Abstract
Summary
Osmotic stress activates the expression of many plant genes through ABA‐dependent as well as ABA‐independent signaling pathways. We report here the characterization of a novel mutant of Arabidopsis thaliana, hos5‐1, which exhibits increased expression of the osmotic stress responsive RD29A gene. The expression of several other stress genes are also enhanced by the hos5‐1 mutation. The enhanced expression is specific to ABA and osmotic stress because low temperature regulation of these genes is not altered in the mutant. Genetic analysis indicated that hos5‐1 is a recessive mutation in a single nuclear gene on chromosome III. Double mutant analysis of hos5‐1 and the ABA‐deficient aba1‐1 as well as the ABA‐insensitive abi1‐1 mutant indicated that the osmotic stress hypersensitivity of hos5‐1 is not affected by ABA deficiency or insensitivity. Furthermore, combined treatments of hos5‐1 with ABA and osmotic stress had an additive effect on RD29A‐LUC expression. These results suggest that the osmotic stress hypersensitivity in hos5‐1 may be ABA‐independent. The germination of hos5‐1 seeds was more resistant to ABA. However, the hos5‐1 mutation did not influence stomatal control and only slightly affected the regulation of growth and proline accumulation by ABA. The hos5‐1 mutation reveals a negative regulator of osmotic stress‐responsive gene expression shared by ABA‐dependent and ABA‐independent osmotic stress signaling pathways.