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Free Content Overexpression of a stress-inducible aldehyde dehydrogenase gene from Arabidopsis thaliana in transgenic plants improves stress tolerance

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In plants, oxidative stress is one of the major causes of damage as a result of various environmental stresses. Oxidative stress is primarily because of the excessive accumulation of reactive oxygen species (ROS). The amplification of ROS damage is further stimulated by the accumulation of toxic degradation products, i.e. aldehydes, arising from reactions of ROS with lipids and proteins. Previously, the isolation of dehydration-inducible genes encoding aldehyde dehydrogenases (ALDHs) was reported from the desiccation-tolerant plant Craterostigma plantagineum and Arabidopsis thaliana. ALDHs belong to a family of NAD(P)+-dependent enzymes with a broad substrate specificity that catalyze the oxidation of various toxic aldehydes to carboxylic acids. Analysis of transcript accumulation revealed that Ath-ALDH3 is induced in response to NaCl, heavy metals (Cu2+ and Cd2+), and chemicals that induce oxidative stress (methyl viologen (MV) and H2O2). To investigate the physiological role and possible involvement of ALDHs in stress protection, we generated transgenic Arabidopsis plants overexpressing Ath-ALDH3. Transgenic lines show improved tolerance when exposed to dehydration, NaCl, heavy metals (Cu2+ and Cd2+), MV, and H2O2. Tolerance of transgenic plants is correlated with decreased accumulation of lipid peroxidation-derived reactive aldehydes (as measured by malondialdehyde) compared to wild-type plants. Increased activity of Ath-ALDH3 appears to constitute a detoxification mechanism that limits aldehyde accumulation and oxidative stress, thus revealing a novel pathway of detoxification in plants. We suggest that Ath-ALDH3 could be used to obtain plants with tolerance to diverse environmental stresses.
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Keywords: abiotic stress; aldehyde dehydrogenase; lipid peroxidation; oxidative stress

Document Type: Research Article

Affiliations: Institute of Botany, University of Bonn, Kirschallee 1, Bonn 53115, Germany

Publication date: August 1, 2003

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