Epigenetic Regulation by Polycomb Complexes from Drosophila to Human and Its Relation to Communicable Disease Pathogenesis

Int J Mol Sci. 2022 Oct 14;23(20):12285. doi: 10.3390/ijms232012285.

Abstract

Although all cells in the human body are made of the same DNA, these cells undergo differentiation and behave differently during development, through integration of external and internal stimuli via 'specific mechanisms.' Epigenetics is one such mechanism that comprises DNA/RNA, histone modifications, and non-coding RNAs that regulate transcription without changing the genetic code. The discovery of the first Polycomb mutant phenotype in Drosophila started the study of epigenetics more than 80 years ago. Since then, a considerable number of Polycomb Group (PcG) genes in Drosophila have been discovered to be preserved in mammals, including humans. PcG proteins exert their influence through gene repression by acting in complexes, modifying histones, and compacting the chromatin within the nucleus. In this article, we discuss how our knowledge of the PcG repression mechanism in Drosophila translates to human communicable disease research.

Keywords: PcG; Polycomb; communicable; pathogenesis.

Publication types

  • Review

MeSH terms

  • Animals
  • Chromatin / genetics
  • Chromatin / metabolism
  • Communicable Diseases* / genetics
  • DNA / metabolism
  • Drosophila / genetics
  • Drosophila / metabolism
  • Drosophila Proteins* / genetics
  • Drosophila Proteins* / metabolism
  • Epigenesis, Genetic
  • Histones / metabolism
  • Humans
  • Mammals / metabolism
  • Polycomb Repressive Complex 1 / genetics
  • Polycomb-Group Proteins / genetics
  • Polycomb-Group Proteins / metabolism
  • RNA / metabolism

Substances

  • Histones
  • Drosophila Proteins
  • Polycomb-Group Proteins
  • Chromatin
  • DNA
  • RNA
  • Polycomb Repressive Complex 1

Grants and funding

This work was supported by the Intramural Research Program of the Center for Biologics Evaluation and Research (CBER), U.S. Food and Drug Administration. This project was also supported in part by Aaron Scholl’s appointment to the Research Participation Program at CBER administered by the Oak Ridge Institute for Science and Education through the US Department of Energy and U.S. Food and Drug Administration.