Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2013 Jul 10:13:145.
doi: 10.1186/1471-2148-13-145.

CpG islands under selective pressure are enriched with H3K4me3, H3K27ac and H3K36me3 histone modifications

Most Mauluda Akhtar  1 , Giovanni Scala, Sergio Cocozza, Gennaro Miele, Antonella Monticelli
Affiliations

CpG islands under selective pressure are enriched with H3K4me3, H3K27ac and H3K36me3 histone modifications

Most Mauluda Akhtar et al. BMC Evol Biol. .

Abstract

Background: Histone modification is an epigenetic mechanism that influences gene regulation in eukaryotes. In particular, histone modifications in CpG islands (CGIs) are associated with different chromatin states and with transcription activity. Changes in gene expression play a crucial role in adaptation and evolution.

Results: In this paper, we have studied, using a computational biology approach, the relationship between histone modifications in CGIs and selective pressure in Homo sapiens. We considered three histone modifications: histone H3 lysine 4 trimethylation (H3K4me3), histone H3 lysine 27 acetylation (H3K27ac) and histone H3 lysine 36 trimethylation (H3K36me3), and we used the publicly available genomic-scale histone modification data of thirteen human cell lines. To define regions under selective pressure, we used three distinct signatures that mark selective events from different evolutionary periods. We found that CGIs under selective pressure showed significant enrichments for histone modifications.

Conclusion: Our result suggests that, CGIs that have undergone selective events are characterized by epigenetic signatures, in particular, histone modifications that are distinct from CGIs with no evidence of selection.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Enrichment of H3K4me3 modification in CpG islands under selective pressure. Black bars represent the fraction of CGIs containing histone modification marks within regions that show signatures of natural selection (HIRs, CEs and 5LSRs). Grey bars represent the fraction of CGIs containing histone modification marks within regions that do not show signatures of selective events. The X-axis indicates the analyzed cell lines. An asterisk (*) above a bar indicates a statistically non-significant difference.
Figure 2
Figure 2
Enrichment of H3K27ac modification in CpG islands under selective pressure. Same notation as in Figure  1.
Figure 3
Figure 3
Enrichment of H3K36me3 modification in CpG islands under selective pressure. Same notation as in Figure  1.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

References

    1. Bird A, Taggart M, Frommer M, Miller OJ, Macleod D. A fraction of the mouse genome that is derived from islands of nonmethylated, CpG-rich DNA. Cell. 1985;40(1):91–99. doi: 10.1016/0092-8674(85)90312-5. - DOI - PubMed
    1. Illingworth RS, Bird AP. CpG islands-“a rough guide”. FEBS Lett. 2009;583(11):1713–1720. doi: 10.1016/j.febslet.2009.04.012. - DOI - PubMed
    1. Larsen F, Gundersen G, Lopez R, Prydz H. CpG islands as gene markers in the human genome. Genomics. 1992;13(4):1095–1107. doi: 10.1016/0888-7543(92)90024-M. - DOI - PubMed
    1. Illingworth RS, Gruenewald-Schneider U, Webb S, Kerr ARW, James KD, Turner DJ, Smith C, Harrison DJ, Andrews R, Bird AP. Orphan CpG islands identify numerous conserved promoters in the mammalian genome. PLoS Genet. 2010;6(9):e1001134. doi: 10.1371/journal.pgen.1001134. - DOI - PMC - PubMed
    1. Jones PA. Functions of DNA methylation: islands, start sites, gene bodies and beyond. Nat Rev Genet. 2012;13(7):484–492. doi: 10.1038/nrg3230. - DOI - PubMed

Publication types

LinkOut - more resources