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DNA repair deficiencies increase the resistance of Arabidopsis Thaliana to Hyaloperonospora Parasitica

Grice, D., Dando, P., Mohr, P., McKenzie, K., Wade, B., Kunz, B. and Cahill, D. 2006, DNA repair deficiencies increase the resistance of Arabidopsis Thaliana to 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. 138-138.

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Title DNA repair deficiencies increase the resistance of Arabidopsis Thaliana to Hyaloperonospora Parasitica
Author(s) Grice, D.
Dando, P.
Mohr, P.
McKenzie, K.
Wade, B.
Kunz, B.
Cahill, D.
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 138
End page 138
Publisher Australian Society for Biochemistry and Molecular Biology Inc
Place of publication Kent Town, S.Aust.
Summary We have found that UV-C treatment of Arabidopsis thaliana induces resistance to the biotrophic pathogen Hyaloperonospora parasitica, and our data suggest UV induced DNA photoproducts are involved (see accompanying abstract by K.G. McKenzie et al.). To address the potential role of DNA damage, we have examined the effect of mutations in nucleotide excision repair (uvr1-1), photoreactivation of cyclobutane pyrimidine dimers (uvr2-1) or flavonoid production (tt5) on the resistance of Arabidopsis to the pathogen with or without pre-inoculation treatment with UV-C. In the mutant backgrounds, UV-C induced pathogen resistance (as measured by decreased conidiophore formation) to the same degree as in the wildtype plants, but much lower UV doses were required (e.g., 100 Jm-2 in the mutant vs. 400 Jm-2 in the wildtype). This is the result expected if damage to DNA rather than a non DNA target is involved. Interestingly, in the absence of UV-C, the tt5 mutation alone resulted in a slight increase in resistance. However, when coupled with uvr1-1, resistance was enhanced to an even greater extent. Remarkably, the tt5 uvr1-1 uvr2-1 triple mutant was completely resistant to the pathogen. Since tt5 mutants are sensitive to reactive oxygen species, which can cause DNA damage susceptible to nucleotide excision repair, our results suggest that in addition to UV photoproducts, an accumulation of endogenous oxidative DNA damage may also trigger resistance to the pathogen. We are currently examining pathogen resistance in other DNA repair deficient mutants, and quantifying UV-C-induced DNA damage in Arabidopsis in order to assess the relationship between damage levels and the extent of 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:30014696

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