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This is surprising, as defective gene silencing underlies developmental abnormalities and disease. Here we delineate the sequence and functional contribution of transcriptional repression mechanisms at high temporal resolution. Inducible entry of the NuRD-interacting transcriptional regulator Ikaros into mouse pre-B cell nuclei triggered immediate binding to target gene promoters. Rapid RNAP2 eviction, transcriptional shutdown, nucleosome invasion, and reduced transcriptional activator binding required chromatin remodeling by NuRD-associated Mi2beta\/CHD4, but were independent of HDAC activity. Histone deacetylation occurred after transcriptional repression. Nevertheless, HDAC activity contributed to stable gene silencing. Hence, high resolution mapping of transcriptional repression reveals complex and interdependent mechanisms that underpin rapid transitions between transcriptional states, and elucidates the temporal order, functional role and mechanistic separation of NuRD-associated enzymatic activities.<\/jats:p>","DOI":"10.7554\/elife.22767","type":"journal-article","created":{"date-parts":[[2017,3,20]],"date-time":"2017-03-20T09:00:13Z","timestamp":1490000413000},"source":"Crossref","is-referenced-by-count":58,"title":["A high-resolution map of transcriptional repression"],"prefix":"10.7554","volume":"6","author":[{"given":"Ziwei","family":"Liang","sequence":"first","affiliation":[{"name":"Lymphocyte Development Group, MRC London Institute of Medical Sciences, Faculty of Medicine, Imperial College London, London, United Kingdom"},{"name":"Epigenetics Section, MRC London Institute of Medical Sciences, Faculty of Medicine, Imperial College London, London, United 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