We screened for mutations that either enhanced or suppressed the abscisic a
cid (ABA)-resistant seed germination phenotype of the Arabidopsis abi1-1 mu
tant. Alleles of the constitutive ethylene response mutant ctr1 and ethylen
e-insensitive mutant ein2 were recovered as enhancer and suppressor mutatio
ns, respectively. Using these and other ethylene response mutants, we showe
d that the ethylene signaling cascade defined by the ETR1, CTR1, and EIN2 g
enes inhibits ABA signaling in seeds. Furthermore, epistasis analysis betwe
en ethylene- and ABA-insensitive mutations indicated that endogenous ethyle
ne promotes seed germination by decreasing sensitivity to endogenous ABA. I
n marked contrast to the situation in seeds, ein2 and etr1-1 roots were res
istant to both ABA and ethylene. Our data indicate that ABA inhibition of r
oot growth requires a functional ethylene signaling cascade, although this
inhibition is apparently not mediated by an increase in ethylene biosynthes
is. These results are discussed in the context of the other hormonal regula
tions controlling seed germination and root growth.