TY - JOUR
T1 - The Effect of Transposon P{GUS·p53.259H} on the Frequency of Tumor Clones in Drosophila melanogaster wtsP2/+ Heterozygotes
AU - Sidorov, R. A.
AU - Belitsky, G. A.
N1 - Funding Information:
This work was supported by the Russian Foundation for Basic Research (grant no. 01-04-49285) and International Science and Technology Center (grant no. 0-832).
PY - 2002/7
Y1 - 2002/7
N2 - We showed that transposon P{GUS · p53.259H}, mapped to chromosome 3 and carrying a dominant mutation p53259H.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 p53259H.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.
AB - We showed that transposon P{GUS · p53.259H}, mapped to chromosome 3 and carrying a dominant mutation p53259H.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 p53259H.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.
UR - http://www.scopus.com/inward/record.url?scp=0346355329&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0346355329&partnerID=8YFLogxK
U2 - 10.1023/A:1016339604917
DO - 10.1023/A:1016339604917
M3 - Article
AN - SCOPUS:0346355329
SN - 1022-7954
VL - 38
SP - 777
EP - 784
JO - Russian Journal of Genetics
JF - Russian Journal of Genetics
IS - 7
ER -