GENETIC CONTROL OF MUTATION IN DROSOPHILA

这个项目的目的是确定DNA修复与 黑腹果蝇的染色体结构和诱变。一种突变 这增加了突变频率(一个突变子)已经被确定并且 特色化的。这个变种人大大降低修复的效果。 X射线诱导的染色体断裂的途径，从而允许先前的 未描述的修复途径有待观察。通过这种新确定的修复 途径断裂的染色体末端被一种新的端粒“封顶”。新的 染色体末端受到其他修复机制的保护，使其免受退化， 但没有有效复制，DNA序列从 有盖子的末端。其中几条染色体末端的DNA已经 测序发现在基因组断裂点的远端没有DNA。这 观察表明，染色体末端的适当复制可能 需要特定的端粒DNA序列，该序列已由 其他的，但染色体的活性是由非DNA成分决定的 端粒的。已分离出封端的稳定的衍生物 并发现获得了端粒特异的DNA序列。这些马厩 目的正在被描述。我们还在开发一种快速检测 突变体以促进遗传分析，并正在研究细胞 诱变子活性的特异性。

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 broken chromosome ends are "capped" with a new telomere. The new chromosome ends are protected from degradation by other repair mechanisms, but are not replicated effectively and DNA sequences are lost from the capped ends. The DNA at the ends of several of these chromosomes have been sequenced and found to have no DNA distal to the genomic breakpoint. This observation suggests that proper replication of the chromosomal end may require a specific telomeric DNA sequence that has been described by others, but that chromosome viability is determined by a non-DNA component of the telomere. Stable derivatives of the capped ends have been isolated and found to have gained a telomere specific DNA sequence. These stable ends are being characterized. We are also developing a rapid assay for the mutator to facilitate genetic analysis and are investigating cell specificity of mutator activity.