Eukaryotic genes are on average more complex than prokaryotic genes in terms of expression regulation, protein length, and protein-domain structure [1-5]. Eukaryotes are also known to have a higher rate of gene duplication than prokaryotes do [6, 7]. Because gene duplication is the primary source of new genes [], the average gene complexity in a genome may have been increased by gene duplication if complex genes are preferentially duplicated. Here, we test this "gene complexity and gene duplicability" hypothesis with yeast genomic data. We show that, on average, duplicate genes from either whole-genome or individual-gene duplication have longer protein sequences, more functional domains, and more cis-regulatory motifs than singleton genes. This phenomenon is not a by-product of previously known mechanisms, such as protein function [10-13], evolutionary rate [14, 15], dosage [11], and dosage balance [16], that influence gene duplicability. Rather, it appears to have resulted from the sub-neo-functionalization process in duplicate-gene evolution [11]. Under this process, complex genes are more likely to be retained after duplication because they are prone to subfunctionalization, and gene complexity is regained via subsequent neofunctionalization. Thus, gene duplication increases both gene number and gene complexity, two important factors in the origin of genomic and organismal complexity.
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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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