The organization of functionally related gene families oftentimes exhibits a non-random genomic distribution as gene clusters that are prevalent throughout divergent eukaryotic organisms. The molecular and cellular functions of the gene families where clustering has been identified vary, and include those involved in basic metabolism, secondary metabolite biosynthesis, and large gene families (e.g. ribosomal proteins). Many of these gene families exhibit transcriptional coregulation, however the roles that clustering plays and the mechanism(s) underlying co-expression are currently understudied. A comprehensive characterization of these relationships would allow for a greater understanding of the implications of genetic editing and engineering to minimize undesired consequences. Here we report the impact of gene clustering and genomic positioning on the expression of large, coregulated gene families in a haploid strain of the budding yeast, Saccharomyces cerevisiae. Computational analysis identifies a significant and complex role for chromatin remodeling as a mechanism underlying cluster transcription. Functional dissection of the 'vitamin metabolic process', 'ribosome biogenesis', and 'ribosomal protein' gene families, characterized the roles for SNF2, JHD2, HIR2, EAF3, and yKU70 dependent chromatin remodeling during steady state transcription as well as the transcriptional response to glucose replenishment. Finally, mining and analysis of transcription profiles reveals significant transcriptional differences between the clustered and unclustered subsets within coregulated families under specific stressors.
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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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