PP2CAAHG3 and FsPP2C1

PP2CA/AHG3 phosphatase is able to rescue the pde1 S. pombe mutant, which is defective in cAMP phosphodiesterase that results in elevated cAMP

amounts and activated cAMP-dependent protein kinase. Possibly, it counteracts the protein kinase A (PKA) in yeast (Kuromori and Yamamoto 1994). However, in plants PP2CA is a strong negative regulator of ABA signal trans-duction, controlling seed germination and stomatal aperture. This was revealed by studies of PP2CA overexpressing plants, ahg3-1 point mutant (causing the loss of PP2C activity) and T-DNA insertion lines pp2ca-1/ahg3-2 and pp2ca-2 (Kuhn et al. 2006; Yoshida et al. 2006). PP2CA/AHG3 plays a major role among PP2Cs in the ABA response in seeds (Yoshida et al. 2006). PP2CA inhibits ABA signal transduction when transiently expressed in isolated protoplasts (Sheen 1998) and its overexpression confers ABA insensitivity in plants (Kuhn et al. 2006). Cold, drought, salt and ABA induce PP2CA expression. Cold- and drought-induced expressions are ABA-dependent as PP2CA expression is reduced in ABA-deficient aba1-1 mutant. Drought-induced expression is ABI1-dependent. Down-regulation of PP2CA accelerates plant development and induces tolerance to cold, suggesting a negative control of the ABA pathway during cold acclimation (Tahtiharju and Palva 2001). PP2CA interacts with AKT2/AKT3 inward rectifying potassium channel protein (Cherel et al. 2002; Vranova et al. 2001) and the highest expression levels of both genes in the phloem vasculature suggests possible interaction in plants (Cherel et al. 2002). An orthologue of PP2CA/AHG3, FsPP2C1 from beech (Fagus sylvatica) (Lorenzo et al. 2001), indicates similarly negative regulation of ABA signalling, as its overexpression in Arabidopsis led to ABA insensitivity, reduced seed dormancy and resistance towards salt and osmotic stresses (Gonzalez-Garcia et al. 2003).

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