A snapshot of histone modifications within transposable elements in Drosophila wild type strains

PLoS One. 2012;7(9):e44253. doi: 10.1371/journal.pone.0044253. Epub 2012 Sep 4.

Abstract

Transposable elements (TEs) are a major source of genetic variability in genomes, creating genetic novelty and driving genome evolution. Analysis of sequenced genomes has revealed considerable diversity in TE families, copy number, and localization between different, closely related species. For instance, although the twin species Drosophila melanogaster and D. simulans share the same TE families, they display different amounts of TEs. Furthermore, previous analyses of wild type derived strains of D. simulans have revealed high polymorphism regarding TE copy number within this species. Several factors may influence the diversity and abundance of TEs in a genome, including molecular mechanisms such as epigenetic factors, which could be a source of variation in TE success. In this paper, we present the first analysis of the epigenetic status of four TE families (roo, tirant, 412 and F) in seven wild type strains of D. melanogaster and D. simulans. Our data shows intra- and inter-specific variations in the histone marks that adorn TE copies. Our results demonstrate that the chromatin state of common TEs varies among TE families, between closely related species and also between wild type strains.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biological Evolution
  • Chromatin / metabolism
  • DNA Copy Number Variations
  • DNA Methylation
  • DNA Transposable Elements*
  • Drosophila / genetics*
  • Drosophila / metabolism
  • Drosophila melanogaster / genetics
  • Drosophila melanogaster / metabolism
  • Epigenesis, Genetic
  • Gene Expression
  • Genetic Variation
  • Genome, Insect
  • Genotype
  • Histones / genetics*
  • Histones / metabolism
  • Protein Processing, Post-Translational*
  • Species Specificity

Substances

  • Chromatin
  • DNA Transposable Elements
  • Histones

Grants and funding

This work was funded by Centre National de Recherche Scientifique (CNRS), the Agence National de la Recherche (ANR)–09–Programe Blanc–0103-01, and Cible 2008 (Région Rhône Alpes) for C. Vieira’s laboratory. Prof. E. Gilson is an associate member of European Union 6th framework program The Epigenome Network of Excellence (NoE), and his laboratory was funded by a European Union 6th framework program grant RISCRAD and ARECA framework program from Canceropole Lyon Auvergne Rhône Alpes. The Swiss National Science Foundation and the State of Geneva fund the work of F. Begeot and M. Delattre. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.