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mu-2:果蝇中的突变基因,可增强末端缺失的诱导。

mu-2: mutator gene in Drosophila that potentiates the induction of terminal deficiencies.

作者信息

Mason J M, Strobel E, Green M M

出版信息

Proc Natl Acad Sci U S A. 1984 Oct;81(19):6090-4. doi: 10.1073/pnas.81.19.6090.

Abstract

An x-ray-dependent mutator on chromosome 3 of Drosophila melanogaster is described that specifically increases the recovery of deletions for chromosomal tip regions. Such deficiencies can be induced on any chromosome. More centromere proximal mutations, as assayed by the sex-linked recessive lethal test, are not increased over the wild-type control. As far as can be determined by genetic, cytological, and molecular assays, the deletions extend to the very end of the chromosome involved. In addition, the frequency of these deletions is directly proportional to x-ray dose, suggesting that they are one-break rearrangements. It is proposed that the mutator is blocked in a major pathway for the repair of DNA double-strand breaks, and that a minor repair pathway is responsible for the addition of new telomeres under these conditions.

摘要

本文描述了黑腹果蝇3号染色体上一种依赖X射线的突变体,它能特异性地提高染色体末端区域缺失的恢复率。这种缺失可在任何染色体上诱导产生。通过性连锁隐性致死试验检测,更靠近着丝粒近端的突变在野生型对照中并未增加。就遗传、细胞学和分子检测所能确定的范围而言,这些缺失延伸至所涉及染色体的最末端。此外,这些缺失的频率与X射线剂量成正比,这表明它们是单断裂重排。有人提出,该突变体在DNA双链断裂修复的主要途径中受阻,而在这些条件下,一条次要的修复途径负责添加新的端粒。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/089d/391865/94ea608018ea/pnas00620-0188-a.jpg

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