Rad51-deficient vertebrate cells accumulate chromosomal breaks prior to cell death

EMBO J. 1998 Jan 15;17(2):598-608. doi: 10.1093/emboj/17.2.598.


Yeast rad51 mutants are viable, but extremely sensitive to gamma-rays due to defective repair of double-strand breaks. In contrast, disruption of the murine RAD51 homologue is lethal, indicating an essential role of Rad51 in vertebrate cells. We generated clones of the chicken B lymphocyte line DT40 carrying a human RAD51 transgene under the control of a repressible promoter and subsequently disrupted the endogenous RAD51 loci. Upon inhibition of the RAD51 transgene, Rad51- cells accumulated in the G2/M phase of the cell cycle before dying. Chromosome analysis revealed that most metaphase-arrested Rad51- cells carried isochromatid-type breaks. In conclusion, Rad51 fulfils an essential role in the repair of spontaneously occurring chromosome breaks in proliferating cells of higher eukaryotes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Avian Proteins
  • B-Lymphocytes / metabolism*
  • B-Lymphocytes / pathology*
  • Cell Death / genetics
  • Cell Line
  • Chickens
  • Chromosome Aberrations / genetics*
  • Cloning, Molecular
  • DNA-Binding Proteins / biosynthesis
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / metabolism
  • G2 Phase / genetics
  • Gene Deletion
  • Gene Expression
  • Gene Targeting
  • Mitosis / genetics
  • Rad51 Recombinase
  • Transfection


  • Avian Proteins
  • DNA-Binding Proteins
  • RAD51 protein, Gallus gallus
  • Rad51 Recombinase