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ATR disruption leads to chromosomal fragmentation and early embryonic lethality.

Although a small decrease in survival and increase in tumor incidence was observed in ATR(+/-) mice, ATR(-/-) embryos die early in development, subsequent to the blastocyst stage and prior to 7.5 days p.c. In culture, ATR(-/-) blastocysts cells continue to cycle into mitosis for 2 days but subsequently fail to expand and die of caspase-dependent apoptosis. Importantly, caspase-independent chromosome breaks are observed in ATR(-/-) cells prior to widespread apoptosis, implying that apoptosis is caused by a loss of genomic integrity. These data show that ATR is essential for early embryonic development and must function in processes other than regulation of p53.

Pubmed ID: 10691732


  • Brown EJ
  • Baltimore D


Genes & development

Publication Data

February 15, 2000

Associated Grants


Mesh Terms

  • Animals
  • Apoptosis
  • Ataxia Telangiectasia Mutated Proteins
  • BRCA1 Protein
  • BRCA2 Protein
  • Blastocyst
  • Caspases
  • Cell Cycle Proteins
  • Cell Transformation, Neoplastic
  • Chromosome Aberrations
  • DNA Repair
  • Fetal Death
  • Gene Expression Regulation, Developmental
  • Gene Targeting
  • Genotype
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mitosis
  • Neoplasm Proteins
  • Neoplasms, Experimental
  • Protein-Serine-Threonine Kinases
  • Transcription Factors