MUTAGEN-SENSITIVE MUTANTS IN DROSOPHILA-MELANOGASTER - EFFECTS ON PRE-MUTATIONAL DAMAGE
MUTAGEN-SENSITIVE MUTANTS IN DROSOPHILA-MELANOGASTER - EFFECTS ON PRE-MUTATIONAL DAMAGE
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DOI：
10.1016/0027-5107(79)90107-6
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发表时间：
1979-01-01
期刊：
影响因子：
--
通讯作者：
WURGLER, FE
中科院分区：
文献类型：
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作者：
GRAF, U;GREEN, MM;WURGLER, FE
D.用X射线、甲磺酸乙酯（EMS）或氮芥（HN 2）诱变来自Basc原种的雄性黑腹果蝇。将相同处理的雄性动物组与不同类型的雌性动物杂交。将幼虫伴性隐性致死作为遗传终点进行评分。所用雌性为X染色体突变纯合子（mus（1）101 D1、mus（1）104 D1、mei-9或mei-41 D5），这些突变导致DNA修复缺陷并增加幼虫的诱变剂敏感性。来自具有正常DNA修复能力的白色种群的雌性作为对照。在成熟精子中诱导的突变前病变仅在受精后由卵母细胞中存在的母体酶系统处理。损伤处理效率的差异可导致母体对从诱变精子中恢复的突变频率的影响。除mus（1）104 D1外，分析的所有突变体均显著改变了1种或多种类型突变前病变的突变固定。mus（1）101 D1原种的影响最大，其中HN 2诱导的DNA交联不会导致伴性隐性致死。突变mus（1）101 D1可能在DNA交联修复的早期步骤中有缺陷。第一组数据清楚地表明，在果蝇中的母体效应的研究是一个有效的工具，分析在体内的功能的修复突变的化学诱导的诱变。
D. melanogaster males from a Basc stock were mutagenized with X-rays, ethyl methanesulfonate (EMS) or nitrogen mustard (HN2). Groups of identically treated males were crossed to different types of females. Larval 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. With the exception of mus(1)104D1, all mutants analyzed significantly modified the mutation fixation of 1 or more types of premutational lesions. The most drastic effect was found with the mus(1)101D1 stock in which HN2-induced DNA cross-links did not lead to sex-linked recessive lethals. The mutant mus(1)101D1 is probably defective in an early step of DNA cross-link repair. The 1st set of data clearly demonstrates that the study of maternal effects in Drosophila is an efficient tool to analyze the in vivo function of repair mutations on chemically-induced mutagenesis.