Transcriptional activation of the budding yeast CLN1 and CLN2 genes during the late G1 phase of the cell cycle has been attributed to a positive feedback loop, wherein the transcription of both genes is stimulated by the accumulation of their protein products. We demonstrate that in cycling cells CLN2 does not play a role in determining the timing of its own transcriptional activation. First, we show that CLN3 alone is sufficient to maximally activate CLN2 transcription. Cells that lack functional CLN1 and CLN2 genes activate the CLN2 promoter with the same kinetics and at the same size as cells in which all three CLN genes are functional. In addition, CLN2 transcription is activated with similar kinetics in cells that have CLN2 as their only functional CLN gene and in CLN-deficient cells. Promoter analysis shows that CLN3-dependent activation of CLN2 transcription is directed primarily through the previously identified UAS1 region although another cis-acting region, UAS2, also can contribute to CLN2 activation under some conditions. The ability to activate transcription of CLN2 is not a unique property of CLN3 because ectopically expressed CLN2 can both activate the endogenous CLN2 promoter and induce Start. We propose that failure of the endogenous CLN2 gene to contribute significantly to activation of its own transcription results from its relative effectiveness at inducing Start, cell cycle progression and, subsequently, inactivation of CLN2 expression.
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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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