Male Drosophila heterozygous for an SD-bearing second chromosome and a normal homolog preferentially transmit the SD chromosome to their offspring. The distorted transmission involves the induced dysfunction of the sperm that receive the SD+ chromosome. The loci on the SD chromosome responsible for causing distortion are the Sd locus the the E(SD) locus. Their target of action on the SD+ chromosome is the Rsps locus. Previous studies of Rsps indicated that deletion of this locus rendered a chromosome insensitive to the action of SD and mapped Rsps physically within the centric heterochromatin of 2R. In this study we have constructed a collection of marked free duplications for the centromeric region of a second chromosome that carried Rsps. The heterochromatic extent of each duplication as well as its sensitivity to distortion was determined. We found that Rsps is the most proximal known locus within the 2R heterochromatin. Furthermore, our results demonstrate that the presence of Rsps is not only necessary but sufficient to confer sensitivity to distortion irrespective of its association with an intact second chromosome or one that pairs meiotically with an SD chromosome. By use of these duplications we increased the usual dosage of Rsps relative to SD to determine whether there was any competition for limited amounts of SD [and/or E(SD)] product. When two Rsps-bearing chromosomes are present within the same spermatocyte nucleus an SD chromosome is capable of causing efficient distortion of both. However, at least in some cases the degree of distortion against a given Rsps was reduced by the presence of an extra dose of Rsps indicating that there was some competition between them. The bearing of these results on present models of segregation distortion are discussed.