Spreading the silence: epigenetic transcriptional regulation during Drosophila development

Dev Genet. 1994;15(6):478-84. doi: 10.1002/dvg.1020150606.


In early Drosophila development a complex cascade of diffusible transcription factors generates an intricate expression pattern of developmental regulators such as the homeotic genes. The mechanism which subsequently maintains the pattern during the rest of development is mainly using epigenetic features for its function. Evidence comes from the analysis of the Polycomb-group (Pc-G), a class of genes which is responsible for maintaining the inactive state of expression. The Pc-G was found to share many parallels to genes involved in heterochromatin formation. Different members of the Pc-G interact in large multiprotein complexes, which apparently can cover and inactivate large chromosomal domains. Specific DNA elements have been identified that are used by the Pc-G proteins to nucleate these specialized domains of silent chromatin. Thus, the Pc-G proteins appear to permanently inactivate genes by generating heterochromatin-like structures which could then be inherited by the daughter cells in an epigenetic manner. Heritable gene silencing is an important but little understood mechanism in pattern formation. Phenomenologically related effects have been observed in many organisms. These range from the transcriptional silencing of the inactive mating type loci in yeast to parental imprinting phenomena and X-chromosome inactivation in mammals. Analysis of these functions in Drosophila provides an excellent model system for studying the molecular basis of such epigenetic mechanisms that use higher order chromatin structures for transcriptional repression.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biological Evolution
  • Cell Compartmentation
  • Cell Nucleus / ultrastructure
  • Drosophila melanogaster / genetics*
  • Gene Expression Regulation, Developmental*
  • Genes, Homeobox*
  • Heterochromatin / physiology
  • Mating Factor
  • Morphogenesis
  • Peptides / genetics
  • Saccharomyces cerevisiae / genetics*
  • Transcription, Genetic


  • Heterochromatin
  • Peptides
  • Mating Factor