دورية أكاديمية
أعرض في EDS

Distinct IL-1α-responsive enhancers promote acute and coordinated changes in chromatin topology in a hierarchical manner.

التفاصيل البيبلوغرافية
العنوان: Distinct IL-1α-responsive enhancers promote acute and coordinated changes in chromatin topology in a hierarchical manner.
المؤلفون: Weiterer SS; Rudolf Buchheim Institute of Pharmacology, Justus Liebig University Giessen, Giessen, Germany., Meier-Soelch J; Rudolf Buchheim Institute of Pharmacology, Justus Liebig University Giessen, Giessen, Germany., Georgomanolis T; Center for Molecular Medicine Cologne, University of Cologne, Cologne, Germany., Mizi A; Center for Molecular Medicine Cologne, University of Cologne, Cologne, Germany.; Department of Pathology, University Medical Center Göttingen, Göttingen, Germany., Beyerlein A; Rudolf Buchheim Institute of Pharmacology, Justus Liebig University Giessen, Giessen, Germany., Weiser H; Rudolf Buchheim Institute of Pharmacology, Justus Liebig University Giessen, Giessen, Germany., Brant L; Department of Pathology, University Medical Center Göttingen, Göttingen, Germany., Mayr-Buro C; Rudolf Buchheim Institute of Pharmacology, Justus Liebig University Giessen, Giessen, Germany., Jurida L; Rudolf Buchheim Institute of Pharmacology, Justus Liebig University Giessen, Giessen, Germany., Beuerlein K; Rudolf Buchheim Institute of Pharmacology, Justus Liebig University Giessen, Giessen, Germany., Müller H; Rudolf Buchheim Institute of Pharmacology, Justus Liebig University Giessen, Giessen, Germany., Weber A; Rudolf Buchheim Institute of Pharmacology, Justus Liebig University Giessen, Giessen, Germany., Tenekeci U; Rudolf Buchheim Institute of Pharmacology, Justus Liebig University Giessen, Giessen, Germany., Dittrich-Breiholz O; Research Core Unit Genomics, Institute of Physiological Chemistry, Medical School Hannover, Hannover, Germany., Bartkuhn M; Institute for Genetics, Justus Liebig University Giessen, Giessen, Germany., Nist A; Genomics Core Facility and Institute of Molecular Oncology, Philipps University Marburg, Marburg, Germany., Stiewe T; Genomics Core Facility and Institute of Molecular Oncology, Philipps University Marburg, Marburg, Germany.; Member of the German Center for Lung Research (DZL), Giessen, Germany., van IJcken WF; Center for Biomics, Erasmus Medical Center, Rotterdam, The Netherlands., Riedlinger T; Institute of Biochemistry, Justus Liebig University Giessen, Giessen, Germany., Schmitz ML; Member of the German Center for Lung Research (DZL), Giessen, Germany.; Institute of Biochemistry, Justus Liebig University Giessen, Giessen, Germany., Papantonis A; Center for Molecular Medicine Cologne, University of Cologne, Cologne, Germany.; Department of Pathology, University Medical Center Göttingen, Göttingen, Germany., Kracht M; Rudolf Buchheim Institute of Pharmacology, Justus Liebig University Giessen, Giessen, Germany.; Member of the German Center for Lung Research (DZL), Giessen, Germany.
المصدر: The EMBO journal [EMBO J] 2020 Jan 02; Vol. 39 (1), pp. e101533. Date of Electronic Publication: 2019 Nov 07.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 8208664 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1460-2075 (Electronic) Linking ISSN: 02614189 NLM ISO Abbreviation: EMBO J Subsets: MEDLINE
أسماء مطبوعة: Publication: 2024- : [London] : Nature Publishing Group
Original Publication: Eynsham, Oxford, England : Published for the European Molecular Biology Organization by IRL Press, [c1982-
مواضيع طبية MeSH: Chromatin/*metabolism , Enhancer Elements, Genetic/*genetics , Gene Expression Regulation/*drug effects , Inflammation Mediators/*metabolism , Interleukin-1alpha/*pharmacology , MAP Kinase Kinase Kinases/*metabolism , NF-kappa B/*metabolism, Binding Sites ; Cells, Cultured ; Chemokines/metabolism ; Chromatin/chemistry ; Chromatin/genetics ; HeLa Cells ; Humans ; MAP Kinase Kinase Kinases/genetics ; NF-kappa B/genetics ; Signal Transduction ; Tumor Necrosis Factor-alpha/pharmacology
مستخلص: How cytokine-driven changes in chromatin topology are converted into gene regulatory circuits during inflammation still remains unclear. Here, we show that interleukin (IL)-1α induces acute and widespread changes in chromatin accessibility via the TAK1 kinase and NF-κB at regions that are highly enriched for inflammatory disease-relevant SNPs. Two enhancers in the extended chemokine locus on human chromosome 4 regulate the IL-1α-inducible IL8 and CXCL1-3 genes. Both enhancers engage in dynamic spatial interactions with gene promoters in an IL-1α/TAK1-inducible manner. Microdeletions of p65-binding sites in either of the two enhancers impair NF-κB recruitment, suppress activation and biallelic transcription of the IL8/CXCL2 genes, and reshuffle higher-order chromatin interactions as judged by i4C interactome profiles. Notably, these findings support a dominant role of the IL8 "master" enhancer in the regulation of sustained IL-1α signaling, as well as for IL-8 and IL-6 secretion. CRISPR-guided transactivation of the IL8 locus or cross-TAD regulation by TNFα-responsive enhancers in a different model locus supports the existence of complex enhancer hierarchies in response to cytokine stimulation that prime and orchestrate proinflammatory chromatin responses downstream of NF-κB.
(© 2019 The Authors. Published under the terms of the CC BY 4.0 license.)
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معلومات مُعتمدة: 162103480 International Deutsche Forschungsgemeinschaſt (DFG); 284237345 International Deutsche Forschungsgemeinschaſt (DFG); 183582903 International Deutsche Forschungsgemeinschaſt (DFG); 268555672 International Deutsche Forschungsgemeinschaſt (DFG); 197785619 International Deutsche Forschungsgemeinschaſt (DFG); 162103480 International Deutsche Forschungsgemeinschaſt (DFG); 183582903 International Deutsche Forschungsgemeinschaſt (DFG); 197785619 International Deutsche Forschungsgemeinschaſt (DFG); 285697699 International Deutsche Forschungsgemeinschaſt (DFG); 290613333 International Deutsche Forschungsgemeinschaſt (DFG); 24676099 International Deutsche Forschungsgemeinschaſt (DFG); 390649896 International Deutsche Forschungsgemeinschaſt (DFG); 111447 International Deutsche Krebshilfe; International Max-Planck Society; 24676099 International Excellence Cluster Cardio-Pulmonary System and Cardio-Pulmonary Institute (EXC 147: Kardiopulmonales System); 390649896 International Cardio-Pulmonary Institute (CPI); International DZL/UGMLC Program; International Center for Molecular Medicine Cologne (ZMMK)
فهرسة مساهمة: Keywords: IL-8; NF-κB; chromatin topology; interleukin-1; tumor necrosis factor-α
سلسلة جزيئية: GEO GSE64224; GSE52470; GSE134436
SRA PRJNA552438
المشرفين على المادة: 0 (Chemokines)
0 (Chromatin)
0 (IL1A protein, human)
0 (Inflammation Mediators)
0 (Interleukin-1alpha)
0 (NF-kappa B)
0 (Tumor Necrosis Factor-alpha)
EC 2.7.11.25 (MAP Kinase Kinase Kinases)
EC 2.7.11.25 (MAP kinase kinase kinase 7)
تواريخ الأحداث: Date Created: 20191109 Date Completed: 20200713 Latest Revision: 20240327
رمز التحديث: 20240327
مُعرف محوري في PubMed: PMC6939198
DOI: 10.15252/embj.2019101533
PMID: 31701553
قاعدة البيانات: MEDLINE
الوصف
تدمد:1460-2075
DOI:10.15252/embj.2019101533