Abstract
Potassium is an essential mineral element for plant growth and development. Although it is known that plants absorb and transport K+ through membrane transporters, it remains unclear how these transporters are regulated. Here we show that the protein kinase CIPK23, encoded by the LKS1 gene, regulates K+ uptake under low-K+ conditions. Lesion of LKS1 significantly reduced K+ uptake and caused leaf chlorosis and growth inhibition, whereas overexpression of LKS1 significantly enhanced K+ uptake and tolerance to low K+. We demonstrate that CIPK23 directly phosphorylates the K+ transporter AKT1 and further find that CIPK23 is activated by the binding of two calcineurin B-like proteins, CBL1 and CBL9. We propose a model in which the CBL1/9-CIPK23 pathway ensures activation of AKT1 and enhanced K+ uptake under low-K+ conditions.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Arabidopsis / genetics
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Arabidopsis / metabolism*
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Arabidopsis Proteins / genetics
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Arabidopsis Proteins / metabolism*
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Base Sequence
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Biological Transport, Active
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Calcium-Binding Proteins / genetics
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Calcium-Binding Proteins / metabolism*
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DNA, Plant / genetics
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Female
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Genes, Plant
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In Vitro Techniques
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Ion Transport
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Models, Biological
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Mutagenesis
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Mutation
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Oocytes / metabolism
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Phenotype
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Plants, Genetically Modified
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Potassium / metabolism
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Potassium Channels / genetics
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Potassium Channels / metabolism*
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Protein Serine-Threonine Kinases / genetics
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Protein Serine-Threonine Kinases / metabolism*
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Recombinant Proteins / genetics
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Recombinant Proteins / metabolism
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Xenopus laevis
Substances
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Arabidopsis Proteins
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CBL protein, Arabidopsis
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Calcium-Binding Proteins
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DNA, Plant
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Potassium Channels
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Recombinant Proteins
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AKT1 protein, Arabidopsis
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CIPK23 protein, Arabidopsis
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Protein Serine-Threonine Kinases
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Potassium