Gene evolution is traditionally considered within the framework of the molecular clock (MC) model whereby each gene is characterized by an approximately constant rate of evolution. Recent comparative analysis of numerous phylogenies of prokaryotic genes has shown that a different model of evolution, denoted the Universal PaceMaker (UPM), which postulates conservation of relative, rather than absolute evolutionary rates, yields a better fit to the phylogenetic data. Here, we show that the UPM model is a better fit than the MC for genome wide sets of phylogenetic trees from six species of Drosophila and nine species of yeast, with extremely high statistical significance. Unlike the prokaryotic phylogenies that include distant organisms and multiple horizontal gene transfers, these are simple data sets that cover groups of closely related organisms and consist of gene trees with the same topology as the species tree. The results indicate that both lineage-specific and gene-specific rates are important in genome evolution but the lineage-specific contribution is greater. Similar to the MC, the gene evolution rates under the UPM are strongly overdispersed, approximately 2-fold compared with the expectation from sampling error alone. However, we show that neither Drosophila nor yeast genes form distinct clusters in the tree space. Thus, the gene-specific deviations from the UPM, although substantial, are uncorrelated and most likely depend on selective factors that are largely unique to individual genes. Thus, the UPM appears to be a key feature of genome evolution across the history of cellular life.
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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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