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|Title:||HIF-dependent and reversible nucleosome disassembly in hypoxia-inducible gene promoters||Authors:||Suzuki N.
|Issue Date:||2018||Publisher:||Elsevier Inc.||Citation:||Suzuki N., Vojnovic N., Lee K.-L., Yang H., Gradin K., Poellinger L. (2018). HIF-dependent and reversible nucleosome disassembly in hypoxia-inducible gene promoters. Experimental Cell Research 366 (2) : 181-191. ScholarBank@NUS Repository. https://doi.org/10.1016/j.yexcr.2018.03.020||Abstract:||Hypoxia causes dramatic changes in gene expression profiles, and the mechanism of hypoxia-inducible transcription has been analyzed for use as a model system of stress-inducible gene regulation. In this study, changes in chromatin organization in promoters of hypoxia-inducible genes were investigated during hypoxia-reoxygenation conditions. Most of the hypoxia-inducible gene promoters were hypersensitive to DNase I under both normal and hypoxic conditions, and our data indicate an immediate recruitment of transcription factors under hypoxic conditions. In some of the hypoxia-inducible promoters, nucleosome-free DNA regions (NFRs) were established in parallel with hypoxia-induced transcription. We also show that the hypoxia-inducible formation of NFRs requires that hypoxia-inducible transcription factors (HIFs) bind to the promoters together with the transcriptional coactivator CBP. Within 1 h after the hypoxia exposure was ended (reoxygenation), HIF complexes were dissociated from the promoter regions. Within 24 h of reoxygenation, the hypoxia-induced transcription returned to basal levels and the nucleosome structure was reassembled in the hypoxia-inducible NFRs. Nucleosome reassembly required the function of the transcriptional coregulator SIN3A. Thus, reversible changes in nucleosome organization mediated by transcription factors are notable features of stress-inducible gene regulation. � 2018 Elsevier Inc.||Source Title:||Experimental Cell Research||URI:||https://scholarbank.nus.edu.sg/handle/10635/164160||ISSN:||00144827||DOI:||10.1016/j.yexcr.2018.03.020|
|Appears in Collections:||Staff Publications|
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