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MEP-1 and a homolog of the NURD complex component Mi-2 act together to maintain germline-soma distinctions in C. elegans.

A rapid cascade of regulatory events defines the developmental fates of embryonic cells. However, once established, these developmental fates and the underlying transcriptional programs can be remarkably stable. Here, we describe two proteins, MEP-1 and LET-418/Mi-2, required for maintenance of somatic differentiation in C. elegans. In animals lacking MEP-1 and LET-418, germline-specific genes become derepressed in somatic cells, and Polycomb group (PcG) and SET domain-related proteins promote this ectopic expression. MEP-1 and LET-418 interact in vivo with the germline-protein PIE-1. Our findings support a model in which PIE-1 inhibits MEP-1 and associated factors to maintain the pluripotency of germ cells, while at later times MEP-1 and LET-418 remodel chromatin to establish new stage- or cell-type-specific differentiation potential.

Pubmed ID: 12507426


  • Unhavaithaya Y
  • Shin TH
  • Miliaras N
  • Lee J
  • Oyama T
  • Mello CC



Publication Data

December 27, 2002

Associated Grants

  • Agency: NICHD NIH HHS, Id: HD33769
  • Agency: NICHD NIH HHS, Id: HD36247

Mesh Terms

  • Adenosine Triphosphatases
  • Animals
  • Autoantigens
  • Caenorhabditis elegans
  • Caenorhabditis elegans Proteins
  • Cell Differentiation
  • Cell Lineage
  • DNA Helicases
  • Embryo, Nonmammalian
  • Gene Expression Regulation, Developmental
  • Germ Cells
  • Histone Deacetylases
  • Mi-2 Nucleosome Remodeling and Deacetylase Complex
  • Nuclear Proteins
  • Transcription Factors