We screened for mutations that either enhanced or suppressed the abscisic acid (ABA)-resistant seed germination phenotype of the Arabidopsis abi1-1 mutant. Alleles of the constitutive ethylene response mutant ctr1 and ethyleneinsensitive mutant ein2 were recovered as enhancer and suppressor mutations, respectively. Using these and other ethylene response mutants, we showed that the ethylene signaling cascade defined by the ETR1 , CTR1 , and EIN2 genes inhibits ABA signaling in seeds. Furthermore, epistasis analysis between ethylene-and ABA-insensitive mutations indicated that endogenous ethylene promotes seed germination by decreasing sensitivity to endogenous ABA. In marked contrast to the situation in seeds, ein2 and etr1-1 roots were resistant to both ABA and ethylene. Our data indicate that ABA inhibition of root growth requires a functional ethylene signaling cascade, although this inhibition is apparently not mediated by an increase in ethylene biosynthesis. These results are discussed in the context of the other hormonal regulations controlling seed germination and root growth.
INTRODUCTIONAbscisic acid (ABA) regulates various aspects of plant growth and development, including seed maturation and dormancy, as well as adaptation to abiotic environmental stresses (Zeevaart and Creelman, 1988; Davies and Jones, 1991). Substantial progress has been made in the characterization of ABA signaling pathways (Busk and Pagès, 1997; Bonetta and McCourt, 1998;Leung and Giraudat, 1998;MacRobbie, 1998). In particular, mutational analyses in Arabidopsis have led to the identification of several genes that control ABA responsiveness. These genetic screens were based primarily on the inhibition of seed germination by applied ABA. The ABA-insensitive ( abi ) mutants abi1 to abi5 are able to germinate in the presence of ABA concentrations that are inhibitory to the wild type (Koornneef et al., 1984;Ooms et al., 1993; Finkelstein, 1994;Nambara et al., 1995). In contrast, germination of the era1 (enhanced response to ABA) to era3 mutant seed is prevented by low concentrations of ABA that ordinarily permit germination of wild-type seed (Cutler et al., 1996). As judged from their impact on seed dormancy, these two sets of mutations also alter the regulation of seed germination by endogenous ABA. Like ABA-deficient mutants (Karssen et al., 1983;Léon-Kloosterziel et al., 1996a), the ABA-insensitive mutants abi1 to abi3 display marked reductions in seed dormancy (Koornneef et al., 1984;Ooms et al., 1993;Nambara et al., 1995). Conversely, the ABA-supersensitive era1 mutation confers enhanced seed dormancy (Cutler et al., 1996).The abi3 , abi4, and abi5 mutants exhibit additional defects in various aspects of seed maturation (Koornneef et al., 1984; Finkelstein and Somerville, 1990;Ooms et al., 1993; Finkelstein, 1994;Parcy et al., 1994;Nambara et al., 1995). The ABI3 and ABI4 genes have been cloned and encode putative transcriptional regulators. ABI3 is orthologous to the maize Viviparous 1 protein (McCarty et al., 1991;Giraudat e...