FEATURE ARTICLE
Tracking Down a Cheating Gene
Some genes will play dirty to gain a selective advantage
Barry Ganetzky
Fateful Meetings
Hiraizumi wisely forgot about the original purpose of his experiments and focused instead on the analysis of the serendipitously discovered SD chromosomes. By chance, it happened that Sandler had made arrangements to join the Crow laboratory as a postdoctoral fellow even before SD was discovered. When it became evident that SD represented an actual instance of meiotic drive, which Sandler had considered from a theoretical standpoint only, he quickly teamed up with Hiraizumi to delve further into the phenomenon.
Over the next several years, Hiraizumi and Sandler provided the framework for the basic understanding of the phenomenon of segregation distortion, on which all subsequent investigations, including my own, have been built.
It did not take long for the two to establish that SD acted only in males; transmission from females was in accord with genetic law. The team also showed that distortion did not depend particularly on the laboratory strain used in the original crosses, since distortion could also be observed when a variety of other chromosomes were paired with SD. Furthermore, the two demonstrated that distortion did not happen as a result of increased mortality of embryos that inherited the non-SD chromosome. Rather, they concluded that distortion was related to a dysfunction in the sperm. That is, some of the sperm (those bearing the non-SD chromosome) in these distorting males failed to develop or function properly and did not participate in fertilization at all.
Most important, Hiraizumi and Sandler showed that distortion was not a property of the SD chromosome itself, but was caused by at least two discrete genes with distinct roles. In later studies, Daniel L. Hartl at the University of Minnesota expanded and clarified the definition of the two key components of the SD chromosomes.
One of these elements is called Sd, a particular gene carried on SD chromosomes. Sd was defined as the gene primarily responsible for causing distortion. The other element is called Responder (Rsp) and was defined as the apparent target of distortion. At least three distinct variants of Rsp have been found in nature and in laboratory strains: Rspi (Responder insensitive) is found on all SD chromosomes, as well as on some non-SD chromosomes; Rsps (Responder sensitive) is found on chromosomes that are sensitive to the action of Sd; and Rspss (Responder super-sensitive), is particularly sensitive to distortion.
Following the initial observations by Hiraizumi and Sandler, studies by several other investigators helped to fill in pieces of the puzzle. James W. Peacock and John Erickson, working at the University of Oregon, demonstrated that meiosis itself proceeds normally in distorting males—chromosomes segregate and are apportioned normally into the immature sperm cells called spermatids. Careful measurements by Hartl and Hiraizumi and by Benedetto Nicoletti and Gianni Trippa at the University of Rome confirmed sperm dysfunction as the ultimate basis of distortion.
Distorting males produce only half as many progeny as normal males even though the embryos produced with their sperm do not experience a greater rate of mortality. The decrease in progeny therefore implied that, compared with normal males, distorting males generate only half as many functional sperm, the vast majority of which contain the SD chromosome and not the homologue. The other half of the sperm—those that received the non-SD chromosome—are eliminated or are otherwise rendered unable to participate in fertilization.
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