Introduction

Abscisic acid (ABA) mediates embryo maturation during late seed development. Maturation involves various morphogenic and biochemical changes including the programming of embryo dormancy and desiccation tolerance. Genetic analysis implicate ABA in the control of dormancy (Koorneef et al., 1984; McCarty et al., 1989). Molecular studies suggest that certain ABA-responsive genes expressed during late embryogenesis are part of a developmental programme leading to desiccation tolerance (Bartels et al., 1988; Dure et al., 1989). Certain of these genes are also expressed in vegetative tissues during osmotic stress (Mundy & Chua, 1988; Gomez et al., 1988), at which time ABA levels rise and growth is inhibited. At present, the connection between ABA effects during embryogenesis and in vegetative tissues is unclear, in part because we do not know the function(s) of most of the major ABA-responsive genes (for reviews, see Skriver & Mundy, 1990; Galau et al., 1991; McCarty & Carson, 1991). However, the hormone mediates responses to osmotic stress, and causes developmental or growth inhibition in both embryonic and vegetative tissues (Smart & Trewavas, 1984; Bensen et al., 1988; Creelman, 1989).

In many fruits, embryo dormancy is broken by environmental cues and physiological factors which initiate germination. In cereal seeds, gibberellic acid (GA) appears to be one such factor by promoting this expression of genes encoding α-amylase and other hydrolases. This effect of GA can be inhibited by ABA (Jacobsen & Beach, 1985; Nolan & Ho, 1988; Huttly & Baulcombe, 1989), an antagonism which may mediate physiological changes controlling the switch from seed quiescence or dormancy to germination.