Chromosome breakage induced by bleomycin in an ataxia telangiectasia lymphoblastoid line: correlation with fragile sites and Epstein-Barr virus DNA localization

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Abstract
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 lp32 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.