Restoration of radiation resistance in ataxia telangiectasia cells by the introduction of normal human chromosome 11.
In order to identify the human chromosome which carries a mutated gene in cells from a patient with the hereditary disorder ataxia telangiectasia belonging to complementation group D (AT-D), we performed chromosome transfer experiments via microcell fusion. A single, pSV2neo-tagged chromosome, either 11 or 12, derived from normal human fibroblasts was introduced into AT-D cells by microcell fusion, and clones which were resistant to the antibiotic G418 were isolated. All 3 hybrid clones containing an additional copy number of chromosome 11 showed a restoration of the resistance of wild-type cells to killing by X-irradiation, whereas all 3 hybrid clones containing an additional copy number of chromosome 12 remained hyper-radiosensitive, like the parental AT cells. The results indicate that a defective gene of AT-D cells is also located on chromosome 11, since a genetic linkage analysis has previously suggested that a defective gene of its complementation group A is located on this chromosome.
Komatsu
K
K
Department of Radiation Biophysics, Nagasaki University School of Medicine, Japan.
Kodama
S
S
Okumura
Y
Y
Koi
M
M
Oshimura
M
M
D001260:Ataxia Telangiectasia / Q000235:genetics* / Q000276:immunology; D002461:Cell Line, Transformed; D002472:Cell Transformation, Viral; D002880:Chromosomes, Human, Pair 11; D002881:Chromosomes, Human, Pair 12; D006801:Humans; D006822:Hybrid Cells; D053652:Nuclear Transfer Techniques; D011836:Radiation Tolerance / Q000235:genetics*; D013539:Simian virus 40