Zhu Jianhua, Fu Xinmiao, Koo Yoon Duck, Zhu Jian-Kang, Jenney Francis E, Adams Michael W W, Zhu Yanmei, Shi Huazhong, Yun Dae-Jin, Hasegawa Paul M, Bressan Ray A
Horticulture and Landscape Architecture Department, Purdue University, West Lafayette, IN 47907, USA.
Mol Cell Biol. 2007 Jul;27(14):5214-24. doi: 10.1128/MCB.01989-06. Epub 2007 May 7.
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.
豆蔻酰化钙传感器SOS3及其相互作用的蛋白激酶SOS2在耐盐性中发挥关键调控作用。这两种蛋白中任何一种发生突变都会使拟南芥植株对盐胁迫高度敏感。我们在此报告了一个名为enh1-1的突变体的分离和特性，该突变体增强了sos3-1的盐敏感性，并且自身也导致盐敏感性增加。ENH1编码一种定位于叶绿体的蛋白，其N端区域有一个PDZ结构域，C端部分有一个铁氧化还原蛋白结构域。已知铁氧化还原蛋白参与某些厌氧细菌中超氧化物的还原。enh1-1突变导致活性氧（ROS）积累增加，尤其是在盐胁迫下。ROS在sos2-1突变体中也积累到更高水平，但在sos3-1突变体中则不然。enh1-1突变不会增强sos2-1的表型。此外，enh1-1和sos2-1突变体，但不是sos3-1突变体，对氧化胁迫表现出更高的敏感性。这些结果表明，ENH1通过参与一条可能涉及SOS2但不涉及SOS3的新的耐盐途径，在盐胁迫产生的活性氧解毒中发挥作用。
