Submitted to: Plant Cell and Environment
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/27/2006
Publication Date: 7/2/2006
Citation: Chen, J., Burke, J.J., Xin, Z., Xu, C., Velten, J.P. 2006. Characterization of the arabidopsis thermosensitive mutant ATTS02 reveals an important role for galactolipids in thermotolerance. Plant Cell and Environment. 29(7):437-1448.
Technical Abstract: Plants are constantly challenged with various abiotic stresses in their natural environment. Elevated temperatures combined with drought during growing season have a detrimental impact on overall plant growth and productivity. Many plants increase their tolerance to high temperatures through an adaptation response known as acquired thermotolerance. To identify the various mechanisms plants have evolved to cope with high temperature stress, we have isolated a series of Arabidopsis mutants that are defective in acquired thermotolerance after a 24 h exposure to 38°C, a temperature treatment that induces thermotolerance in wild-type plants. One of these mutants, atts02, was characterized in detail. The expression of several heat shock proteins (HSPs) in high temperature treated atts02 mutant was similar to identically treated wild-type plants, suggesting that thermosensitivity in the atts02 mutant was not caused by a defect in the production of HSPs. The mutated gene in atts02 was identified by positional cloning to be digalactosyldiacylglycerol synthase 1 (DGD1). Thermosensitivity in atts02 was associated with 1) a decreased ratio of digalactosyldiacyl glycerol (DGDG) to monogalactosyldiacylglycerol (MGDG), resulting from reduced levels of DGDG in and the inability to increase activity DGDG content upon high temperature treatment; and 2) increased levels of unsaturated MGDG and DGDG lipid species derived from endoplasmic reticulum (ER) biosynthetic pathways, especially after high temperature treatment. The increased unsaturation of ER-derived MGDG was associated with a concomitant increase in the saturation of MGDG derived from plastid (BETTER THAN PROKARYOTIC???) pathways in the high temperature treated mutants, suggesting that plants may possess inherent compensatory mechanisms to partially offset a deficiency caused by this mutation.