A mutant ofNicotiana plumbaginifolia, CKR1, isolated on the basis of its enhanced resistance to cytokinins was found to have a greater tendency to wilt than the wild type (Blonstein et al., 1991, Planta183, 244–250). Further characterisation has shown that the wiltiness in the mutant is not caused by an insensitivity to abscisic acid (ABA) because the external application of ABA leads to stomatal closure and phenotypic reversion. The basal ABA level in the mutant is<20 of that in the wild type. Following stress, the ABA level in wild-type leaves increases by approx 9-to 10-fold while the mutant shows only a slight increase. This deficiency in ABA is unlikely to be the consequence of accelerated catabolism as the levels of two major metabolites of ABA, phaseic and dihydrophaseic acid, are also much reduced in the mutant. The qualitative and quantitative distributions of carotenoids, the presumed presursors of ABA, are the same for the leaves of both wild type and mutant. Biosynthesis of ABA at the C15 level was investigated by feeding xanthoxin (Xan) to detached leaves. Wild-type leaves convert between 9–19 of applied Xan to ABA while the mutant converts less than 1. The basal level oftrans-ABA-alcohol (t-ABA-alc) is 3-to 10-fold greater in the mutant and increases by a further 2.5-to 6.0-fold after stress. This indicates that the lesion in the wilty mutant ofN. plumbaginifoliaaffects the conversion of ABA-aldehyde to ABA, as in theflaccaandsitiensmutants of tomato and thedroopymutant of potato (Taylor et al., 1988, Plant Cell Environ.11, 739–745; Duckham et al., 1989, J. Exp. Bot.217, 901–905). Wild-type tomato andN. plumbaginifolialeaves can converttrans-Xan intot-ABA-alc, and Xan into ABA, while those offlaccaand the wiltyN. plumbaginifoliamutant convert both Xan andt-Xan tot-
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