GENETIC CONTROL OF MUTATION IN DROSOPHILA

突变率是由基因控制的。 在细菌和酵母中， 诱导突变的频率可以增加或减少， 阻断一种或另一种DNA修复途径。 该项目旨在 确定果蝇中DNA修复和突变之间的关系 黑腹菌 正在采取三种方法：（1）突变体， 增加突变频率（一个增变因子）已被确定，映射， 和表征了 这种突变子阻止染色体断裂的修复 特别是在卵母细胞中，从而允许先前未描述的修复， 过程要观察。 在这个过程中，断裂的染色体被“修复”， 允许末端缺失的恢复。 (2)DNA的相互作用 修复缺陷突变体和转座因子已被观察到， 双突变体组合。 没有一个修复缺陷突变体被检测到 影响转座子诱导的突变率， 尽管mei-41位点的突变体阻止了重组， 携带转座子的染色体的传递。 (3)非整倍性是指 作为一个遗传终点来检测。 诱导非整倍体的化学物质正在被 鉴定为研究有丝分裂和减数分裂的探针。

Mutation rates are under genetic control. In bacteria and yeast, the frequency of induced mutations can be either increased or decreased by blocking one or another pathway of DNA repair. This project is designed to determine the relationship between DNA repair and mutagenesis in Drosophila melanogaster. Three approaches are being taken: (1) A mutant which increases the mutation frequency (a mutator) has been identified, mapped, and characterized. This mutator blocks repair of chromosome breaks specifically in oocytes, thereby allowing a previously undescribed repair process to be observed. In this process broken chromosomes are "healed", allowing the recovery of terminal deletions. (2) The interaction of DNA repair-defective mutants and transposable elements has been observed in double mutant combinations. None of the repair-defective mutants examined to date influence the rates of transposon-induced mutation or recombination, although mutants at the mei-41 locus prevent the transmission of transposon-bearing chromosomes. (3) Aneuploidy is being examined as a genetic endpoint. Chemicals that induce aneuploidy are being identified as probes to investigate mitosis and meiosis.