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Depositordc.contributorWaclaw, Bartlomiej
Funderdc.contributor.otherThe Royal Society of Edinburghen_UK
Spatial Coveragedc.coverage.spatialUKen
Spatial Coveragedc.coverage.spatialUNITED KINGDOMen
Data Creatordc.creatorWaclaw, Bartlomiej
Data Creatordc.creatorCholewa-Waclaw, Justyna
Data Creatordc.creatorShah, Ruth
Data Creatordc.creatorWebb, Shaun
Data Creatordc.creatorChhatbar, Kashyap
Data Creatordc.creatorRamsahoye, Bernard
Data Creatordc.creatorPusch, Oliver
Data Creatordc.creatorYu, Miao
Data Creatordc.creatorGreulich, Philip
Data Creatordc.creatorBird, Adrian
Date Accessioneddc.date.accessioned2019-06-07T16:17:30Z
Date Availabledc.date.available2019-06-07T16:17:30Z
Citationdc.identifier.citationWaclaw, Bartlomiej; Cholewa-Waclaw, Justyna; Shah, Ruth; Webb, Shaun; Chhatbar, Kashyap; Ramsahoye, Bernard; Pusch, Oliver; Yu, Miao; Greulich, Philip; Bird, Adrian. (2019). Supplementary data for the manuscript "Quantitative modelling predicts the impact of DNA methylation on RNA polymerase II traffic", [dataset]. University of Edinburgh. School of Physics and Astronomy. https://doi.org/10.7488/ds/2568.en
Persistent Identifierdc.identifier.urihttps://hdl.handle.net/10283/3351
Persistent Identifierdc.identifier.urihttps://doi.org/10.7488/ds/2568
Dataset Description (abstract)dc.description.abstractPatterns of gene expression are primarily determined by proteins that locally enhance or repress transcription. While many transcription factors target a restricted number of genes, others appear to modulate transcription levels globally. An example is MeCP2, an abundant methylated-DNA binding protein that is mutated in the neurological disorder Rett Syndrome. Despite much research, the molecular mechanism by which MeCP2 regulates gene expression is not fully resolved. Here we integrate quantitative, multi-dimensional experimental analysis and mathematical modelling to show that MeCP2 is a novel type of global transcriptional regulator whose binding to DNA creates "slow sites" in gene bodies. Waves of slowed-down RNA polymerase II formed behind these sites travel backward and indirectly affect initiation, reminiscent of defect-induced shock waves in non-equilibrium physics transport models. This mechanism differs from conventional gene regulation mechanisms, which often involve direct modulation of transcription initiation. Our findings point to a genome-wide function of DNA methylation that may account for the reversibility of Rett syndrome in mice. Moreover, our combined theoretical and experimental approach provides a general method for understanding how global gene expression patterns are choreographed.en_UK
Dataset Description (TOC)dc.description.tableofcontentsSee Readme.txten_UK
Languagedc.language.isoengen_UK
Publisherdc.publisherUniversity of Edinburgh. School of Physics and Astronomyen_UK
Rightsdc.rightsCreative Commons Attribution 4.0 International Public Licenseen
Subjectdc.subjectMeCP2en_UK
Subjectdc.subjectgene expressionen_UK
Subjectdc.subjecttranscriptionen_UK
Subjectdc.subjectRNA-seqen_UK
Subjectdc.subjectChIP-seqen_UK
Subjectdc.subjectATAC-seqen_UK
Subjectdc.subjectmathematical modelen_UK
Subject Classificationdc.subject.classificationBiological Sciencesen_UK
Titledc.titleSupplementary data for the manuscript "Quantitative modelling predicts the impact of DNA methylation on RNA polymerase II traffic"en_UK
Typedc.typedataseten_UK

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