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.
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