An effect of centromere function on the behavior of ring-X chromosomes in Drosophila melanogaster.

Abstract

It is shown that under the influence of an autosomal meiotic mutant that causes abnormalities in meiotic centromere function (mei-S332), ring-X chromosomes are frequently nonrecoverable. Evidence is presented that this nonrecoverability is caused by a failure of sister ring-chromatids to successfully effect an equational separation with resultant dominant lethality. Because mei-S332 results in meiotic abnormalities only after replication has been completed, and because ring chromosomes are normally transmitted with approximately the same efficiency as rod chromosomes, it is suggested that during replication in normal meioses, sister ring-chromatids form mutually interlocked ring complexes that are resolved without genetic consequences at anaphase II, with the resolution owing at least in part to normal centromere function.