Abstract

A hypothesis developed in two earlier papers (Capell and Dörffling 1993, Janowiak and Dörffling 1996), but critically reinvestigated recently by Ristic et al. 1998 was tested again with new material and methods. According to the hypothesis, chilling tolerant maize genotypes accumulate abscisic acid (ABA) faster and in higher amounts than chilling sensitive genotypes when exposed to chilling stress. This relationship is in accordance with a suggested protective role of ABA against chilling injury. The hypothesis was tested in two ways: first by investigating 20 new maize genotypes with defined differences in chilling tolerance, second by manipulating the endogenous level of ABA during a low temperature treatment by applying the ABA biosynthesis inhibitor norflurazon and measuring the resulting chilling tolerance. Results of the first approach showed that the accumulation of ABA in the third leaves determined by an indirect ELISA after two days of chilling at 4 °C was significantly correlated with chilling tolerance as measured by necrotic injury and by ϕPSII of the 20 tested genotypes. Accumulation of ABA induced by low temperature was significantly higher in the group of chilling tolerant genotypes than in that of chilling sensitive ones. It was inversely related to chilling-induced water loss. Results of the second experiment showed that norflurazon-treated seedlings were less chilling tolerant and accumulated less ABA than untreated ones. Application of ABA compensated the reduction in chilling tolerance by norflurazon. It is concluded that the results support the above mentioned hypothesis that chilling tolerance in maize is related to the ability to accumulate ABA as a protective agent against chilling injury.

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