A major obstacle in understanding the role of GSTs in infected plants is the fact that the endogenous, physiological substrates of GST isoenzymes are in most cases not known. Among the possible substrates are fatty acid hydroperoxides, which are major products of oxidative membrane damage and can be also produced by lipoxygenase action. Bartling et al. (1993) isolated a cDNA clone for a novel GST from Arabidopsis. The encoded protein catalysed the decomposition of several fatty acid hydroperoxides into the corresponding hydroxy-acids, with the concomitant formation of GSSG (Figure 4). However, the enzyme did not use H202 as substrate. These data confirmed that GSTs contribute to the protection against oxidative damage to membranes in plants.
Ethacrynic acid, which resembles naturally occurring alkenals accumulating during oxidative stress (Croft et al. 1993), was used as a model GST substrate (Edwards 1996). Exposure of pea epicotyls to a fungal cell wall elicitor or GSH markedly stimulated the GST activity toward ethacrynic acid, which was not detectable in water-treated controls. It is important to note that elicitations did not increase GST activities towards the generally used xenobiotic substrates l-chloro-2,4-dinitrobenzene or fluorodifen. Fungal elicitor and GSH treatments resulted also in the accumulation of the phy-toalexin pisatin. It is possible that elicitor-induced GSTs function to conju gate toxic alkenals, which might accumulate in plants during oxidative stress (Edwards 1996).
The artificial elevation of GST in plant tissues can provide valuable information on the role of GST in infected plants. Recently a substantial induction of GST activity was observed in Xanthi-nc tobacco leaf discs treated with the monoterpene compound (S)-carvone. Tobacco leaf discs with induced GST activities were infected by TMV 2 days after (S)-carvone pre-treatment. The induction of GST activity markedly suppressed the development of necrotic lesions induced by TMV, but did not decrease the foliar virus concentration. These results confirmed previous suppositions about the protective role of GST in virus-infected tobacco leaves (Gullner et al. 1999). GST activities of soybean cells were markedly increased by 2 days incubations with BTH and salicylic acid, but the resistance of the treated cell cultures toward infections was not investigated (Knorzer et al. 1999).
Summarizing the above reports on GST, it seems that the role of GSTs in infected plants is the suppression of necrotic disease symptoms by the detoxification of toxic lipid hydroperoxides that derive from peroxidation of cell membranes. In the future, this supposition may be confirmed by the study of transgenic plants overexpressing GST isoenzymes and of transformants expressing GSTs in antisense direction. Tobacco plants have been transformed with genes encoding GST (Roxas et al. 1997, Thompson et al. 1998). These transgenic tobacco plants overexpressing GST were more resistant towards abiotic stress effects than wild type plants. The effects of microbial infections on these transgenic plants have not been reported yet.
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