Yeast complementation reveals a role for an Arabidopsis thaliana late embryogenesis abundant (LEA)-like protein in oxidative stress tolerance.
A functional cloning approach using the oxidant-sensitive yeast mutant, Deltayap1, was employed to identify plant genes involved in tolerance of oxidative stress. In this screen, we identified an Arabidopsis late embryogenesis-abundant (LEA)-like protein, AtLEA5, which increased the tolerance of Deltayap1 cells to the oxidants H(2)O(2), diamide, menadione and tert-butyl hydroperoxide. Unlike canonical LEAs, AtLEA5 is constitutively expressed in roots and reproductive organs but not in seeds. In leaves of short-day grown plants, AtLEA5 transcripts exhibited a diurnal pattern of regulation, where transcripts were repressed in the light and abundant in the dark. Expression of AtLEA5 in leaves was induced by oxidants, ABA and dehydration. Use of abi1-1 (ABA-insensitive) and aba1-1 (ABA-deficient) Arabidopsis mutants indicated that drought induction of AtLEA5 required ABA synthesis but was independent of the ABI1 gene product. Abscisic acid and H(2)O(2) induction of AtLEA5 was also independent of the OXI1 protein kinase. Constitutive overexpression of AtLEA5 resulted in increased root growth and shoot biomass, both in optimal conditions and under H(2)O(2) stress. However, in comparison with wild type, photosynthesis in overexpressing plants was more susceptible to drought. These features suggest that AtLEA5 has a unique function among LEA proteins in that it plays a specific role in protection against oxidative stress involving decreased photosynthesis. This protein functions as part of a complex network of defences that contribute to robustness of plants under stress by minimizing the negative effects of oxidation.[1]References
- Yeast complementation reveals a role for an Arabidopsis thaliana late embryogenesis abundant (LEA)-like protein in oxidative stress tolerance. Mowla, S.B., Cuypers, A., Driscoll, S.P., Kiddle, G., Thomson, J., Foyer, C.H., Theodoulou, F.L. Plant J. (2006) [Pubmed]
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