Chromosome breakage induced by bleomycin in an ataxia telangiectasia lymphoblastoid line: correlation with fragile sites and Epstein-Barr virus DNA localization.
We have analyzed the distribution of bleomycin-induced breaks in a subline of the ATL9 lymphoblastoid line, derived from peripheral lymphocytes of an ataxia telangiectasia patient, transformed in vitro by Epstein-Barr virus (EBV). As reported elsewhere (Caporossi et al., 1988), the major feature of this subline, ATL9/g, is a stable achromatic gap at 1p32 in one of the chromosomes 1, overlapping a preferential site of EBV localization. The results of this paper show that this gap is highly sensitive to bleomycin-induced damage. In addition, the breaks induced by bleomycin in ATL9 cells are distributed nonrandomly and are preferentially localized in bands where fragile sites have been mapped.
Caporossi
D
D
Department of Public Health and Cell Biology, II University of Rome, Italy.
Tedeschi
B
B
Vernole
P
P
Porfirio
B
B
Nicoletti
B
B
D001260:Ataxia Telangiectasia / Q000235:genetics / Q000473:pathology*; D001761:Bleomycin / Q000494:pharmacology*; D002461:Cell Line, Transformed; D002871:Chromosome Banding; D043283:Chromosome Fragile Sites; D002873:Chromosome Fragility; D002874:Chromosome Mapping; D002875:Chromosomes / Q000187:drug effects* / Q000648:ultrastructure; D004249:DNA Damage; D004279:DNA, Viral; D004854:Herpesvirus 4, Human / Q000235:genetics; D006801:Humans; D007945:Leukemia, Lymphoid / Q000235:genetics / Q000473:pathology*; D014170:Transformation, Genetic / Q000235:genetics
D004279:DNA, Viral; D001761:Bleomycin