FIERY1 encoding an inositol polyphosphate 1-phosphatase is a negative regulator of abscisic acid and stress signaling in Arabidopsis

Abstract

The plant hormone abscisic acid (ABA) plays a wide range of important roles in plant growth and development, including embryogenesis, seed dormancy, root and shoot growth, transpiration, and stress tolerance. ABA and various abiotic stresses also activate the expression of numerous plant genes through undefined signaling pathways. To gain insight into ABA and stress signal transduction, we conducted a genetic screen based on ABA-and stress-inducible gene transcription. Here we report the identification of an Arabidopsis mutation, fiery1 (fry1), which results in super-induction of ABA-and stress-responsive genes. Seed germination and postembryonic development of fry1 are more sensitive to ABA or stress inhibition. The mutant plants are also compromised in tolerance to freezing, drought, and salt stresses. Map-based cloning revealed that FRY1 encodes an inositol polyphosphate 1-phosphatase, which functions in the catabolism of inositol 1, 4, 5-trisphosphate (IP 3 ). Upon ABA treatment, fry1 mutant plants accumulated more IP 3 than did the wild-type plants. These results provide the first genetic evidence indicating that phosphoinositols mediate ABA and stress signal transduction in plants and their turnover is critical for attenuating ABA and stress signaling.

Enhancement of Abscisic Acid Sensitivity and Reduction of Water Consumption in Arabidopsis by Combined Inactivation of the Protein Phosphatases Type 2C ABI1 and HAB1

“…era1, abh1, and gcr1) with enhanced response to ABA have been shown to cause reduced water consumption (Pei et al, 1998;Hugouvieux et al, 2001;Pandey and Assmann, 2004), many examples of mutants that do not match this assertion are known. For instance, the fry1 and sad1 mutants, which show ABAhypersensitive inhibition of seed germination and superinduction of ABA-responsive genes, have compromised tolerance to drought stress (Xiong et al, 2001a(Xiong et al, , 2001b. Likewise, the calcineurin B-like 9, the calcineurin B-like-interacting protein kinase, and the APETALA2-like ABA repressor 1 mutants, which display ABA hypersensitivity and enhanced expression of ABA signaling genes, do not correlate with stresstolerance phenotypes Pandey et al, , 2005.…”

“…For instance, recessive mutations leading to ABA hypersensitivity were found in the era1 (Cutler et al, 1996), abh1 ), fry1 (Xiong et al, 2001b), hypersensitive to ABA1 (hab1; Leonhardt et al, 2004;Saez et al, 2004), sad1 (Xiong et al, 2001a), and gcr1 (Pandey and Assmann, 2004) mutants. The intragenic revertants of abi1-1 and abi1-1R1 to R7 also carry recessive mutations that lead to enhanced responsiveness to ABA (Gosti et al, 1999).…”

Role for cytoplasmic nucleotide hydrolysis in hepatic function and protein synthesis

“…In addition, the identification of a phenotypically related human skeletal disease resulting from mutations in gPAPP confirms that Golgi-resident 3′-nucleotidase activity is essential for sulfation-dependent processes such as cartilage formation and long bone growth (14). Conversely, functional studies in bacteria and yeast have implicated the more ancient cytosolic 3′-nucleotidase Bpnt1 in numerous sulfation-independent processes, including salt tolerance and methionine biosynthesis (15)(16)(17)(18)(19)(20)(21)(22)(23). Thus, although it is clear that gPAPP is essential for proper Golgimediated sulfation, the role of Bpnt1 in mammals and its potential connection to cytosolic sulfation remains unclear.…”

Salt Stress Signaling and Mechanisms of Plant Salt Tolerance

“…The fry1 mutation leads to sustained accumulation of IP 3 and hypersensitivity to ABA, cold and salt stress. Thus, IP 3 plays a crucial role in cytosolic Ca 2+ oscillations during ABA, salt and cold stress signaling (26).…”

“…Excess Na + -induced membrane depolarization may activate mechanosensitive Ca 2+ channels to generate Ca 2+ signature under salt stress (4,17). Pharmacological studies and genetic analysis have shown the involvement of inositol 1,4,5-tris phosphate (IP 3 )-gated Ca 2+ channels in the regulation of Ca 2+ signature during salt stress (24)(25)(26). The FRY1 locus of Arabidopsis encodes an inositol polyphosphate 1-phosphatase, which catabolizes IP 3 .…”