“…In seed, both mutations reduce dormancy and the sensitivity of germination to the inhibitory effects of ABA (Koornneef et al, 1984;Finkelstein and Somerville, 1990). In vegetative tissues, both mutants display ABA-resistant seedling growth, abnormal stomatal regulation, and defects in various ABA-induced morphological and molecular responses (Koornneef et al, 1984;Finkelstein and Somerville, 1990;Schnall and Quatrano, 1992;Finkelstein, 1994b;Gosti et al, The cloning and characterization of the ABl7 gene (Leung et al, 1994;Meyer et al, 1994) revealed that it encodes a protein composed of a nove1 N-terminal segment and a C-terminal domain that is an active protein serine/threonine phosphatase 2C (PP2C) (Bertauche et al, 1996). In guard cells, ABI1 appears to relay, together with counteracting protein kinases, ABA signals to stomatal regulation in that defects in stomatal closure caused by the abi7-7 mutant gene can be partially suppressed by kinase antagonists (Armstrong et al, 1995).…”