Abstract

In order to investigate the effects of a permanent increase in cellular H(2)O(2) on cation homeostasis we have studied a T-DNA insertion mutant of the Arabidopsis CATALASE 2 gene. This mutant (cat2-1) exhibits 20% of wild-type leaf catalase activity and accumulates more H(2)O(2) than the wild type under normal growth conditions. In addition to reduced size, a pale green color and great reduction in secondary roots, the cat2-1 mutant exhibited increased sensitivity to H(2)O(2), NaCl, norspermidine, high light and cold stress. On the other hand, the germination of the cat2-1 mutant is more tolerant to lithium than the wild type. This novel phenotype cannot be explained by changes in lithium transport. Actually, the uptake of lithium (and of other toxic cations such as sodium and norspermidine) is increased in the cat2-1 mutant while K(+) levels were decreased. The lithium tolerance of this mutant seems to result both from insensitivity to the inhibitory ethylene induced by this cation and a reduced capability for ethylene production. Accordingly, induction by ethylene of responsive genes such as PR4 and EBP/ERF72 is decreased in cat2-1. Mutants insensitive to ethylene such as etr1-1 and ein3-3 are lithium tolerant, and inhibition of ethylene biosynthesis with 2-aminoisobutyrate protects against lithium toxicity. Microarray analysis of gene expression indicates that the expression of genes related to cation transport and ethylene synthesis and perception was not altered in the cat2-1 mutant, suggesting that H(2)O(2) modulates these processes at the protein level. These results uncover a cross-talk between oxidative stress, cation homeostasis and ethylene.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.