ArticlePloS one2007
Determining physical constraints in transcriptional initiation complexes using DNA sequence analysis.
Article in PloS one, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed.
- Quantitative analysis of transcription factor binding and expression using calling cards reporter arrays.Nucleic acids research · 2020Article
- Spatial promoter recognition signatures may enhance transcription factor specificity in yeast.PloS one · 2013Article
- Probing the informational and regulatory plasticity of a transcription factor DNA-binding domain.PLoS genetics · 2012Article
- The fitness landscapes of cis-acting binding sites in different promoter and environmental contexts.PLoS genetics · 2010Article
- Dissection of combinatorial control by the Met4 transcriptional complex.Molecular biology of the cell · 2010Article
- Organization of developmental enhancers in the Drosophila embryo.Nucleic acids research · 2009Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Eukaryotic gene expression is often under the control of cooperatively acting transcription factors whose binding is limited by structural constraints. By determining these structural constraints, we can understand the "rules" that define functional cooperativity. Conversely, by understanding the rules of binding, we can infer structural characteristics. We have developed an information theory based method for approximating the physical limitations of cooperative interactions by comparing sequence analysis to microarray expression data. When applied to the coordinated binding of the sulfur amino acid regulatory protein Met4 by Cbf1 and Met31, we were able to create a combinatorial model that can correctly identify Met4 regulated genes. Interestingly, we found that the major determinant of Met4 regulation was the sum of the strength of the Cbf1 and Met31 binding sites and that the energetic costs associated with spacing appeared to be minimal.
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Registered trials
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