Molecular Genetics and Genomics

, Volume 287, Issue 7, pp 591–606

The maize b1 paramutation control region causes epigenetic silencing in Drosophila melanogaster

Original Paper

DOI: 10.1007/s00438-012-0702-z

Cite this article as:
McEachern, L.A. & Lloyd, V.K. Mol Genet Genomics (2012) 287: 591. doi:10.1007/s00438-012-0702-z


Paramutation is an epigenetic process in which a combination of alleles in a heterozygous organism results in a meiotically stable change in expression of one of the alleles. The mechanisms underlying paramutation are being actively investigated, and examples have been described in both plants and mammals, suggesting that it may utilize epigenetic mechanisms that are widespread and evolutionarily conserved. Paramutation at the well-studied maize b1 locus requires a control region consisting of seven 853 bp tandem repeats. To study the conservation of the epigenetic mechanisms underlying seemingly unique epigenetic processes such as paramutation, we created transgenic Drosophilamelanogaster carrying the maize b1 control region adjacent to the Drosophilawhite reporter gene. We show that the b1 tandem repeats cause silencing of the white reporter in Drosophila. A single copy of the tandem repeat sequence is sufficient to cause silencing, and silencing strength increases as the number of tandem repeats increases. Additionally, transgenic lines with the full seven tandem repeats demonstrate evidence of either pairing-sensitive silencing and silencing in trans, or epigenetic activation in trans. These trans-interactions are dependent on repeat number, similar to maize b1 paramutation. Also, as in maize, the tandem repeats are bidirectionally transcribed in Drosophila. These results indicate that the maize b1 tandem repeats function as an epigenetic silencer and mediate trans-interactions in Drosophila, and support the hypothesis that the mechanisms underlying such epigenetic processes are conserved.


EpigeneticsParamutationTandem repeatsSilencingDrosophila melanogaster

Supplementary material

438_2012_702_MOESM1_ESM.doc (57 kb)
Supplementary material 1 (DOC 57 kb)

Copyright information

© Springer-Verlag 2012

Authors and Affiliations

  1. 1.Department of BiologyDalhousie UniversityHalifaxCanada
  2. 2.Department of BiologyMount Allison UniversitySackvilleCanada
  3. 3.Department of PhysiologyDalhousie UniversityHalifaxCanada