Science (American Association for the Advancement of Science), 2021-06, Vol.372 (6548), p.1349-1353
2021
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- Autor(en) / Beteiligte
- Titel
- NF-κB dynamics determine the stimulus specificity of epigenomic reprogramming in macrophages
- Ist Teil von
- Science (American Association for the Advancement of Science), 2021-06, Vol.372 (6548), p.1349-1353
- Ort / Verlag
- United States: The American Association for the Advancement of Science
- Erscheinungsjahr
- 2021
- Quelle
- American Association for the Advancement of Science
- Beschreibungen/Notizen
- The epigenome of macrophages can be reprogrammed by extracellular cues, but the extent to which different stimuli achieve this is unclear. Nuclear factor κB (NF-κB) is a transcription factor that is activated by all pathogen-associated stimuli and can reprogram the epigenome by activating latent enhancers. However, we show that NF-κB does so only in response to a subset of stimuli. This stimulus specificity depends on the temporal dynamics of NF-κB activity, in particular whether it is oscillatory or non-oscillatory. Non-oscillatory NF-κB opens chromatin by sustained disruption of nucleosomal histone-DNA interactions, enabling activation of latent enhancers that modulate expression of immune response genes. Thus, temporal dynamics can determine a transcription factor's capacity to reprogram the epigenome in a stimulus-specific manner.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0036-8075eISSN: 1095-9203DOI: 10.1126/science.abc0269Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8489855
- Format
- –
- Schlagworte
- Animals, Cell activation, Cell Nucleus - metabolism, Chromatin, Chromatin - metabolism, Deoxyribonucleic acid, DNA, DNA - metabolism, Dynamics, Enhancer Elements, Genetic, Enhancers, Epigenome, Gene expression, Gene Expression Regulation, Gene regulation, Genes, Histones, Histones - metabolism, Immune response, Inflammation, Inflammatory response, Macrophages, Macrophages - immunology, Macrophages - metabolism, MAP Kinase Signaling System, Methylation, Mice, Mice, Inbred C57BL, Mice, Knockout, Models, Biological, NF-kappa B - metabolism, NF-KappaB Inhibitor alpha - genetics, NF-KappaB Inhibitor alpha - metabolism, NF-κB protein, Nucleosomes - metabolism, Signal Transduction, Stimuli, Transcription activation, Transcription Factor RelA - metabolism, Transcription factors, Transcription, Genetic