Genome-wide Mapping of HATs and HDACs Reveals Distinct Functions in Active and Inactive Genes
Histone acetyltransferases (HATs) and deacetylases (HDACs) function antagonistically to control histone acetylation. As acetylation is a histone mark for active transcription, HATs have been associated with active and HDACs with inactive genes. We describe here genome-wide mapping of HATs and HDACs...
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| Published in | Cell Vol. 138; no. 5; pp. 1019 - 1031 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
04.09.2009
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0092-8674 1097-4172 1097-4172 |
| DOI | 10.1016/j.cell.2009.06.049 |
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| Abstract | Histone acetyltransferases (HATs) and deacetylases (HDACs) function antagonistically to control histone acetylation. As acetylation is a histone mark for active transcription, HATs have been associated with active and HDACs with inactive genes. We describe here genome-wide mapping of HATs and HDACs binding on chromatin and find that both are found at active genes with acetylated histones. Our data provide evidence that HATs and HDACs are both targeted to transcribed regions of active genes by phosphorylated RNA Pol II. Furthermore, the majority of HDACs in the human genome function to reset chromatin by removing acetylation at active genes. Inactive genes that are primed by MLL-mediated histone H3K4 methylation are subject to a dynamic cycle of acetylation and deacetylation by transient HAT/HDAC binding, preventing Pol II from binding to these genes but poising them for future activation. Silent genes without any H3K4 methylation signal show no evidence of being bound by HDACs. |
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| AbstractList | Histone acetyltransferases (HATs) and deacetylases (HDACs) function antagonistically to control histone acetylation. As acetylation is a histone mark for active transcription, HATs have been associated with active and HDACs with inactive genes. We describe here genome-wide mapping of HATs and HDACs binding on chromatin and find that both are found at active genes with acetylated histones. Our data provide evidence that HATs and HDACs are both targeted to transcribed regions of active genes by phosphorylated RNA Pol II. Furthermore, the majority of HDACs in the human genome function to reset chromatin by removing acetylation at active genes. Inactive genes that are primed by MLL-mediated histone H3K4 methylation are subject to a dynamic cycle of acetylation and deacetylation by transient HAT/HDAC binding, preventing Pol II from binding to these genes but poising them for future activation. Silent genes without any H3K4 methylation signal show no evidence of being bound by HDACs. Histone acetyltransferases (HATs) and histone deacetylases (HDACs) function antagonistically to control histone acetylation states that are crucial to many cellular processes. We describe here genome-wide mapping experiments that reveal that both HATs (CBP, p300, PCAF, Tip60, MOF) and HDACs (HDAC1, HDAC2, HDAC3, HDAC6) on chromatin are positively correlated with gene expression and histone acetylation. We provide evidence that Tip60 and HDAC6 are targeted to transcribed regions of active genes by phosphorylated RNA Pol II. Our results indicate that MLL-mediated H3K4 methylation primes chromatin to facilitate histone acetylation. Our data suggest that the majority of HDACs in the human genome function to reset chromatin by removing acetylation in active genes; the dynamic cycle of acetylation and deacetylation by transient HAT/HDAC binding prevents Pol II from binding to the genes primed by H3K4 methylation and poises them for future activation. Histone acetyltransferases (HATs) and deacetylases (HDACs) function antagonistically to control histone acetylation. As acetylation is a histone mark for active transcription, HATs have been associated with active and HDACs with inactive genes. We describe here genome-wide mapping of HATs and HDACs binding on chromatin and find that both are found at active genes with acetylated histones. Our data provide evidence that HATs and HDACs are both targeted to transcribed regions of active genes by phosphorylated RNA Pol II. Furthermore, the majority of HDACs in the human genome function to reset chromatin by removing acetylation at active genes. Inactive genes that are primed by MLL-mediated histone H3K4 methylation are subject to a dynamic cycle of acetylation and deacetylation by transient HAT/HDAC binding, preventing Pol II from binding to these genes but poising them for future activation. Silent genes without any H3K4 methylation signal show no evidence of being bound by HDACs.Histone acetyltransferases (HATs) and deacetylases (HDACs) function antagonistically to control histone acetylation. As acetylation is a histone mark for active transcription, HATs have been associated with active and HDACs with inactive genes. We describe here genome-wide mapping of HATs and HDACs binding on chromatin and find that both are found at active genes with acetylated histones. Our data provide evidence that HATs and HDACs are both targeted to transcribed regions of active genes by phosphorylated RNA Pol II. Furthermore, the majority of HDACs in the human genome function to reset chromatin by removing acetylation at active genes. Inactive genes that are primed by MLL-mediated histone H3K4 methylation are subject to a dynamic cycle of acetylation and deacetylation by transient HAT/HDAC binding, preventing Pol II from binding to these genes but poising them for future activation. Silent genes without any H3K4 methylation signal show no evidence of being bound by HDACs. |
| Author | Barski, Artem Schones, Dustin E. Peng, Weiqun Zang, Chongzhi Zhao, Keji Wang, Zhibin Cui, Kairong |
| AuthorAffiliation | 1 Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, NIH, Bethesda, MD 2 Department of Physics, The George Washington University, D.C 3 These authors contributed equally to this work |
| AuthorAffiliation_xml | – name: 1 Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, NIH, Bethesda, MD – name: 3 These authors contributed equally to this work – name: 2 Department of Physics, The George Washington University, D.C |
| Author_xml | – sequence: 1 givenname: Zhibin surname: Wang fullname: Wang, Zhibin organization: Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA – sequence: 2 givenname: Chongzhi surname: Zang fullname: Zang, Chongzhi organization: Department of Physics, The George Washington University, Washington D.C. 20052, USA – sequence: 3 givenname: Kairong surname: Cui fullname: Cui, Kairong organization: Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA – sequence: 4 givenname: Dustin E. surname: Schones fullname: Schones, Dustin E. organization: Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA – sequence: 5 givenname: Artem surname: Barski fullname: Barski, Artem organization: Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA – sequence: 6 givenname: Weiqun surname: Peng fullname: Peng, Weiqun organization: Department of Physics, The George Washington University, Washington D.C. 20052, USA – sequence: 7 givenname: Keji surname: Zhao fullname: Zhao, Keji email: zhaok@nhlbi.nih.gov organization: Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19698979$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Acetylation Cell Line DNA Gene Expression Genome, Human Histone Acetyltransferases - genetics Histone Acetyltransferases - metabolism Histone Deacetylase Inhibitors Histone Deacetylases - genetics Histone Deacetylases - metabolism Histones - metabolism Humans Methylation Phosphorylation RNA Polymerase II - metabolism |
| Title | Genome-wide Mapping of HATs and HDACs Reveals Distinct Functions in Active and Inactive Genes |
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