Background: In yeast, 14-3-3 proteins bind to hundreds of phosphorylated proteins and play a role in the regulation of many processes including tolerance to NaCl. However, the mechanism of 14-3-3 involvement in the cell answer to salt or osmotic stresses is weakly understood.
Methods: We studied the role of the Saccharomyces cerevisiae 14-3-3 homologs Bmh1 and Bmh2 in the regulation of alkali-metal-cation homeostasis using the genetic-interaction approach. Obtained results were confirmed with the Bimolecular-Fluorescence-Complementation method.
Results: Deletion of BMH1, encoding the major 14-3-3 isoform, resulted in an increased sensitivity to Na+, Li+ and K+ and to cationic drugs but did not affect membrane potential. This bmh1Δ phenotype was complemented by overexpression of BMH2. Testing the genetic interaction between BMH genes and genes encoding plasma-membrane cation transporters revealed, that 14-3-3 proteins neither interact with the potassium uptake systems, nor with the potassium-specific channel nor with the Na+(K+)-ATPases. Instead, a genetic interaction was identified between BMH1 and NHA1 which encodes an Na+(K+)/H+ antiporter. In addition, a physical interaction between 14-3-3 proteins and the Nha1 antiporter was shown. This interaction does not depend on the phosphorylation of the Nha1 antiporter by Hog1 kinase. Our results uncovered a previously unknown interaction partner of yeast 14-3-3 proteins and provided evidence for the previously hypothesized involvement of Bmh proteins in yeast salt tolerance.
General significance: Our results showed for the first time that the yeast 14-3-3 proteins and an alkali-metal-cation efflux system interact and that this interaction enhances the cell survival upon salt stress.
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Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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Site | Modification | Modifier | Source | Reference |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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Evidence ID | Analyze ID | File | Description |
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