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Molecular and Cellular Biology, July 2007, p. 5214-5224, Vol. 27, No. 14
0270-7306/07/$08.00+0 doi:10.1128/MCB.01989-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Department of Horticulture and Landscape Architecture, Purdue University, West Lafayette, Indiana 47907,1 Department of Botany and Plant Sciences, University of California, Riverside, California 92521,2 Division of Applied Life Science (BK21 Program) and Environmental Biotechnology National Core Research Center, Gyeongsang National University, Jinju 660-701, South Korea,3 Department of Biochemistry and Molecular Biology, University of Georgia, Athens, Georgia 30602,4 Department of Chemistry and Biochemistry, Texas Tech University, Lubbock, Texas 794095
Received 23 October 2006/ Returned for modification 20 December 2006/ Accepted 4 April 2007
The myristoylated calcium sensor SOS3 and its interacting protein kinase, SOS2, play critical regulatory roles in salt tolerance. Mutations in either of these proteins render Arabidopsis thaliana plants hypersensitive to salt stress. We report here the isolation and characterization of a mutant called enh1-1 that enhances the salt sensitivity of sos3-1 and also causes increased salt sensitivity by itself. ENH1 encodes a chloroplast-localized protein with a PDZ domain at the N-terminal region and a rubredoxin domain in the C-terminal part. Rubredoxins are known to be involved in the reduction of superoxide in some anaerobic bacteria. The enh1-1 mutation causes enhanced accumulation of reactive oxygen species (ROS), particularly under salt stress. ROS also accumulate to higher levels in sos2-1 but not in sos3-1 mutants. The enh1-1 mutation does not enhance sos2-1 phenotypes. Also, enh1-1 and sos2-1 mutants, but not sos3-1 mutants, show increased sensitivity to oxidative stress. These results indicate that ENH1 functions in the detoxification of reactive oxygen species resulting from salt stress by participating in a new salt tolerance pathway that may involve SOS2 but not SOS3.
Published ahead of print on 7 May 2007.
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