Cyclin-dependent kinases (CDKs) drive the cell cycle through the phosphorylation of substrates that function in genome duplication and cell division. The existence of multiple cyclin subunits and their distinct cell cycle-regulated expression suggests that cyclins impart unique specificities to CDK-substrate interactions that are critical for normal cellular function. This study shows that the combination of early cell cycle expression and deletion of the CDK inhibitor Saccharomyces Wee1 (Swe1) enables the mitotic B-type (Clb) cyclins Clb2, Clb3, and Clb4 of Saccharomyces cerevisiae to initiate S phase with similar effectiveness as the S-phase cyclin Clb5. Although in vivo analysis indicates preferential phosphorylation of a replication substrate by Clb5-Cdk1, this difference is relatively minor compared with the impact of transcriptional control and Swe1 regulation. Indeed, early expressed Clb2-Cdk1 can activate all essential Clb-Cdk substrates in a strain lacking all other Clbs and Swe1. Thus, Swe1 regulation and expression timing are key mechanisms that sequester the broad activity of Clb2-Cdk1 from critical substrates. Furthermore, the ability of Swe1 to inhibit the activity of different B-type cyclins in replication initiation correlates with the normal expression timing of those cyclins, with no apparent in vivo inhibition of Clb5 and Clb6, moderate inhibition of Clb3 and Clb4, and strong inhibition of Clb2. Hence, Swe1 appears to reinforce the temporal activity of cyclins established through transcriptional control. The conserved nature of CDK function suggests that similar mechanisms regulate CDK specificity in multicellular organisms.
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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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