The computational prediction of nucleosome positioning from DNA sequence now allows for in silico investigation of the molecular evolution of biophysical properties of the DNA molecule responsible for primary chromatin organization in the genome. To discern what signal components driving nucleosome positioning in the yeast genome are potentially targeted by natural selection, we compare the performance of various models predictive of nucleosome positioning within the context of a simple statistical test, the repositioned mutation test. We demonstrate that while nucleosome occupancy is driven largely by translational exclusion in response to AT content, there is also a strong signature of evolutionary conservation of regular patterns within nucleosomal DNA sequence related to the structural organization of the nucleosome core (e.g., 10-bp dinucleotide periodicity). We also use computer simulations to investigate hypothetical coding and regulatory constraints on the ability of sequence properties affecting nucleosome formation to adaptively evolve. Our results demonstrate that natural selection may act independently on different DNA sequence properties responsible for local chromatin organization. Furthermore, at least with respect to the deformation energy of the DNA molecule in the nucleosome, the presence of the genetic code has greatly restricted the ability of sequences to evolve the dynamic nucleosome organization typically observed in promoter regions.
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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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