A very good description of histone marks¶
Reference¶
Copied from: https://github.com/mdozmorov/genomerunner_web/wiki/Histone-marks
Summary¶
Individual histone marks can be looked up using [Google](https://www.google.com/), [PubMed](http://www.ncbi.nlm.nih.gov/pubmed), and [HIstome: The Histone Infobase](http://www.actrec.gov.in/histome/)
Good reviews or histone modifications:
Zhou, Vicky W., Alon Goren, and Bradley E. Bernstein. “Charting Histone Modifications and the Functional Organization of Mammalian Genomes.” Nature Reviews. Genetics 12, no. 1 (January 2011): 7–18. [doi:10.1038/nrg2905](http://www.nature.com/nrg/journal/v12/n1/full/nrg2905.html). [https://www.ncbi.nlm.nih.gov/pubmed/21116306](https://www.ncbi.nlm.nih.gov/pubmed/21116306)
Barski, Artem, Suresh Cuddapah, Kairong Cui, Tae-Young Roh, Dustin E. Schones, Zhibin Wang, Gang Wei, Iouri Chepelev, and Keji Zhao. “High-Resolution Profiling of Histone Methylations in the Human Genome.” Cell 129, no. 4 (May 18, 2007): 823–37. [doi:10.1016/j.cell.2007.05.009](http://www.cell.com/cell/abstract/S0092-8674(07)00600-9). [https://www.ncbi.nlm.nih.gov/pubmed/17512414](http://www.cell.com/cell/abstract/S0092-8674(07)00600-9)
Hoffman, Michael M., Jason Ernst, Steven P. Wilder, Anshul Kundaje, Robert S. Harris, Max Libbrecht, Belinda Giardine, et al. “Integrative Annotation of Chromatin Elements from ENCODE Data.” Nucleic Acids Research 41, no. 2 (January 2013): 827–41. https://doi.org/10.1093/nar/gks1284. [https://academic.oup.com/nar/article-lookup/doi/10.1093/nar/gks1284](https://academic.oup.com/nar/article-lookup/doi/10.1093/nar/gks1284) - Chromatin states called by both ChromHMM and Segway. 25 states, description of each.
Spatial distribution of histone marks¶
From Wang, Zhibin, Dustin E. Schones, and Keji Zhao. “Characterization of Human Epigenomes.” Current Opinion in Genetics & Development 19, no. 2 (April 2009): 127–34. https://doi.org/10.1016/j.gde.2009.02.001. - Concise description of main histone marks, their roles in transcription, and the corresponding studies. Figure 2 - schematic distribution of histone marks with respect to genes-TSSs.
Basic histone marks¶
Histone Marks |
Functional Annotation |
References |
|---|---|---|
H3K4me1 |
Enhancer (active, intermediate and poised) |
Heintzman ND et.al. 2007 (PMID: 17277777), Hu G et.al. 2013 (PMID: 23260488), Herz HM et.al. 2012 (PMID: 23166019 ) |
H3K4me1/H3K27ac |
Active Enhancer |
Creyghton MP et al. 2010 (PMID: 21106759 ), Heintzman ND et.al. 2009 (PMID: 19295514), Rada-Iglesias A et.al. 2011 (PMID: 21160473 ) |
H3K4me1/H3K27me3 |
Poised Developmental Enhancer |
Creyghton MP et al. 2010 (PMID: 21106759 ), Rada-Iglesias A et.al. 2011 (PMID: 21160473 ) |
H3K4me3 |
Promoters |
Bernstein BE et.al. 2005 (PMID: 15680324), Kim TH et.al. 2005 (PMID: 15988478), Pokholok DK et.al. 2005 (PMID: 16122420 ) |
H3K4me3/H3K27me3 |
Bivalent/Poised Promoter |
Bernstein BE et.al. 2006 (PMID: 16630819) |
H3K9ac |
Active Enhancer |
Karmodiya K et.al., 2012 (PMID: 22920947) |
H3K9me3 |
Heterochromatin, can mark poised enhancers |
Mikkelsen TS et.al. 2007 (PMID: 17603471), Zentner GE et.al. 2011 (PMID: 21632746) |
H3K14ac |
Active Enhancer |
Karmodiya . et.al., 2012 (PMID: 22920947) |
H3K27ac |
Active Enhancer |
Creyghton MP et.al. 2010 (PMID: 21106759 ), Zentner GE et.al. 2011 (PMID: 21632746) |
H3K27me3 |
Polycomb Repressed Regions, poised enhancers |
Bernstein BE et.al. 2006 (PMID: 16630819), Lee TI et.al. 2006 (PMID: 16630818), Zentner GE et.al. 2011 (PMID: 21632746) |
H3K36me3 |
Transcribed Gene Body, Active enhancers |
Barski A et al. 2007 (PMID: 17512414), Zentner GE et.al. 2011 (PMID: 21632746) |
H3K56ac |
Active Enhancer |
Skalska L et.al. 2015 (PMID: 26069324) |
H4K16ac |
Active Enhancer |
Taylor GC et.al. 2013 (PMID: 23990607) |
H2A.Z/H2A.Zac |
Poised and active enhancers |
Hu G et.al. 2013 (PMID: 23260488), Ku M 2012 (PMID: 23034477), Dalvai M et.al. 2013 (PMID: 23637611) |
Detailed description¶
Histone Marks |
Description |
|---|---|
H2AK5ac |
The DSB-induced acetylation of H2AX lysine 5 is required for further ubiquitination and occurs independently of the phosphorylation of H2AX. K5 acetylation-dependent ubiquitination of H2A.X by the TIP60-UBC13 complex causes its release from damaged chroma |
H2AK9ac |
H2AK9 acetylation shows a robust peak at the transcription start site (TSS) of active and poised genes (PMID: 18552846). Site also confirmed by Mass Spectrometry (PMID: 12937907). |
H2az |
H2A.Z is a sequence variant of Histone H2A. H2AZ appears to alter nucleosome stability, is partially redundant with nucleosome remodeling complexes, and is involved in transcriptional control. [11893489] |
H2BK120ac |
Shown to be enriched at the Transcription start site (TSS) and along gene bodies (PMID: 18552846). |
H2BK12ac |
H2BK12 shown to be enriched at the Transcription start site (TSS) and along gene bodies (PMID: 18552846). H2BK12 acetylation is found at differentially methylated regions of imprinted genes (PMID: 20693536). |
H2BK15ac |
Acetylated H2BK15 levels are reported to rise after RGC-32 knockdown in colon cancer cell lines (PMID: 19883641). |
H2BK20ac |
H2BK20 is shown to be heavily deacetylated on exposure to Nickel(II) which is supposed to be carcinogenic (PMID: 16283522). Shown to be enriched at the Transcription start site (TSS) and along gene bodies (PMID: 18552846). |
H2BK5ac |
H2BK5 acetylation shows a robust peak at the transcription start site (TSS) of active and poised genes (PMID: 18552846). |
H3K14ac |
Histone H3K14 acetylation is critical for the recruitment of TFIID at the IFN-gamma locus and hence important for eliciting proper immune response (PMID: 12419248). In mice, acetylation by CLOCK at H3 Lys-14, is thought to initiate chromatin remodelling |
H3K18ac |
H3K18 acetylation shows a robust peak at the transcription start site (TSS) of active and poised genes (PMID: 18552846). |
H3K23ac |
H3K23 acetylation and H3K4 methylation are part of a non-canonical histone signature which is recognised by chromatin regulator tripartite motif-containing 24 (TRIM24) that binds chromatin and oestrogen receptor to activate the oestrogen-dependent genes |
H3K23me2 |
H3K23me2 |
H3k27ac |
Histone H3 (acetyl K27). As with H3K9ac, associated with transcriptional initiation and open chromatin structure. It remains unknown whether acetylation has can have different consequences depending on the specific lysine residue targeted. In general, though, there appears to be high redundancy. Histone acetylation is notable for susceptibility to small molecules and drugs that target histone deacetylases. |
H3K27ac |
Histone H3 (acetyl K27). As with H3K9ac, associated with transcriptional initiation and open chromatin structure. It remains unknown whether acetylation has can have different consequences depending on the specific lysine residue targeted. In general, though, there appears to be high redundancy. Histone acetylation is notable for susceptibility to small molecules and drugs that target histone deacetylases. |
H3k27me3 |
Histone H3 (tri-methyl K27). Marks promoters that are silenced by Polycomb proteins in a given lineage; large domains are found at inactive developmental loci. |
H3K36me3 |
Histone H3 (tri-methyl K36). Marks regions of RNAPII elongation, including coding and non-coding transcripts. |
H3k36me3b |
Histone H3 (tri-methyl K36) marks actively transcribed chromatin regions |
H3K4ac |
H3K4 acetylation marks are shown to be enriched at the Transcription start site (TSS) and along gene bodies (PMID: 18552846). |
H3K4me1 |
Histone H3 (mono methyl K4). Is associated with enhancers, and downstream of transcription starts. |
H3K4me2 |
Histone H3 (di methyl K4). Marks promoters and enhancers. Most CpG islands are marked by H3K4me2 in primary cells. May be associated also with poised promoters. |
H3K4me3 |
Histone H3 (tri methyl K4). Marks promoters that are active or poised to be activated. |
H3K56ac |
H3K56ac levels in human cells are differentially regulated at telomeres and globally in response to cell cycle arrest (PMID: 19625767). During DNA damage, H3K56 acetylation levels increased, and this acetylated H3K56 is also localised at the DNA repair sites. It also colocalised with other proteins involved in DNA damage signalling pathways such as phospho-ATM, Chk2, and p53 demonstrating its involvement in DNA damage repair (PMID: 20587414 ). |
H3K79me1 |
Dynamics of H3K79 monomethylation has been studied in terms of old and new histones and it has been found that the rate of methylation is almost equal for both types of histones (PMID: 20699226). |
H3K79me2 |
H3K79me2 is a mark of the transcriptional transition region - the region between the initiation marks (K4me3, etc) and the elongation marks (K36me3). |
H3K9ac |
Histone H3 (acetyl K9). As with H3K27ac, associated with transcriptional initiation and open chromatin structure. It remains unknown whether acetylation can have different consequences depending on the specific lysine residue targeted. In general, though, there appears to be high redundancy. Histone acetylation is notable for susceptibility to small molecules and drugs that target histone deacetylases. |
H3K9K14ac |
Histone H3 (acetyl K9 or K14). Transcription activation mark, from [20159609]. |
H3K9me1 |
Histone H3 (mono-methyl K9). Is associated with active and accessible regions. NOTE CONTRAST to H3K9me3 which is associated with repressive heterochromatic state. |
H3K9me3 |
Histone H3 (tri methyl K9). Is associated with repressive heterochromatic state (silenced chromatin). NOTE CONTRAST to H3K9me1 which is associated with active and accessible regions. |
H3R17me2 |
CARM1 dependent methylation of H3R17 leads to the activation of E2F1 promoter indicating its role in gene activation (PMID: 18172323). H3R17me2 is important for transcriptional activation of MHC II HLA-DRA genes (PMID: 17478518) |
H4K12ac |
Shown to be enriched at the transcription start site (TSS) and along gene bodies (PMID: 18552846). H4K12ac is required for unperturbed progression to S phase (PMID: 16387653). |
H4K20 |
Transcription associated |
H4K20me1 |
Histone H4 (mono-methyl K20). Is associated with active and accessible regions. In mammals, PR-Set7 specifically catalyzes H4K20 monomethylation. NOTE CONTRAST to H3K20me3 which is associated with heterochromatin and DNA repair. |
H4K5ac |
Hyperacetylated histone H4 marks transcriptionally active regions of the chromatin (PMID: 8343956). H4K5ac is required for unperturbed progression to S phase (PMID: 16387653). Shown to be enriched at the transcription start site (TSS) and along gene bodie |
H4K8ac |
Hyperacetylated histone H4 marks transcriptionally active regions of the chromatin (PMID: 8343956). H4K5ac is required for unperturbed progression to S phase (PMID: 16387653). Shown to be enriched at the transcription start site (TSS) and along gene bodie |
H4K91ac |
H4K91 acetylation shows a robust peak at the transcription start site (TSS) of active and poised genes (PMID: 18552846). |