Proceedings of the National Academy of Sciences of the United States of America · 2000
Abnormal development of Purkinje cells and lymphocytes in Atm mutant mice.
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Borghesani P R, Alt F W, Bottaro A, Davidson L, Aksoy S, Rathbun G A, Roberts T M, Swat W, Segal R A, Gu Y
Аннотация
Motor incoordination, immune deficiencies, and an increased risk of cancer are the characteristic features of the hereditary disease ataxia-telangiectasia (A-T), which is caused by mutations in the ATM gene. Through gene targeting, we have generated a line of Atm mutant mice, Atm(y/y) mice. In contrast to other Atm mutant mice, Atm(y/y) mice show a lower incidence of thymic lymphoma and survive beyond a few months of age. Atm(y/y) mice exhibit deficits in motor learning indicative of cerebellar dysfunction. Even though we found no gross cerebellar degeneration in older Atm(y/y) animals, ectopic and abnormally differentiated Purkinje cells were apparent in mutant mice of all ages. These findings establish that some neuropathological abnormalities seen in A-T patients also are present in Atm mutant mice. In addition, we report a previously unrecognized effect of Atm deficiency on development or maintenance of CD4(+)8(+) thymocytes. We discuss these findings in the context of the hypothesis that abnormal development of Purkinje cells and lymphocytes contributes to the pathogenesis of A-T.
Предметные рубрики MeSH
AnimalsAtaxia TelangiectasiaAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCerebellumDNA-Binding ProteinsFemaleFlow CytometryGene Expression Regulation, DevelopmentalLife ExpectancyLymphocytesMaleMiceMice, Mutant StrainsNeoplasms, ExperimentalProtein Serine-Threonine KinasesPsychomotor PerformancePurkinje CellsTumor Suppressor Proteins