Formation of a Polycomb-Domain in the Absence of Strong Polycomb Response Elements

PLoS Genet. 2016 Jul 28;12(7):e1006200. doi: 10.1371/journal.pgen.1006200. eCollection 2016 Jul.

Abstract

Polycomb group response elements (PREs) in Drosophila are DNA-elements that recruit Polycomb proteins (PcG) to chromatin and regulate gene expression. PREs are easily recognizable in the Drosophila genome as strong peaks of PcG-protein binding over discrete DNA fragments; many small but statistically significant PcG peaks are also observed in PcG domains. Surprisingly, in vivo deletion of the four characterized strong PREs from the PcG regulated invected-engrailed (inv-en) gene complex did not disrupt the formation of the H3K27me3 domain and did not affect inv-en expression in embryos or larvae suggesting the presence of redundant PcG recruitment mechanism. Further, the 3D-structure of the inv-en domain was only minimally altered by the deletion of the strong PREs. A reporter construct containing a 7.5kb en fragment that contains three weak peaks but no large PcG peaks forms an H3K27me3 domain and is PcG-regulated. Our data suggests a model for the recruitment of PcG-complexes to Drosophila genes via interactions with multiple, weak PREs spread throughout an H3K27me3 domain.

Publication types

  • Research Support, N.I.H., Intramural

MeSH terms

  • Animals
  • Chromatin / genetics*
  • DNA-Binding Proteins / biosynthesis
  • DNA-Binding Proteins / genetics*
  • Drosophila melanogaster / genetics
  • Gene Expression Regulation, Developmental
  • Genome, Insect
  • Histone Demethylases / genetics
  • Imaginal Discs / growth & development
  • Imaginal Discs / metabolism
  • Larva / genetics
  • Larva / growth & development
  • Polycomb-Group Proteins / biosynthesis
  • Polycomb-Group Proteins / chemistry
  • Polycomb-Group Proteins / genetics*
  • Protein Binding / genetics
  • Protein Domains / genetics
  • Response Elements / genetics*

Substances

  • Chromatin
  • DNA-Binding Proteins
  • Polycomb-Group Proteins
  • Histone Demethylases

Grant support

This work was supported by the Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.