Loss-of-function mutations in DET2 gene lead to an enhanced resistance to oxidative stress in Arabidopsis
Brassinosteroids (BRs) play an essential role in plant growth and development, and have been implicated in many physiological responses. However, little is known about the role of BRs in the plant response to oxidative stress. In this study, we identified a novel insertion allele (det2‐9) of the DET...
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Published in | Physiologia plantarum Vol. 123; no. 1; pp. 57 - 66 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK; Malden, USA
Munksgaard International Publishers
01.01.2005
Blackwell |
Subjects | |
Online Access | Get full text |
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Summary: | Brassinosteroids (BRs) play an essential role in plant growth and development, and have been implicated in many physiological responses. However, little is known about the role of BRs in the plant response to oxidative stress. In this study, we identified a novel insertion allele (det2‐9) of the DET2 gene in Arabidopsis based on molecular, physiological and genetic approaches. We found that the det2 mutant exhibited an enhanced resistance to oxidative stress. The enhanced oxidative stress resistance in det2 plants was correlated with a constitutive increase in superoxide dismutase (SOD) activity and increased transcript levels of the defence gene catalase (CAT). To our knowledge, these results demonstrate, for the first time, that loss‐of‐function mutations in the DET2 gene lead to an enhanced oxidative stress resistance in Arabidopsis. A general explanation is that the long‐term BR deficiency in the det2 mutant results in a constant in vivo physiological stress that, in turn, activates the constitutive expression of some defence genes and, consequently, the activities of related enzymes. |
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Bibliography: | istex:D3D031AB961D2CAA2B428455C7E75AA55AF32557 ark:/67375/WNG-1KJ2F7VH-2 ArticleID:PPL432 Edited by J. B. Reid ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0031-9317 1399-3054 |
DOI: | 10.1111/j.1399-3054.2004.00432.x |