ATPP2CA Negatively Regulates ABA Responses during Cold Acclimation and Interacts with the Potassium Channel AKT3

Abstract

The phytohormone abscisic acid (ABA) regulates diverse developmental and physiological responses, including seed maturation, dormancy and germination as well as guard cell closure. ABA also mediates adaptive responses to abiotic environmental stresses such as drought (Leung and Giraudat, 1998). The role of ABA in cold acclimation has been the center of much debate. However, several lines of evidence suggest that the ABA may have an important role in the cold acclimation process. First, application of ABA at normal growth temperatures can induce an increase in freezing tolerance in a wide range of plants, including Arabidopsis (Guy, 1990Lång et al., 1989). Furthermore, endogenous ABA levels increase transiently in response to low temperature (Lång et al., 1994). In addition, the ABA-deficient mutants of Arabidopsis, aba1 and aba4, are severely impaired in their ability to cold-acclimate (Heino et al., 1990; Gilmour and Thomashow, 1991). However, application of ABA could suppress the impaired cold-acclimation phenotype (Heino et al., 1990). In addition to mutants in ABA biosynthesis, also Arabidopsis mutants defective in ABA responsiveness appear to affect cold acclimation. The ABA-insensitive mutant abi1 is impaired in development of freezing tolerance (Mäntylä et al., 1995) as well as in the cold-induced expression of several cold-responsive genes (Lång and Palva, 1992; Nordin et al., 1993). Identification of ABI1 as a protein phosphatase 2C (Leung et al., 1994; Meyer et al., 1994) suggested that protein dephosphorylation might be involved in cold signal transduction.