The closely related related phosphatases ABI1 and ABI2 are negative regulators of ABA signalling according to genetic studies of several mutations and T-DNA insertion lines (Gosti et al. 1999; Merlot et al. 2001; Yoshida et al. 2006). (Semi)-dominant abi1-1 and abi2-1 mutations carry the same Gly to Asp amino acid substitution, which is located near to the Mg2+ binding site and reduces the phosphatase activity. These mutations cause an ABA-insensitivity, reduced seed dormancy, abnormal stomata regulation, defects in drought responses (Bertauche et al. 1996; Leung et al. 1994, 1997; Meyer et al. 1994; Rodriguez et al. 1998) and lead to salt tolerance (Ohta et al.
2003). Both ABI1 and abi1-1 proteins inhibit ABA signal transduction to ABA-responsive gene promoters HVA1 and RBCS in isolated protoplasts (Sheen 1998) as well as KIN2 and Rd29A promoters in cells microinjected with recombinant proteins (Wu et al. 2003). The N-terminal part of ABI1 contains a putative Ca2+-binding domain (Leung et al. 1994; Meyer et al. 1994;), and ABI1 action was placed downstream of Ca2+ in the ABA pathway (Wu et al. 2003).
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