| First Author | Laposa RR | Year | 2004 |
| Journal | FASEB J | Volume | 18 |
| Issue | 7 | Pages | 896-8 |
| PubMed ID | 15033931 | Mgi Jnum | J:118485 |
| Mgi Id | MGI:3699668 | Doi | 10.1096/fj.03-0903fje |
| Citation | Laposa RR, et al. (2004) Atm-null mice exhibit enhanced radiation-induced birth defects and a hybrid form of embryonic programmed cell death indicating a teratological suppressor function for ATM. FASEB J 18(7):896-8 |
| abstractText | ATM (ataxia-telangiectasia mutated) is a genotoxic stress transducer. In this first report of Atm-dependent birth defects, Atm-null embryos were uniquely susceptible to low-dose (0.5 Gy) radiation, exhibiting severe runting, tail anomalies, and lethality, independent of cell cycle arrest or insulin-like growth factor 1. This treatment enhanced levels of p53 protein and central nervous system (CNS) apoptosis in wild-type mice, but not Atm-null mutants, at 6 h postirradiation. At 48 h, however, this pattern was reversed, with Atm-null mice exhibiting high levels of a hybrid form of programmed cell death within the CNS. Even heterozygous Atm-deficient embryos were radiosensitive to a higher radiation dose of 2 Gy. These results show that Atm is a novel teratologic suppressor gene protecting embryos from pathological cell death and teratogenesis initiated by even mild DNA damage. |
