Graf U, Green M M, Würgler F E
Mutat Res. 1979 Nov;63(1):101-12. doi: 10.1016/0027-5107(79)90107-6.
Drosophila melanogaster males from a Basc stock were mutagenized with either X-rays, ethyl methanesulfonate (EMS), or nitrogen mustard (HN2). Groups of identically treated males were crossed to different types of female. Sex-linked recessive lethals were scored as a genetic end point. The females used were homozygous for X-chromosomal mutations (mus(1)101D1, mus(1)104D1, mei-9 or mei-41D5) which lead to defective DNA repair and which increase the mutagen sensitivity of larvae. Females from a white stock with normal DNA repair capacities served as controls. The premutational lesions induced in mature sperm are only processed after insemination by the maternal enzyme systems present in the oocytes. Differences in the efficiency of the processing of lesions can lead to maternal effects on the frequency of mutations recovered from mutagenized sperm. It was found that, with the exception of mus(1)104D1, all mutants analysed significantly modify the mutation fixation of one or more types of premutational lesions. The most drastic effect is found with the mus(1)101D1 stock in which HN2-induced DNA cross-links do not lead to sex-linked recessive lethals. It is assumed that mus(1)101D1 is defective in an early step of DNA cross-link repair. Our first set of data clearly demonstrates that the study of maternal effects in Drosophila is an efficient tool to analyse the in vivo function of repair mutations on chemically induced mutagenesis.
用X射线、甲磺酸乙酯（EMS）或氮芥（HN2）对来自Basc品系的黑腹果蝇雄性进行诱变处理。将经过相同处理的雄性果蝇分组与不同类型的雌性果蝇杂交。以性连锁隐性致死作为遗传终点。所使用的雌性果蝇对于X染色体突变（mus(1)101D1、mus(1)104D1、mei-9或mei-41D5）是纯合的，这些突变会导致DNA修复缺陷，并增加幼虫的诱变敏感性。来自具有正常DNA修复能力的白眼品系的雌性果蝇作为对照。成熟精子中诱导的前突变损伤只有在授精后由卵母细胞中存在的母体酶系统进行处理。损伤处理效率的差异可导致母体对从诱变精子中回收的突变频率产生影响。结果发现，除了mus(1)104D1之外，所有分析的突变体都显著改变了一种或多种类型前突变损伤的突变固定。在mus(1)101D1品系中发现了最显著的影响，其中HN2诱导的DNA交联不会导致性连锁隐性致死。据推测，mus(1)101D1在DNA交联修复的早期步骤中存在缺陷。我们的第一组数据清楚地表明，在果蝇中研究母体效应是分析修复突变在化学诱导诱变中的体内功能的有效工具。
