Suppression of X-ray-induced chromosome aberrations in ataxia telangiectasia cells by introduction of a normal human chromosome 11.
We studied X-ray-induced chromosome aberrations in ataxia telangiectasia (AT) cells containing an introduced chromosome 11 or 12 derived from normal human fibroblasts. We used microcell-mediated chromosome transfer to introduce the normal chromosomes into AT cells belonging to complementation group D. Cells were irradiated with 1 Gy of X-rays in the G2 phase. All 5 hybrid clones with an introduced chromosome 11 showed a reduction in the frequency of chromatid-type aberrations to normal levels, whereas all 4 hybrid clones with an introduced chromosome 12 failed to show this reduction. This finding, taken together with our previous report that chromosome 11 can restore radioresistant cell killing in AT cells, indicates that a defective gene on chromosome 11 in AT cells is responsible for the hypersensitivity to not only cell killing but also chromosome aberrations. Our results suggest that a putative AT gene on chromosome 11 plays an important role in the repair process of radiation-induced DNA damage that leads to chromosome aberrations.
Kodama
S
S
Department of Radiation Biophysics, Nagasaki University School of Medicine, Japan.
Komatsu
K
K
Okumura
Y
Y
Oshimura
M
M
D000818:Animals; D001260:Ataxia Telangiectasia / Q000235:genetics*; D002470:Cell Survival / Q000235:genetics / Q000528:radiation effects; D002478:Cells, Cultured; D002869:Chromosome Aberrations; D002880:Chromosomes, Human, Pair 11; D002881:Chromosomes, Human, Pair 12; D004249:DNA Damage; D004260:DNA Repair; D005347:Fibroblasts / Q000528:radiation effects; D016195:G2 Phase / Q000528:radiation effects; D006801:Humans; D007621:Karyotyping; D051379:Mice