Sensory transcription networks generally control rapid and reversible gene expression responses to external stimuli. Developmental transcription networks carry out slow and irreversible temporal programs of gene expression during development. It is important to understand the design principles that underlie the structure of sensory and developmental transcription networks. Cascades, which are chains of regulatory reactions, are a basic structural element of transcription networks. When comparing databases of sensory and developmental transcription networks, a striking difference is found in the distribution of cascade lengths. Here, we suggest that delay times in the responses of the network present a design constraint that influences the network architecture. We experimentally studied the response times in simple cascades constructed of well-characterized repressors in Escherichia coli. Accurate kinetics at high temporal resolution was measured using green fluorescent protein (GFP) reporters. We find that transcription cascades can show long delays of about one cell-cycle time per cascade step. Mathematical analysis suggests that such a delay is characteristic of cascades that are designed to minimize the response times for both turning-on and turning-off gene expression. The need to achieve rapid reversible responses in sensory transcription networks may help explain the finding that long cascades are very rare in databases of E.coli and Saccharomyces cerevisiae sensory transcription networks. In contrast, long cascades are common in developmental transcription networks from sea urchin and from Drosophila melanogaster. Response delay constraints are likely to be less important for developmental networks, since they control irreversible processes on the timescale of cell-cycles. This study highlights a fundamental difference between the architecture of sensory and developmental transcription networks.
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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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