Disney J E, Barth A L, Shultz L D
Jackson Laboratory, Bar Harbor, ME 04609.
Cytogenet Cell Genet. 1992;59(1):39-44. doi: 10.1159/000133196.
The murine severe combined immunodeficiency (scid) mutation interferes with normal recombination of immunoglobulin and T-cell receptor genes. This immunologic defect results in a lack of fully differentiated B and T cells in scid/scid mice. Animals homozygous for the scid mutation also display increased sensitivity to the damaging effects of ionizing radiation. We report here our observations of high frequencies of radiation-induced chromatid interchanges and intrachanges in bone marrow cells and fibroblasts from scid/scid mice. The presence of these aberrant chromosome structures suggests that a delay in strand rejoining underlies the increased sensitivity of scid/scid mice to ionizing radiation. The scid mutation may provide important clues for understanding the relationship between mitotic recombination and DNA repair in higher eukaryotic cells.
小鼠严重联合免疫缺陷(scid)突变会干扰免疫球蛋白和T细胞受体基因的正常重组。这种免疫缺陷导致scid/scid小鼠中缺乏完全分化的B细胞和T细胞。scid突变纯合子动物对电离辐射的损伤作用也表现出更高的敏感性。我们在此报告我们对scid/scid小鼠骨髓细胞和成纤维细胞中辐射诱导的染色单体互换和内部互换高频现象的观察结果。这些异常染色体结构的存在表明,链重新连接延迟是scid/scid小鼠对电离辐射敏感性增加的基础。scid突变可能为理解高等真核细胞中有丝分裂重组与DNA修复之间的关系提供重要线索。