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The Segregation distorter (SO) phenomenon in Drosophila melanogaster is characterized by the preferential recovery of Distorter second chromosomes in the progeny of heterozygous males. In some crosses, virtually all of the offspring of such males will carry the SD chromosome (compared to the expected 50% based on Mendelian segregation), and it is now known that the aberrant segregation ratios are due to the dysfunction of sperm carrying the nonSD homologue (HARTL, HIRAIZUMI and CROW 1967; NICOLETTI, TRIPPA and DEMARCO 196’7). The SD system consists essentially of two interacting sites: Sd, which is located close to the centromere-but outside of the heterochromatic region-on the left arm of chromosome ZZ and Responder (Rsp), which is located in the right centromeric heterochromatin, also of chromosome ZZ (SANDLER and HIRAIZUMI 1960; HIRAIZUMI and NAKAZIMA 1967; HARTL 1974; GANETSKY 1977; BRITTNACHER and GANETSKY 1983; SHARP, HILLIKER and HOLM 1985). HARTL (1973) proposed that the Sd locus produces a multimeric regulatory protein that may interact differently with the Responder-sensitive (Rsp’) and Responder-insensitive (Rspi) alleles. In his model, HARTL proposed that normal sperm function depends on the interaction of the Sd+ product with the Rsp locus. The model that we are proposing here is formally very similar to HARTL’S (1973) model, but it differs from the original in the following ways: We propose that neither the Sd locus nor the Rsp locus produces wild-type products that are necessary for normal sperm development. Moreover, we propose that while there is, indeed, a product of Sd that interacts with Rsp, this product is a nucleic acid molecule rather than a protein. Specifically, this DNA molecule is a copy of the Sd element itself, and its mode of action at the Rsp locus is one of chromosome disruption due to insertion at this site. Our model has implications both for the origin and the maintenance of Segregation Distortion systems. Briefly, the model is as follows: The Sd element entered the D. melanogaster genome, probably by horizontal gene transfer, and inserted into a number of chromosomal sites by replicative transposition. Original insertion sites need not have included the Sd site on chromosome ZZ. By chance, insertions in the right centromeric heterochromatin led to chromosome disruption and consequent

IS THE SEGREGATION DISTORTION PHENOMENON IN DROSOPHILA DUE TO RECURRENT ACTIVE GENETIC TRANSPOSITION?