ABA-Hypersensitive Germination1 encodes a protein phosphatase 2C, an essential component of abscisic acid signaling in Arabidopsis seed
- PMID: 17461784
- DOI: 10.1111/j.1365-313X.2007.03107.x
ABA-Hypersensitive Germination1 encodes a protein phosphatase 2C, an essential component of abscisic acid signaling in Arabidopsis seed
Abstract
The phytohormone abscisic acid (ABA) regulates physiologically important stress and developmental responses in plants. To reveal the mechanism of response to ABA, we isolated several novel ABA-hypersensitive Arabidopsis thaliana mutants, named ahg (ABA-hypersensitive germination). ahg1-1 mutants showed hypersensitivity to ABA, NaCl, KCl, mannitol, glucose and sucrose during germination and post-germination growth, but did not display any significant phenotypes in adult plants. ahg1-1 seeds accumulated slightly more ABA before stratification and showed increased seed dormancy. Map-based cloning of AHG1 revealed that ahg1-1 has a nonsense mutation in a gene encoding a novel protein phosphatase 2C (PP2C). We previously showed that the ahg3-1 mutant has a point mutation in the AtPP2CA gene, which encodes another PP2C that has a major role in the ABA response in seeds (Yoshida et al., 2006b). The levels of AHG1 mRNA were higher in dry seeds and increased during late seed maturation--an expression pattern similar to that of ABI5. Transcriptome analysis revealed that, in ABA-treated germinating seeds, many seed-specific genes and ABA-inducible genes were highly expressed in ahg1-1 and ahg3-1 mutants compared with the wild-type. Detailed analysis suggested differences between the functions of AHG1 and AHG3. Dozens of genes were expressed more strongly in the ahg1-1 mutant than in ahg3-1. Promoter-GUS analyses demonstrated both overlapping and distinct expression patterns in seed. In addition, the ahg1-1 ahg3-1 double mutant was more hypersensitive than either monogenic mutant. These results suggest that AHG1 has specific functions in seed development and germination, shared partly with AHG3.
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