Translational repression of cyclin E prevents precocious mitosis and embryonic gene activation during C. elegans meiosis

Dev Cell. 2009 Sep;17(3):355-64. doi: 10.1016/j.devcel.2009.08.003.


Germ cells, the cells that give rise to sperm and egg, maintain the potential to recreate all cell types in a new individual. This wide developmental potential, or totipotency, is manifested in unusual tumors called teratomas, in which germ cells undergo somatic differentiation. Although recent studies have implicated RNA regulation, the mechanism that normally prevents the loss of germ cell identity remains unexplained. In C. elegans, a teratoma is induced in the absence of the conserved RNA-binding protein GLD-1. Here, we demonstrate that GLD-1 represses translation of CYE-1/cyclin E during meiotic prophase, which prevents germ cells from re-entering mitosis and inducing embryonic-like transcription. We describe a mechanism that prevents precocious mitosis in germ cells undergoing meiosis, propose that this mechanism maintains germ cell identity by delaying the onset of embryonic gene activation until after fertilization, and provide a paradigm for the possible origin of human teratomas.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3' Untranslated Regions
  • Animals
  • Animals, Genetically Modified
  • Caenorhabditis elegans
  • Caenorhabditis elegans Proteins / chemistry
  • Caenorhabditis elegans Proteins / physiology*
  • Cell Cycle
  • Cyclin B / metabolism
  • Cyclin E / biosynthesis*
  • Cyclin E / metabolism
  • Fertilization
  • Gene Expression Regulation*
  • Germ Cells / metabolism
  • Meiosis*
  • Mitosis*
  • Models, Biological
  • Protein Biosynthesis*


  • 3' Untranslated Regions
  • Caenorhabditis elegans Proteins
  • Cyclin B
  • Cyclin E
  • GLD-1 protein, C elegans