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Cytogenetic manifestations associated with the reversion, by gene amplification, at the HGPRT locus in V79 Chinese hamster cells

Published online by Cambridge University Press:  14 April 2009

A. Di Leonardo ,
C. Agnese ,
P. Cavolina ,
A. Maddalena ,
G. Sciandrello  and
R. Randazzo
A. Di Leonardo
Affiliation:
Department of Cell and Developmental Biology ‘A. Monroy’, University of Palermo, via Archiraft 22, 90123 Palermo, Italy
C. Agnese
Affiliation:
Department of Cell and Developmental Biology ‘A. Monroy’, University of Palermo, via Archiraft 22, 90123 Palermo, Italy
P. Cavolina
Affiliation:
Department of Cell and Developmental Biology ‘A. Monroy’, University of Palermo, via Archiraft 22, 90123 Palermo, Italy
A. Maddalena
Affiliation:
Department of Cell and Developmental Biology ‘A. Monroy’, University of Palermo, via Archiraft 22, 90123 Palermo, Italy
G. Sciandrello
Affiliation:
Department of Cell and Developmental Biology ‘A. Monroy’, University of Palermo, via Archiraft 22, 90123 Palermo, Italy
R. Randazzo
Affiliation:
Department of Cell and Developmental Biology ‘A. Monroy’, University of Palermo, via Archiraft 22, 90123 Palermo, Italy
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Summary

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Some HGPRT spontaneous revertants were isolated from a mutant line (E2) of V79 Chinese hamster cells and phenotypically characterized. Dot–Blot hybridization with a 32P-Iabelled HGPRT probe revealed an increase in the number of HGPRT sequences in some of these revertants, suggesting the occurrence of gene amplification. Cytogenetic analysis performed in three of these revertants showed a characteristic abnormally banding region (ABR) on the elongated p arm of the X chromosome. In Situ hybridization in one revertant (RHE2) showed that the amplified sequences reside on the p+ arm of the X chromsome in two different localizations. Because of the very probable clonal origin of the revertant, these features indicate that the amplified sequences might rearrange after their integration into the chromosome.

Type
Research Article
Information
Genetics Research , Volume 53 , Issue 3 , June 1989 , pp. 201 - 206
Copyright
Copyright © Cambridge University Press 1989

References

Brennand, J., Chinault, A. C., Konecki, D. S., Melton, D. W. and Caskey, C. T. (1982). Cloned cDNA sequences of the hypoxanthine / guanine phosphoribosyltransferase gene from a mouse neuroblastoma cell line found to have amplified genomic sequences. Proceedings of the National Academy of Sciences USA 79, 1950–1954.CrossRefGoogle ScholarPubMed
Cowell, J. K. (1982). Double minutes and homogeneously staining regions may be due to breakage–fusion–bridge cycles following telomere loss. Chromosoma 88, 216–221.Google Scholar
Farrell, S. A. & Worton, R. G. (1977). Chromosome loss is responsible for segregation at the HPRT locus in Chinese hamster cell hybrids. Somatic Cell Genetics 3, 539–551.CrossRefGoogle ScholarPubMed
Fenwick, R. G. jr, Fuscoe, J. C. & Caskey, C. T. (1984). Amplification versus mutation as a mechanism for reversion of an HGPRT mutation. Somatic Cell and Molecular Genetics 10, 71–84.Google Scholar
Fuscoe, J. C., O'Neil, J. P., Machanoff, R. & Hsie, A. W. (1982). Quantification and analysis of reverse mutations at the HGPRT locus in Chinese hamster cells. Molecular and Cellular Biology 3, 1086–1096.Google Scholar
Gusella, J. A., Varsanyi, A., Kao, F. T., Jones, C., Puck, T. T., Keys, C., Orkin, S. & Housman, D. (1979). Precise localization of human β-globin gene complex on chromosome 11. Proceedings of the National Academy of Sciences USA 76, 1086–1096.Google Scholar
Hahn, P., Kapp, L. N., Morgan, W. F. & Painter, R. (1986). Chromosomal changes without DNA overproduction in hydroxyurea-treated mammalian cells: implications for gene amplification. Cancer Research 46, 4607–4612.Google Scholar
Hamlin, J. L., Milbrandt, J. D., Heintz, N. H. & Azizkhan, J. C. (1984). DNA sequence amplification. International Review of Cytology 90, 31–82.CrossRefGoogle ScholarPubMed
Harper, M. E., & Saunders, G. F. (1981). Localization of single copy DNA sequence on G-banded human chromosomes by in situ hybridization. Chromosoma 83, 431–439.Google Scholar
Kaufman, R. J., Brown, P. C. & Schimke, R. T. (1979). Amplified dihydrofolate reductase genes in unstably resistant cells are associated with double minute chromosomes. Proceedings of the National Academy of Sciences USA 76, 5669–5673.CrossRefGoogle ScholarPubMed
Kaufman, R. J., Sharp, P. A. & Latt, S. A. (1983). Evolution of chromosome regions containing transfected and amplified dihydrofolate reductase sequences. Molecular and Cellular Biology 3, 699–711.Google Scholar
Lewis, J. A., Biedler, J. L., & Melera, P. W. (1982). Gene amplification accompanies low level increases in the activity of dihydrofolate reductase in antifolate-resistant Chinese hamster lung cells containing abnormally banding chromosomes. Journal of Cell Biology 94, 418–424.Google Scholar
Maniatis, T., Fritsch, E. F. & Sambrook, J. (1982). Molecular Cloning. A Laboratory Manual. Cold Spring Harbor Laboratory.Google Scholar
Mariani, B. D. & Schimke, R. T. (1984). Gene amplification in a single cell-cycle in Chinese hamster ovary cells. Journal of Biological Chemistry 259, 1901–1910.CrossRefGoogle Scholar
McClintock, B. (1941). The stability of broken ends of chromosomes in Zea Mays, Genetics 26, 234–282.Google Scholar
Melton, D. W., Konecki, D. S., Ledbetter, D. H., Hejmanik, J. F. & Caskey, C. T. (1981). In vitro translation of hypoxanthine-guanine phosphoribosyltransferase mRNA: characterization of a mouse neuroblastoma cell line that has elevated levels of hypoxanthine-guanine phosphoribosyltransferase protein. Proceedings of the National Academy of Sciences USA 78, 6977–6980.Google Scholar
Morgan, W. F., Bodycote, J., Ferro, M. L., Hahn, P. J., Kapp, L. N., Pantelias, G. E. & Painter, R. B. (1986). A cytogenetic investigation of DNA replication after hydroxyurea treatment: implication for gene amplification. Chromosoma 93, 191–196.CrossRefGoogle ScholarPubMed
Patterson, D., Vannais, D. B., Niswander, L. A. & Davidson, J. N. (1985). Identification and localization of DNA alteration in Chinese hamster ovary cells mutants (Urd−) defective in the first three enzymes of the novo pyrimidine synthesis. Somatic Cell and Molecular Genetics 11, 379–390.Google Scholar
Roberts, J. M. & Axel, R. (1982). Gene amplification and gene correction in somatic cells. Cell 29, 109–119.Google Scholar
Sager, R., Gadi, I. K., Stephens, L. & Garbowy, C. T. (1985). Gene amplification: an example of accelerated evolution in tumorigenic cells. Proceedings of the National Academy of Sciences USA 82, 7015–7019.Google Scholar
Schimke, R. T., Sherwood, S. W., Hill, A. B. & Johnston, R. N. (1986). Overreplication and recombination of DNA in higher eukaryotes: potential consequences and biological implications. Proceedings of the National Academy of Sciences USA 83, 2157–2161.Google Scholar
Seabright, M. (1971). A rapid banding technique for human chromosomes. Lancet ii, 971–972.Google Scholar
Stark, G. R. (1986). DNA amplification in drug resistant cells and in tumors. Cancer Surveys 5, 1–23.Google Scholar
Steglich, C., Grens, A. & Scheffer, I. E. (1985). Chinese hamster cells deficient in ornithine decarboxylase activity: reversion by gene amplification and by azacytidine treatment. Somatic Cell and Molecular Genetics 11, 11–23.Google Scholar
Sumner, A. T. (1972). A simple technique for demonstrating centromeric heterochromatin. Experimental Cell Research 75, 304–306.CrossRefGoogle ScholarPubMed
Zabel, B. U., Naylor, S. L., Sakaguchi, A. J., Bell, G. I. & Shows, T. B. (1983). High resolution chromosomal localization of human genes for amylase, proopiomelanocortin, somatostatin and a DNA fragment (D3S1) by in situ hybridization. Proceedings of the National Academy of Sciences U.S.A. 80, 6932–6936.Google Scholar
Zownir, O., Fuscoe, J. C., Fenwick, R. & Morrow, J. (1984). Gene amplification as a mechanism for reversion at the HGPRT locus in V79 Chinese hamster cells. Journal of Cellular Physiology 119, 341–348.Google Scholar