GENETIC CONTROL OF MUTATION IN DROSOPHILA

这个项目的目的是确定DNA 果蝇的染色体修复、染色体结构和诱变 黑腹菌 一种增加突变频率的突变（a 突变体）已经被鉴定和表征。 这个变异者 大大降低了X射线诱导的修复途径的功效 染色体断裂，从而允许以前未描述的修复， 路要观察。 通过这个新发现的修复途径 个别断裂的染色体末端被“修复”， 末端缺失的恢复。 染色体分布 可以治愈的骨折已经在几个层面上进行了检查。 （一） 该突变基因只在雌性生殖细胞中起作用，而不在雄性或雌性生殖细胞中起作用。 体细胞 (2)中断可以在 常染色质 (3)增变因子增加了细胞中断裂的恢复， 异染色质，但断裂不恢复为终端 删除。 相反，它们是类似于 来自野生型雌性的重排。 因此，当突变体 其本身对常染色质没有不同的影响， 异染色质，愈合过程可能是特定的 常染色质 (4)末端缺失的断点是 随机分布，表明特定的DNA序列是 而不是愈合过程所必需的 (5)DNA序列 正在从缺陷染色体中丢失，这表明 断裂末端的新端粒并不像 原始的端粒复制染色体的过程 DNA末端的缺失和替换。 终端 这些缺失中的几个的限制性片段已经被 克隆的 我们计划对每个片段的DNA进行测序， 与已知的端粒序列进行比对 我们也 开发突变子的快速测定，以促进插入 突变和转座子标签。

This project is designed to determine the relationship between DNA repair, chromosome structure and mutagenesis in Drosophila melanogaster. A mutation that increases the mutation frequency (a mutator) has been identified and characterized. This mutator greatly reduces the efficacy of a repair pathway for x-ray induced chromosome breaks, thereby allowing a previously undescribed repair pathway to be observed. By this newly identified repair pathway individual broken chromosome ends are "healed," allowing the recovery of terminal deletions. The distribution of chromosome breaks that can be healed has been examined at several levels. (1) The mutator acts only in the female germline, not in males or somatic cells. (2) Breaks can be recovered anywhere in the euchromatin. (3) The mutator increases the recovery of breaks in the heterochromatin, but the breaks are not recovered as terminal deletions. Rather, they are rearrangements similar to the rearrangements from wild-type females. Thus, while the mutator itself does not have differential effects on euchromatin and heterochromatin, the healing process may be specific to euchromatin. (4) The breakpoints of the terminal deletions are distributed randomly, suggesting that specific DNA sequences are not required for the healing process to occur. (5) DNA sequences are being lost from the deficient chromosomes, suggesting that the neotelomeres on the broken ends are not as effective as the original telomeres and that the process of replicating chromosome ends involves loss and replacement of DNA sequences. The terminal restriction fragments of several of these deletions have been cloned. We plan to sequence the DNA of each fragment in order to compare it with the sequence of known telomeres. We are also developing a rapid assay for the mutator to facilitate insertional mutagenesis and transposon tagging.