| First Author | Brown EJ | Year | 2000 |
| Journal | Genes Dev | Volume | 14 |
| Issue | 4 | Pages | 397-402 |
| PubMed ID | 10691732 | Mgi Jnum | J:60768 |
| Mgi Id | MGI:1353879 | Doi | 10.1101/gad.14.4.397 |
| Citation | Brown EJ, et al. (2000) ATR disruption leads to chromosomal fragmentation and early embryonic lethality. Genes Dev 14(4):397-402 |
| abstractText | 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. |
