Title:
Epigenetic histone modifications of human transposable elements: genome defense versus exaptation

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dc.contributor.author Huda, Ahsan en_US
dc.contributor.author Mariño-Ramírez, Leonardo en_US
dc.contributor.author Jordan, I. King en_US
dc.contributor.corporatename Georgia Institute of Technology. School of Biology en_US
dc.date.accessioned 2011-12-22T19:59:36Z
dc.date.available 2011-12-22T19:59:36Z
dc.date.issued 2010-01-25
dc.description © 2010 Huda et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. en_US
dc.description DOI: 10.1186/1759-8753-1-2 en_US
dc.description.abstract Background: Transposition is disruptive in nature and, thus, it is imperative for host genomes to evolve mechanisms that suppress the activity of transposable elements (TEs). At the same time, transposition also provides diverse sequences that can be exapted by host genomes as functional elements. These notions form the basis of two competing hypotheses pertaining to the role of epigenetic modifications of TEs in eukaryotic genomes: the genome defense hypothesis and the exaptation hypothesis. To date, all available evidence points to the genome defense hypothesis as the best explanation for the biological role of TE epigenetic modifications. Results: We evaluated several predictions generated by the genome defense hypothesis versus the exaptation hypothesis using recently characterized epigenetic histone modification data for the human genome. To this end, we mapped chromatin immunoprecipitation sequence tags from 38 histone modifications, characterized in CD4+ T cells, to the human genome and calculated their enrichment and depletion in all families of human TEs. We found that several of these families are significantly enriched or depleted for various histone modifications, both active and repressive. The enrichment of human TE families with active histone modifications is consistent with the exaptation hypothesis and stands in contrast to previous analyses that have found mammalian TEs to be exclusively repressively modified. Comparisons between TE families revealed that older families carry more histone modifications than younger ones, another observation consistent with the exaptation hypothesis. However, data from within family analyses on the relative ages of epigenetically modified elements are consistent with both the genome defense and exaptation hypotheses. Finally, TEs located proximal to genes carry more histone modifications than the ones that are distal to genes, as may be expected if epigenetically modified TEs help to regulate the expression of nearby host genes. Conclusions: With a few exceptions, most of our findings support the exaptation hypothesis for the role of TE epigenetic modifications when vetted against the genome defense hypothesis. The recruitment of epigenetic modifications may represent an additional mechanism by which TEs can contribute to the regulatory functions of their host genomes. en_US
dc.identifier.citation Huda, A., Mariño-Ramírez, L. and I.K. Jordan, 2010. Epigenetic histone modifications of human transposable elements: genome defense versus exaptation. Mobile DNA 1:2 en_US
dc.identifier.doi 10.1186/1759-8753-1-2
dc.identifier.issn 1759-8753
dc.identifier.uri http://hdl.handle.net/1853/42112
dc.language.iso en_US en_US
dc.publisher Georgia Institute of Technology en_US
dc.publisher.original BioMed Central en_US
dc.subject Genome evolution en_US
dc.subject Transposable elements en_US
dc.subject Transposition en_US
dc.subject Genome defense en_US
dc.subject Exaptation en_US
dc.title Epigenetic histone modifications of human transposable elements: genome defense versus exaptation en_US
dc.type Text
dc.type.genre Article
dspace.entity.type Publication
local.contributor.author Jordan, I. King
local.contributor.corporatename College of Sciences
local.contributor.corporatename School of Biological Sciences
relation.isAuthorOfPublication 1c155699-6f2d-418d-83cd-9e1424896d4f
relation.isOrgUnitOfPublication 85042be6-2d68-4e07-b384-e1f908fae48a
relation.isOrgUnitOfPublication c8b3bd08-9989-40d3-afe3-e0ad8d5c72b5
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