title: Receptor Signaling Directs Global Recruitment of Pre-existing Transcription Factors to Inducible Elements.
abstract: Gene expression programs are largely regulated by the tissue-specific expression of lineage-defining transcription factors or by the inducible expression of transcription factors in response to specific stimuli. Here I will review our own work over the last 20 years to show how specific activation signals also lead to the wide-spread re-distribution of pre-existing constitutive transcription factors to sites undergoing chromatin reorganization. I will summarize studies showing that activation of kinase signaling pathways creates open chromatin regions that recruit pre-existing factors which were previously unable to bind to closed chromatin. As models I will draw upon genes activated or primed by receptor signaling in memory T cells, and genes activated by cytokine receptor mutations in acute myeloid leukemia. I also summarize a hit-and-run model of stable epigenetic reprograming in memory T cells, mediated by transient Activator Protein 1 (AP-1) binding, which enables the accelerated activation of inducible enhancers.
authors.affiliation: Institute of Cancer and Genomic Sciences, Institute of Biomedical Research, University of Birmingham, U.K.
authors.forename: Peter N
authors.initials: PN
authors.lastname: Cockerill
mesh_terms: D000818:Animals; D057890:Epigenomics; D006801:Humans; D007938:Leukemia / Q000235:genetics / Q000378:metabolism*; D009154:Mutation / Q000235:genetics; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology; D018808:Transcription Factor AP-1 / Q000235:genetics / Q000378:metabolism; D014158:Transcription, Genetic / Q000235:genetics / Q000502:physiology
chemical_list: D018808:Transcription Factor AP-1
keywords: Transcription; epigenetics; immunological memory; leukemia