Potter M, Sanford K K, Parshad R, Tarone R E, Price F M, Mock B, Huppi K
Laboratory of Genetics, National Cancer Institute, Bethesda, Maryland 20892.
Genomics. 1988 Apr;2(3):257-62. doi: 10.1016/0888-7543(88)90010-9.
Early-passage skin fibroblasts from different inbred and congenic strains of mice were X-irradiated (1 Gy), and the number of chromatid breaks was determined at 2.0 h after irradiation. The cells from DBA/2N, C3H/HeN, STS/A, C57BL/6N, BALB/cJ, and AKR/N had 25 to 42 chromatid breaks per 100 metaphase cells (efficient repair phenotype). NZB/NJ had greater than 78 and BALB/cAn had 87 to 110 chromatid breaks per 100 cells (inefficient repair phenotype). Differences between BALB/cAn and BALB/c. DBA/2 congenic strains which carry less than 1% of the DBA/2 genome indicate that two genes, one on chromosome 1 linked to bcl-2-Pep-3 and the other on chromosome 4 closely linked to Fv-1, affect the efficiency with which the cells repair radiation-induced chromatin damage.
对来自不同近交系和同源近交系小鼠的早期传代皮肤成纤维细胞进行X射线照射(1戈瑞),并在照射后2.0小时测定染色单体断裂数。来自DBA/2N、C3H/HeN、STS/A、C57BL/6N、BALB/cJ和AKR/N的细胞每100个中期细胞有25至42条染色单体断裂(高效修复表型)。NZB/NJ每100个细胞有超过78条染色单体断裂,BALB/cAn每100个细胞有87至110条染色单体断裂(低效修复表型)。携带不到1% DBA/2基因组的BALB/cAn和BALB/c、DBA/2同源近交系之间的差异表明,两个基因,一个位于与bcl-2-Pep-3连锁的1号染色体上,另一个位于与Fv-1紧密连锁的4号染色体上,影响细胞修复辐射诱导的染色质损伤的效率。