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1 Departments of Molecular Biology and Genetics,
2 Comparative Medicine, and
3 Oncology, The Johns Hopkins University School of Medicine, Baltimore, Maryland
To examine the role of ataxia-telangiectasia mutated (Atm) in telomere function, we generated Atm and telomerase null mice (Atm-/- mTR-/- iG6 mice). These mice exhibited increased germ cell death and chromosome fusions compared with either Atm-/- or mTR-/- iG6 mice. Furthermore, the Atm-/- mTR-- iG6 mice had a delayed onset and reduced incidence of thymic lymphoma compared with Atm-/- mice. The tumors in the Atm-/- mTR-/- iG6 mice showed increased apoptosis and anaphase bridges. Finally, lymphomas from Atm-/- mTR-/- iG6 mice were derived from CD8 immature, single-positive T cells, whereas Atm-/- lymphomas were from CD4+CD8+ double-positive T cells. We propose that Atm protects short telomeres and that Atm deficiency cooperates with short telomeres, leading to increased cell death, decreased tumorigenesis, and increased overall survival.
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