The delayed leaf senescence mutants of Arabidopsis, ore1, ore3, and ore9 are tolerant to oxidative stress

Reactive oxygen species play a critical role in mediating the oxidative damage that causes senescence in a variety of aerobic organisms, from yeast to mammals. Genetic studies of these organisms have revealed that extended longevity is frequently associated with an increased resistance to stress. Ho...

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Published inPlant and cell physiology Vol. 45; no. 7; pp. 923 - 932
Main Authors Woo, H.R. (Pohang Univ. of Science and Technology, Kyungbuk (Korea R.)), Kim, J.H, Nam, H.G, Lim, P.O
Format Journal Article
LanguageEnglish
Published Japan Oxford University Press 01.07.2004
Oxford Publishing Limited (England)
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Summary:Reactive oxygen species play a critical role in mediating the oxidative damage that causes senescence in a variety of aerobic organisms, from yeast to mammals. Genetic studies of these organisms have revealed that extended longevity is frequently associated with an increased resistance to stress. However, the relationship between life span and oxidative stress tolerance in plants is poorly understood. We have investigated the responses to oxidative stress in the delayed leaf senescence mutants of Arabidopsis thaliana, ore1, ore3, and ore9. The detached leaves of these mutants exhibit increased tolerance to various types of oxidative stress. The ore1, ore3, and ore9 mutants were also more tolerant to oxidative stress at the level of the whole plant, as determined by measuring physiological and molecular changes associated with oxidative stress. However, the activities of antioxidant enzymes were similar or lower in the mutants, as compared to wild type. These results suggest that the increased resistance to oxidative stress in the ore1, ore3, and ore9 mutants is not due to enhanced activities of these antioxidant enzymes. Taken together, our findings provide genetic evidence that oxidative stress tolerance is linked to control of leaf longevity in plants.
Bibliography:F30
2005003152
F62
local:pch110
Received November 17, 2003; Accepted April 30, 2004
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content type line 23
ISSN:0032-0781
1471-9053
DOI:10.1093/pcp/pch110