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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Turker, M.S. et al.

Turker, Gage, Rose, Ponomareva, Tischfield, Stambrook, Barlow, Wynshaw-Boris,

Solid tissues removed from ATM homozygous deficient mice do not exhibit a mutator phenotype for second-step autosomal mutations.

The presence of increased frequencies of blood-derived and solid tumors in ataxia-telangiectasia (A-T) patients, coupled with a role for the ATM (A-T mutation) protein in detecting specific forms of DNA damage, has led to the assumption of a mutator phenotype in A TM-deficient cells. Supporting this assumption are observations of increased rates of chromosomal aberrations and intrachromosomal homologous recombinational events in the cells of A-T patients. We have bred mice with knockout mutations for the selectable Aprt (adenine phosphoribosyltransferase) locus and the Atm locus to examine the frequency of second-step autosomal mutations in Atm-deficient cells. Two solid tissues were examined: (a) the ear, which yields predominately mesenchymal cells; and (b) the kidney, which yields predominately epithelial cells. We report here the lack of a mutator phenotype for inactivating autosomal mutations in solid tissues of the Atm-deficient mice.[1]

References

Solid tissues removed from ATM homozygous deficient mice do not exhibit a mutator phenotype for second-step autosomal mutations. Turker, M.S., Gage, B.M., Rose, J.A., Ponomareva, O.N., Tischfield, J.A., Stambrook, P.J., Barlow, C., Wynshaw-Boris, A. Cancer Res. (1999) [Pubmed]

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