The Effect of Transposon P{GUS · p53.259H} on the Frequency of Tumor Clones in Drosophila melanogaster wtsP2/+ Heterozygotes

The Effect of Transposon P{GUS · p53.259H} on the Frequency of Tumor Clones in Drosophila... We showed that transposon P{GUS · p53.259H}, mapped to chromosome 3 and carrying a dominant mutation p53 259H.GUS, has a positive effect on the frequency of spontaneous and carcinogen-induced tumor mosaic clones warts – in Drosopila melanogaster heterozygotes for the tumor suppressor gene warts located in the same chromosome. The transposon effect could be explained either by the arrest of apoptosis in the cells expressing mutant p53 259H.GUS gene and containing carcinogen-induced pre-mutations, and/or by genetic instability introduced into chromosome 3 by the P{GUS · p53.259H} transposon itself. The effect of the P{GUS · p53.259H} appeared to be carcinogen-specific. It substantially increased the frequency of tumors induced by supermutagenic platinum complex, oxoplatin, and did not increase the frequencies of tumors induced by polycyclic aromatic hydrocarbons, benzo(α)pyrene and pyrene. In the spectrum of mutations induced by all carcinogens tested, somatic recombination events prevailed over somatic mutations. Hence, carcinogen-specificity of the P{GUS · p53.259H} effect cannot be explained by preferential induction of somatic mutations or somatic recombination by one of the carcinogens. Organ-specificity of the increased frequency of mosaic warts – clones induced by P{GUS · p53.259H} was established. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Russian Journal of Genetics Springer Journals

The Effect of Transposon P{GUS · p53.259H} on the Frequency of Tumor Clones in Drosophila melanogaster wtsP2/+ Heterozygotes

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Publisher
Kluwer Academic Publishers-Plenum Publishers
Copyright
Copyright © 2002 by MAIK “Nauka/Interperiodica”
Subject
Biomedicine; Human Genetics
ISSN
1022-7954
eISSN
1608-3369
D.O.I.
10.1023/A:1016339604917
Publisher site
See Article on Publisher Site

Abstract

We showed that transposon P{GUS · p53.259H}, mapped to chromosome 3 and carrying a dominant mutation p53 259H.GUS, has a positive effect on the frequency of spontaneous and carcinogen-induced tumor mosaic clones warts – in Drosopila melanogaster heterozygotes for the tumor suppressor gene warts located in the same chromosome. The transposon effect could be explained either by the arrest of apoptosis in the cells expressing mutant p53 259H.GUS gene and containing carcinogen-induced pre-mutations, and/or by genetic instability introduced into chromosome 3 by the P{GUS · p53.259H} transposon itself. The effect of the P{GUS · p53.259H} appeared to be carcinogen-specific. It substantially increased the frequency of tumors induced by supermutagenic platinum complex, oxoplatin, and did not increase the frequencies of tumors induced by polycyclic aromatic hydrocarbons, benzo(α)pyrene and pyrene. In the spectrum of mutations induced by all carcinogens tested, somatic recombination events prevailed over somatic mutations. Hence, carcinogen-specificity of the P{GUS · p53.259H} effect cannot be explained by preferential induction of somatic mutations or somatic recombination by one of the carcinogens. Organ-specificity of the increased frequency of mosaic warts – clones induced by P{GUS · p53.259H} was established.

Journal

Russian Journal of GeneticsSpringer Journals

Published: Oct 13, 2004

References

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