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Published on March 31, 2006; 10.1104/pp.106.079038


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Received February 10, 2006
Returned for revision February 28, 2006
Accepted March 19, 2006

G-protein complex mutants are hypersensitive to ABA-regulation of germination and post-germination development

Sona Pandey , Jin-Gui Chen , Alan M. Jones , and Sarah M. Assmann *

Department of Biology, Pennsylvania State University, University Park, Pennsylvania 16802-5301
Departments of Biology and Pharmacology, University of North Carolina, Chapel Hill, North Carolina 27599-3280

* Corresponding author; email: sma3{at}psu.edu.

Abscisic acid (ABA) plays regulatory roles in a host of physiological processes throughout plant growth and development. Seed germination, early seedling development, stomatal guard cell functions, and acclimation to adverse environmental conditions are key processes regulated by ABA. Recent evidence suggests that signaling processes in both seeds and guard cells involve heterotrimeric G proteins. To assess new roles for the Arabidopsis G{alpha} subunit (GPA1), the G{beta} subunit (AGB1), and the candidate G-protein-coupled receptor (GCR1) in ABA signaling during germination and early seedling development, we utilized knock-out mutants lacking one or more of these components. Our data show that GPA1, AGB1, and GCR1 each negatively regulates ABA signaling in seed germination and early seedling development. Plants lacking AGB1 have greater ABA hypersensitivity than plants lacking GPA1, suggesting that AGB1 is the predominant regulator of ABA and that GPA1 affects the efficacy of AGB1 execution. GCR1 acts upstream of GPA1 and AGB1 for ABA signaling pathways during germination and early seedling development: gcr1 gpa1 double mutants exhibit a gpa1 phenotype and agb1 gcr1 and agb1 gcr1 gpa1 mutants exhibit an agb1 phenotype. Contrary to the scenario in guard cells, where GCR1 and GPA1 have opposite effects on ABA signaling during stomatal opening, GCR1 acts in concert with GPA1 and AGB1 in ABA signaling during germination and early seedling development. Thus, cell- and tissue-specific functional interaction in response to a given signal such as ABA may determine the distinct pathways regulated by the individual members of the G-protein complex.




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