This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Turker, M. S. Articles by Wynshaw-Boris, A. Search for Related Content PubMed PubMed Citation Articles by Turker, M. S. Articles by Wynshaw-Boris, A.

Solid Tissues Removed from Atm Homozygous Deficient Mice Do Not Exhibit a Mutator Phenotype for Second-Step Autosomal Mutations¹

Center for Research on Occupational and Environmental Toxicology, Oregon Health Sciences University, Portland, Oregon 97201 [M. S. T., B. M. G., J. A. R., O. N. P.]; Department of Genetics, Rutgers, the State University of New Jersey, Piscataway, New Jersey 08854 [J. A. T.]; Department of Cell Biology, Neurobiology, and Anatomy, University of Cincinnati, College of Medicine, Cincinnati, Ohio 45267-0521 [P. J. S.]; and Genetic Disease Research Branch, National Human Genome Research Institute, NIH, Bethesda, Maryland 20892 [C. B., A. W-B.]

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 ATM-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.

This article has been cited by other articles:

				M. S. Turker Autosomal mutation in somatic cells of the mouse Mutagenesis, January 1, 2003; 18(1): 1 - 6. [Abstract] [Full Text] [PDF]

				O. N. Ponomareva, J. A. Rose, M. Lasarev, J. Rasey, and M. S. Turker Tissue-specific Deletion and Discontinuous Loss of Heterozygosity Are Signatures for the Mutagenic Effects of Ionizing Radiation in Solid Tissues Cancer Res., March 1, 2002; 62(5): 1518 - 1523. [Abstract] [Full Text] [PDF]

				A. J.R. Bishop and R. H. Schiestl Homologous recombination as a mechanism for genome rearrangements: environmental and genetic effects Hum. Mol. Genet., October 1, 2000; 9(16): 2427 - 2334. [Abstract] [Full Text] [PDF]

				A. J. R. Bishop, C. Barlow, A. J. Wynshaw-Boris, and R. H. Schiestl Atm Deficiency Causes an Increased Frequency of Intrachromosomal Homologous Recombination in Mice Cancer Res., January 1, 2000; 60(2): 395 - 399. [Abstract] [Full Text]