HAB1 and HAB2 are closely related to ABI1 and ABI2 and also negatively regulate the ABA signalling pathway (Rodriguez et al. 1998; Saez et al. 2004). This was shown by studying the T-DNA insertion mutants hab1-1 and hab2ds (Leonhardt et al. 2004; Saez et al. 2004; Yoshida et al. 2006). Double mutants abi1-2/hab1-1 and abi1-3/hab1-1 display enhanced responsiveness to ABA and sensitivity to NaCl or mannitol. The enhancement in ABA-mediated stomatal closure, leading to reduced water loss in these lines, indicates overlapping functions of ABI1 and HAB1 (Saez et al. 2006). Conversely, constitutive overexpression of HAB1 leads to ABA insensitivity, impaired stomatal closure, ABA-resistant root growth, and reduction of ABA-induced gene expression. These support a negative role in the ABA pathway. Seeds of HAB1 overexpressing plants germinate on inhibitory concentrations of ABA, man-nitol and paclobutrazol, indicating that HAB1 may promote seed germination by negatively regulating ABA responses in seeds (Saez et al. 2004). Introduction of abi1-1-like mutation into HAB1 (hab1G246D) led to reduced phosphatase activity and to a strong ABA insensitivity of seeds in hab1G246D overexpressing plants. The strong ABI phenotype of hab1G246D, which is similar to ahg3G145D (Robert et al. 2006) and opposite to the ABA hypersensitivity of the HAB1 T-DNA insertion mutant, indicates a dominant mutation.
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