Segregation distortion was first discovered in a natural population of Drosophila melanogaster in Madison, Wisconsin (Sandler et al., 1959). About 3% of the second chromosomes extracted from this population are found to cause grossly aberrant segregation in males. They are called segregation distorter (SD) chromosomes, and males heterozygous for SD produce 95% or more of SD-bearing progeny instead of the expected one-to-one ratio. Segregation in females is normal. The nonMendelian segregation in males comes about because SD causes the dysfunction of a large fraction of sperm bearing its homologue (Hartl et al., 1967; Nicoletti et al., 1967). The process of dysfunction can be observed directly in the electron microscope (Tokuyasu et al., 1972), but the molecular basis of distortion is only guessed at (see Hartl, 1973, for example). SD chromosomes carry a complex polygenic set of suppressors and enhancers (Miklos, 1972), but two major loci involved in the phenomenon have been identified (Sandler and Hiraizumi, 1960; Hartl, 1974). These two loci are located in or near the centromeric heterochromatin. The leftmost one is known as Sd, the rightmost one as Rsp. Genetically, SD chromosomes are Sd Rsp, normal chromosomes are Sd+ Rsp+. The Sd allele is necessary for distortion to occur and Rsp responds to the action of Sd. Thus, whereas segregation in Sd Rsp+ / Sd+ Rsp+ and Sd+ Rsp / Sd+ Rsp+ males is normal, males of genotype Sd Rsp / Sd+ Rsp+ produce an excess of Sd Rsp-bearing offspring and those of genotype Sd Rsp+ / Sd+ Rsp produce a deficiency of Sd Rsp+bearing offspring. Most important for purposes of this paper, Sd Rsp / Sd+ Rsp males exhibit normal segregation. Natural populations of Drosophila melanogaster contain high frequencies of suppressors of SD. Some of these are sexlinked, others are autosomal. The frequency of suppressor-bearing X chromosomes is about 85% in both a Japanese population and one in Madison. Autosomal suppressors, principally on chromosome 2, reach frequencies of about 45% in Madison but are fairly rare in Japan (Kataoka, 1967; Hartl, 1970a). Suppression of distortion by the sex-linked suppressors is due to a gene located at approximately 47 on the chromosome map (Kataoka, 1967). The genetic basis of the second chromosomal suppressors is the subject of this report. The study was based on 75 second chromosomes extracted from a wild population near Raleigh, North Carolina. Thirty-six of these chromosomes carry suppressors of SD. The vast majority of these suppressors are genotypically Sd+ Rsp; they are able to suppress distortion because they carry one of the components of the SD system. The Rsp element of segregation distortion therefore is present at remarkably and unexpectedly high frequencies in some natural populations. ' This work was supported by grants numbered GM19551 and GM21732 from the National Institutes of Health. D. L. H. is supported by Research Career Award GM2301.