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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.

ATR disruption leads to chromosomal fragmentation and early embryonic lethality