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Phosphorylation at murine Serine 18 (human Serine 15) is a critical regulatory process for the tumor suppressor function of p53. p53Ser18 residue is a substrate for  ataxia-telangiectasia mutated  (ATM) and  ATM-related  (ATR) protein kinases. Studies of mice with a germ-line mutation that replaces Ser18 with Ala ( p53 S18A   mice) have demonstrated that loss of phosphorylation of p53Ser18 leads to the development of tumors, including lymphomas, fibrosarcomas, leukemia and leiomyosarcomas. The predominant lymphoma is B-cell lymphoma, which is in contrast to the lymphomas observed in  Atm −/−   animals. This observation and the fact that multiple kinases phosphorylate p53Ser18 suggest Atm-independent tumor suppressive functions of p53Ser18. Therefore, in order to examine p53Ser18 function in relationship to ATM, we analyzed the lifespan and tumorigenesis of mice with combined mutations in p53Ser18 and  Atm . Surprisingly, we observed no cooperation in survival and tumorigenesis in compound  p53 S18A   and  Atm −/−   animals. However, we observed embryonic lethality in the compound mutant animals. In addition, the homozygous p53Ser18 mutant allele impacted the weight of  Atm −/−   animals. These studies examine the genetic interaction of p53Ser18 and  Atm in vivo . Furthermore, these studies demonstrate a role of p53Ser18 in regulating embryonic survival and motor coordination.

Loss of p53 Ser18 and Atm Results in Embryonic Lethality without Cooperation in Tumorigenesis