Arabidopsis decuple mutant reveals the importance of SnRK2 kinases in osmotic stress responses in vivo
KAUST DepartmentDesert Agriculture Initiative
Biological and Environmental Sciences and Engineering (BESE) Division
Online Publication Date2011-01-10
Print Publication Date2011-01-25
Permanent link to this recordhttp://hdl.handle.net/10754/561701
MetadataShow full item record
AbstractOsmotic stress associated with drought or salinity is a major factor that limits plant productivity. Protein kinases in the SNF1-related protein kinase 2 (SnRK2) family are activated by osmotic stress, suggesting that the kinases are involved in osmotic stress signaling. However, due to functional redundancy, their contribution to osmotic stress responses remained unclear. In this report, we constructed an Arabidopsis line carrying mutations in all 10 members of the SnRK2 family. The decuple mutant snrk2.1/2/3/4/5/6/7/8/9/10 grew poorly under hyperosmotic stress conditions but was similar to the wild type in culture media in the absence of osmotic stress. The mutant was also defective in gene regulation and the accumulation of abscisic acid (ABA), proline, and inositol 1,4,5-trisphosphate under osmotic stress. In addition, analysis of mutants defective in the ABA-activated SnRK2s (snrk2.2/3/6) and mutants defective in the rest of the SnRK2s (snrk2.1/4/5/7/8/9/10) revealed that SnRK2s are a merging point of ABA-dependent and -independent pathways for osmotic stress responses. These results demonstrate critical functions of the SnRK2s in mediating osmotic stress signaling and tolerance.
CitationFujii, H., Verslues, P. E., & Zhu, J.-K. (2011). Arabidopsis decuple mutant reveals the importance of SnRK2 kinases in osmotic stress responses in vivo. Proceedings of the National Academy of Sciences, 108(4), 1717–1722. doi:10.1073/pnas.1018367108
SponsorsWe thank the Arabidopsis Biological Resource Center for providing the T-DNA insertion mutants. This work was supported by National Institutes of Health Grant R01GM059138 (to J.-K.Z.).
PubMed Central IDPMC3029766
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