Chromatin immune precipitation followed by high-throughput sequencing (Chip-Seq), investigate the genome-wide distribution of all histone modifications. Lysine residues within histones di or tri-methylated in Saccharomyces cerevisiae have been studied earlier. Tri-methylation of Lys 4 of histone H3K4me3 correlates with transcriptional activity, but little is known about this methylation state in human. It was also previously proved that deposition of H3K4me2 modification at TSS is associated with gene repression in the yeast cell. Overlapping non-coding RNA (ncRNA) transcript assumes a crucial role in this repression. Here, we examine the H3K4me2 and H3K4me3 methylation dynamics at the TSS region of human genes across the ENCODE (https://www. encode project. org/) Consortium 8 cell lines GM12878, H1-hESC, HeLa-S3, HepG2, HSMM, HUVEC, K562 and NHEK, we identified clear divergence of histone modification profiles in H1-hESC with respect to others. While, H3K4me2 modifications were found to be associated with the vast majority of genes in the H1-hESC with a significantly decreased amount in other differentiated cell lines, H3K4me3 modification showed completely reverse trends. By the process of differentiation, a distinct set of genes lose H3K4me2 in H1-hESCand gain H3K4me3 in differentiated cell, thereby, enhancing the expression level of the corresponding genes. On the level of gene ontology molecular function classification, these genes are mostly associated with protein binding, nucleotide binding, DNA binding and ATP binding. Other than that, signaling and receptor activity, metal ion binding and phosphorylation-dephosphorylating action can be correlated with these genes. We expect a crosstalk between the change of methylation status and gene functionality, as all these functions can be allied to transcriptional regulation and gene activation, which once again is linked to H3K4me3 mark.
| Published in | Biomedical Sciences (Volume 1, Issue 3) |
| DOI | 10.11648/j.bs.20150103.11 |
| Page(s) | 18-33 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2015. Published by Science Publishing Group |
Epigenetic, H3K4me2, H3K4me3, RNA-Seq, Chip-Seq, UCSC, Methylation Dynamics
| [1] | K. Luger, A. W. Mader, R. K. Richmond, D. F. Sargent, andT. J. Richmond, “Crystal structure of the nucleosome core particle at 2. 8A resolution” Nature, vol. 389, pp. 251–260, September 1997. |
| [2] | T. Kouzarides, “Chromatin modifications and their function”, Cell, vol. 128, pp. 693–705, February 2007. |
| [3] | R. Marmorstein, and R. C. Trievel, “Histone modifying enzymes: structures, mechanisms, and specificities” Biochim. Biophys. Acta, vol. 1789, pp. 58–68, January 2009. |
| [4] | J. F. Couture, andR. C. Trievel, “Histone-modifying enzymes: encrypting an enigmatic epigenetic code” Curr. Opin. Struct. Biol, vol. 16, pp. 753–760, October 2006. |
| [5] | V. W. Zhou, A. Goren, andB. E. Bernstein, “Charting histone modifications and the functional organization of mammalian genomes” Nat. Rev. Genet, vol. 12, pp. 7– 18, November 2011. |
| [6] | J. C. Black, andJ. R. Whetstine, “Chromatin landscape: methylation beyond transcription” Epigenetics, vol. 6, pp. 9-15, January 2011. |
| [7] | D. K. Pokholok, C. T. Harbison, andS. Levine, “Genome-wide map of nucleosome acetylation and methylation in yeast” Cell, vol. 122, pp. 517–527, August 2005. |
| [8] | E. Vallas, S. Sanchez-Molina, andM. A. Martinex-Balbaz, “Role of histone modifications in marking and activating genes through mitosis” J Biol. Chem.,vol. 280, pp. 42592-42600, December 2005. |
| [9] | T. Y. Roh, W. C. Ngau, and K. Cui, “High-resolution genome-wide mapping of histone modifications” Nat. Biotechnol, vol. 22, pp. 1013–1016, August 2004. |
| [10] | W. E. Farrell, “Epigenetics of pituitary tumors: an update” CurrOpinEndocrinol Diabetes Obes. vol. 21, pp. 299-305, August 2014. |
| [11] | N. D. Heintzman, R. K. Stuart, G. Hon, Y. Fu, C. W. Ching, R. D. Hawkins, L. O. Barrera, S. Van Calcar, C. Qu, and K. A. Ching, “Distinct and predictive chromatin signatures of transcriptional promoters and enhancers in the human genome, ” Nat. Genet, vol. 39, pp. 311–318, March 2006. |
| [12] | B. E. Bernstein, T. S. Mikkelsen, X. Xie, M. Kamal, D. J. Huebert, J. Cuff, B. Fry, A. Meissner, M. Wernig, and K. Plath, “A bivalent chromatin structure marks key developmental genes in embryonic stem cells” Cell, vol. 125, pp. 315–326, April 2006. |
| [13] | T. Y. Roh, S. Cuddapah, and K. Cui, “The genomic landscape of histone modifications in human T cells” Proc. Natl. Acad. Sci. USA, vol. 103, pp. 15782– 15787, October 2006. |
| [14] | A. Barski, S. Cuddapah, K. Cui, T. Y. Roh, D. E. Schones, Z. Wang, G. Wei, I. Chepelev, andK. Zhao, “High-resolution profiling of histone methylations in the human genome” Cell, vol. 129, pp. 823–837, May 2007. |
| [15] | G. E. Crawford, I. E. Holt, and J. Whittle, “Genome-wide mapping of DNasehypersensitive sites using massively parallel signature sequencing (MPSS)”, Genome Res, vol. 16, pp. 123–131, January 2006. |
| [16] | A. Visel, M. J. Blow, and Z. Li, “ChIP-seq accurately predicts tissue-specificactivity of enhancers” Nature, vol. 457, pp. 854–858, February 2009. |
| [17] | N. D. Heintzman, G. C. Hon, and R. D. Hawkins, “Histone modifications at human enhancers reflect global cell-type-specific gene expression” Nature, vol. 459, pp. 108–112, May 2009. |
| [18] | K. Ishihara, M. Oshimura, and M. Nakao, “CTCF-dependent chromatin insulator is linked to epigenetic remodeling” Mol. Cell, vol. 23, pp. 733–742, September2006. |
| [19] | P. A. Jones, and D. Takai, “The role of DNA methylation in mammalian epigenetics”, Science, vol. 293, pp. 1068–1070, August 2001. |
| [20] | T. K. Kim, M. Hemberg, J. M. Gray, and et al “Widespread transcription at neuronal activity-regulated enhancers” Nature, vol. 465, pp. 182–187, May 2010. |
| [21] | K. Polyak, “Breast cancer: origins and evolution,” J. Clin. Invest,vol. 117, pp. 3155– 3163, November 2007. |
| [22] | D. S. Johnson, A. Mortazavi, and R. M. Myers, “Genome-wide mapping of in vivo protein-DNA interactions” Science, vol. 316, pp. 1497–1502, June 2007. |
| [23] | T. Y. Roh, andK. Zhao, “High-resolution genome wide chromatin modifications by GMAT”Methods Mol. Biol, vol. 387, pp. 95-108, May 2007. |
| [24] | A. Sanyal, B. R. Lajoie, G. Jain and J. Dekker. “The long-range interaction landscape of gene promoters” Nature, vol. 6, pp. 109-113, September 2012. |
| [25] | T. Kim, Z. Xu, S. Clauder-Münster, L. M. Steinmetz, and S. Buratowski, “Set3HDAC mediates effects of overlapping noncoding transcription on gene induction kinetics, ” Cell, vol. 150 (6), pp. 1158-69, September2012. |
| [26] | R. Schneider, A. J. Bannister, F. A. Myers, A. A. Thorne, C. Crane-Robinson, andT. Kouzarides, “Histone H3 lysine 4 methylation patterns in highereukaryotic genes, ” Nature Cell Biology, vol. 6, pp. 73-77. January 2004. |
| [27] | H. Santos-Rosa, R. Schneider, A. J. Bannister, J. Sherriff, B. E. Bernstein, E. N. C TolgaEmre, S. L. Schreiber, J. Mellor, andT. Kouzarides, “Active genes are tri-methylated at K4 of histone H3, ” Nature, vol. 419, pp. 407-411, September2002. |
| [28] | C. M. Koch, R. M. Andrews, and P. Flicek, “The landscape of histone modifications across 1% of the human” Genome Res, vol. 17, pp. 691-707, June 2007. |
| [29] | B. E. Bernstein, E. L. Humphrey, R. L. Erlich, R. Schneider, P. Bouman, J. S. Liu, T. Kouzarides, and S. L. Schreiber, “Methylation of histone H3 Lys 4 in coding regions ofactive genes, ” Proc. Natl. Acad. Sci. USA, vol. 99, pp. 8695–8700, June 2002. |
| [30] | M. Ashburner, C. A. Ball, J. A. Blake, D. Botstein, H. Butler, J. M. Cherry, A. P. Davis, K. Dolinski, S. S. Dwight, J. T. Eppig, M. A. Harris, D. P. Hill, L. Issel-Tarver, A. Kasarskis, S. Lewis, J. C. Matese, J. E. Richardson, M. Ringwald, G. M. Rubin, and G. Sherlock, “Gene ontology: tool for the unification of biology. The Gene Ontology Consortium” Nat Genet, vol. 25 (1), pp. 25-9, May 2000. |
APA Style
Smarajit Das, Pijush Das, Sanga Mitra, Medhanjali Dasgupta, Jayprokas Chakrabarti, et al. (2015). Epigenetic Transfiguration of H3K4me2 to H3K4me3 During Differentiation of Embryonic Stem Cell into Non-embryonic Cells. Biomedical Sciences, 1(3), 18-33. https://doi.org/10.11648/j.bs.20150103.11
ACS Style
Smarajit Das; Pijush Das; Sanga Mitra; Medhanjali Dasgupta; Jayprokas Chakrabarti, et al. Epigenetic Transfiguration of H3K4me2 to H3K4me3 During Differentiation of Embryonic Stem Cell into Non-embryonic Cells. Biomed. Sci. 2015, 1(3), 18-33. doi: 10.11648/j.bs.20150103.11
Share This Article
Twitter
Linked In
Facebook
Copy
Download@article{10.11648/j.bs.20150103.11,
author = {Smarajit Das and Pijush Das and Sanga Mitra and Medhanjali Dasgupta and Jayprokas Chakrabarti and Eric Larsson},
title = {Epigenetic Transfiguration of H3K4me2 to H3K4me3 During Differentiation of Embryonic Stem Cell into Non-embryonic Cells},
journal = {Biomedical Sciences},
volume = {1},
number = {3},
pages = {18-33},
doi = {10.11648/j.bs.20150103.11},
url = {https://doi.org/10.11648/j.bs.20150103.11},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.bs.20150103.11},
abstract = {Chromatin immune precipitation followed by high-throughput sequencing (Chip-Seq), investigate the genome-wide distribution of all histone modifications. Lysine residues within histones di or tri-methylated in Saccharomyces cerevisiae have been studied earlier. Tri-methylation of Lys 4 of histone H3K4me3 correlates with transcriptional activity, but little is known about this methylation state in human. It was also previously proved that deposition of H3K4me2 modification at TSS is associated with gene repression in the yeast cell. Overlapping non-coding RNA (ncRNA) transcript assumes a crucial role in this repression. Here, we examine the H3K4me2 and H3K4me3 methylation dynamics at the TSS region of human genes across the ENCODE (https://www. encode project. org/) Consortium 8 cell lines GM12878, H1-hESC, HeLa-S3, HepG2, HSMM, HUVEC, K562 and NHEK, we identified clear divergence of histone modification profiles in H1-hESC with respect to others. While, H3K4me2 modifications were found to be associated with the vast majority of genes in the H1-hESC with a significantly decreased amount in other differentiated cell lines, H3K4me3 modification showed completely reverse trends. By the process of differentiation, a distinct set of genes lose H3K4me2 in H1-hESCand gain H3K4me3 in differentiated cell, thereby, enhancing the expression level of the corresponding genes. On the level of gene ontology molecular function classification, these genes are mostly associated with protein binding, nucleotide binding, DNA binding and ATP binding. Other than that, signaling and receptor activity, metal ion binding and phosphorylation-dephosphorylating action can be correlated with these genes. We expect a crosstalk between the change of methylation status and gene functionality, as all these functions can be allied to transcriptional regulation and gene activation, which once again is linked to H3K4me3 mark.},
year = {2015}
}
TY - JOUR T1 - Epigenetic Transfiguration of H3K4me2 to H3K4me3 During Differentiation of Embryonic Stem Cell into Non-embryonic Cells AU - Smarajit Das AU - Pijush Das AU - Sanga Mitra AU - Medhanjali Dasgupta AU - Jayprokas Chakrabarti AU - Eric Larsson Y1 - 2015/10/14 PY - 2015 N1 - https://doi.org/10.11648/j.bs.20150103.11 DO - 10.11648/j.bs.20150103.11 T2 - Biomedical Sciences JF - Biomedical Sciences JO - Biomedical Sciences SP - 18 EP - 33 PB - Science Publishing Group SN - 2575-3932 UR - https://doi.org/10.11648/j.bs.20150103.11 AB - Chromatin immune precipitation followed by high-throughput sequencing (Chip-Seq), investigate the genome-wide distribution of all histone modifications. Lysine residues within histones di or tri-methylated in Saccharomyces cerevisiae have been studied earlier. Tri-methylation of Lys 4 of histone H3K4me3 correlates with transcriptional activity, but little is known about this methylation state in human. It was also previously proved that deposition of H3K4me2 modification at TSS is associated with gene repression in the yeast cell. Overlapping non-coding RNA (ncRNA) transcript assumes a crucial role in this repression. Here, we examine the H3K4me2 and H3K4me3 methylation dynamics at the TSS region of human genes across the ENCODE (https://www. encode project. org/) Consortium 8 cell lines GM12878, H1-hESC, HeLa-S3, HepG2, HSMM, HUVEC, K562 and NHEK, we identified clear divergence of histone modification profiles in H1-hESC with respect to others. While, H3K4me2 modifications were found to be associated with the vast majority of genes in the H1-hESC with a significantly decreased amount in other differentiated cell lines, H3K4me3 modification showed completely reverse trends. By the process of differentiation, a distinct set of genes lose H3K4me2 in H1-hESCand gain H3K4me3 in differentiated cell, thereby, enhancing the expression level of the corresponding genes. On the level of gene ontology molecular function classification, these genes are mostly associated with protein binding, nucleotide binding, DNA binding and ATP binding. Other than that, signaling and receptor activity, metal ion binding and phosphorylation-dephosphorylating action can be correlated with these genes. We expect a crosstalk between the change of methylation status and gene functionality, as all these functions can be allied to transcriptional regulation and gene activation, which once again is linked to H3K4me3 mark. VL - 1 IS - 3 ER -
Information
Email: