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

Abstract

An X-ray-dependent mutator on chromosome 3 of D. 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 fas as can be determined by genetic, cytological, and molecular assays, the deletions extend to they very end of the chromosome involved. The frequency of these deletions is directly proportional to X-ray dose, suggesting that they are 1-break rearrangements. The mutator could be blocked in a major pathway for the repair of DNA double-strand breaks; a minor repair pathway could be responsible for the addition of new telomeres under these conditions.