Ataxia-telangiectasia (AT) is a rare human autosomal recessive disease characterized by hypersensitivity to ionizing radiation, neurological disorders, immunodeficiency, chromosomal instability and a high incidence of cancers. It was thought that the cause for hypersensitivity was due to the putative DNA repair gene deficiency. Recently, studies on genetic linkage analysis of families with AT carriers had suggested that a genetic defect in a region of chromosome 11 q 22~23 was responsible for the AT disorder. The SV 40-transformed AT5BIVA cells (group D), from skin fibroblast of AT patients, was hypersensitive to Gamma-ray. The karyotype analysis had previously shown there were abnormalities of chromosome 11, 13,14,15 and 22 in AT5BIVA cells. In order to study the molecular mechanism of hyper-radiosensitivity in AT cells and to map DNA repair gene, a new strategy to introduce intact chromosomes into AT 5 BIVA cells by the technique of microcell-mediated chromosome transfer (MMCT) was used.,Two human×mouse hybrid cells (FD 3 and FD 8) and a mouse cell line (LM/TK,-,) were used. FD 3 cells contain human chromosome 11 while FD 8 does not, The microcells of these three cell lines were prepared and fused with AT 5 BIVA cells. After twice selection by 3 Gy ,γ-, irradiation, the clones which were resistant to γ-irradiation were isolated. AT/FD 3-1 cells, the AT 5 BIVA×FD 3 mircocell fused hybrid, showed enhancement of radioresistance. Karyotype analysis had also shown AT/FD 3-1 cells contained an additional copy of chromosome 11. The results indicated the genes responsible for cell resistance to ionizing irradiation existed in human chromosome 11.