabidopsis thaliana resistant to the biotrophic Oomycete pathogen Hyaloperonospora parasitica. The UV treatment induces an incompatible response in a dose-dependent fashion, and is still effective upon pathogen inoculation up to seven days after UV exposure. The degree of resistance diminishes with time but higher doses result in greater levels of resistance, even after seven days. Furthermore, the effect is systemic, occurring in parts of the plant that have not been irradiated. Incubation in the dark post?irradiation and prior to infection reduces the UV dose required to generate a specific level of pathogen resistance without affecting the duration of resistance. These observations, plus the inability of plants to photoreactivate UV photoproducts in the dark, strongly suggest that DNA damage induces the resistance phenotype. Currently, we are assessing the influence of DNA repair defects on UV-induced resistance, following the expression of a number of defence?related genes post-UV-C irradiation, and assessing the effect of UV in plant mutants deficient in specific signalling molecules involved in resistance.
Notes Reproduced with the kind permission of the copyright owner.
Language eng
Field of Research 060704 Plant Pathology
Socio Economic Objective 970105 Expanding Knowledge in the Environmental Sciences
HERDC Research category E3 Extract of paper
Copyright notice ©2006, Australian Society for Biochemistry and Molecular Biology
Persistent URL http://hdl.handle.net/10536/DRO/DU:30014699

Document type: Conference Paper
Collections: School of Life and Environmental Sciences
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