Genome stability of vtc1, tt4, and tt5 Arabidopsis thaliana mutants impaired in protection against oxidative stress

Summary Reactive oxygen species (ROS) are formed upon normal cellular metabolism or influence of environmental factors and, at normal levels, they play an important physiological role. However, at elevated levels, radicals are toxic and extremely dangerous to all cellular components, including DNA....

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Veröffentlicht in:The Plant journal : for cell and molecular biology 2004-04, Vol.38 (1), p.60-69
Hauptverfasser: Filkowski, Jody, Kovalchuk, Olga, Kovalchuk, Igor
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Sprache:eng
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Zusammenfassung:Summary Reactive oxygen species (ROS) are formed upon normal cellular metabolism or influence of environmental factors and, at normal levels, they play an important physiological role. However, at elevated levels, radicals are toxic and extremely dangerous to all cellular components, including DNA. To efficiently protect themselves, plants have developed sophisticated mechanisms for radical screening and scavenging. In this paper, we analyzed the genome stability of several plant mutants impaired in the protection against free radicals. We crossed the well‐known uidA recombination reporter line 651 to flavonoid (tt4 and tt5) and Vitamin C (vtc1)‐deficient plants. We found that in all lines tested, both spontaneous and induced (UVC and Rose Bengal (RB)) recombination was higher than in the original 651 parental line. The mRNA expression levels of various DNA repair (RAD1, RAD54‐like, MSH3) as well as radical scavenging genes (GPx1, CAT, FSD3) exhibited substantial differences in both control and induced conditions. Our data show that plants impaired in certain aspects of the protection against elevated levels of free radicals induce the production of scavenging enzymes earlier than wild‐type (wt) plants, and the higher level of radical species results in the increased incidence of spontaneous double‐strand breaks resulting in a higher expression of DNA repair genes.
ISSN:0960-7412
1365-313X
DOI:10.1111/j.1365-313X.2004.02020.x