GENETIC CONTROL OF MUTATION IN DROSOPHILA

这个项目的目的是确定DNA修复与 果蝇的染色体结构和诱变。 增加突变频率的突变(变异体)已经被 在MU2基因中进行了鉴定和鉴定。变种人非常多 降低伽玛射线引起的染色体断裂的修复效率 卵母细胞，从而允许先前未描述的修复途径 观察到的。通过这一新发现的修复途径，断裂的染色体末端 被一种新的端粒“封顶”。突变子突变似乎扰乱了 卵母细胞中的染色质结构，而不是精子染色体，因此 卵母细胞的染色体没有得到正确的修复。鉴于MU2突变 也影响有丝分裂重组，有理由预计 MU2蛋白可能与体细胞染色体相关。这是 通过观察证实，MU2突变也增强了杂色， 也就是说，它们似乎促进了异染色质的形成。我们计划 寻找其他可能与MU2相互作用的基因产物 染色质。突变子基因已经用150个嵌套的集合进行了定位 删除到5千个基数的区域。一个候选的同源基因 到这个区域的基因已经被克隆和测序。该序列没有 与数据库中的任何其他基因都有很强的相似性。基因组学 包括转录单位的区域将被重新引入到 以确定与MU2突变的互补性。

This project is designed to determine the relationships among DNA repair, chromosome structure, and mutagenesis in Drosophila melanogaster. Mutations that increase the mutant frequency (mutators) have been identified in the mu2 gene and characterized. The mutators greatly reduce the efficacy of repair of gamma-ray-induced chromosome breaks in oocytes, 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. Mutator mutations appear to disrupt chromatin structure in the oocyte, but not the sperm chromosomes, so that oocyte chromosomes are not repaired properly. Given that mu2 mutations also affect mitotic recombination, it is reasonable to expect that the MU2 protein would associate with somatic cell chromosomes. This is confirmed by the observation that mu2 mutations also enhance variegation, that is they appear to enhance the formation of heterochromatin. We plan to look for other gene products that might interact with MU2 in chromatin. The mutator gene has been mapped using a nested set of 150 deletions to a region of 5 kilobasepairs. A candidate cDNA homologous to this region has been cloned and sequenced. The sequence does not have a strong resemblance to any other genes in the database. The genomic region including the transcription unit will be reintroduced into the genome to ascertain complementation with mu2 mutations.