FEATURE ARTICLE
Tracking Down a Cheating Gene
Some genes will play dirty to gain a selective advantage
Barry Ganetzky
Fratricide
Taken together, these results all indicate that SD manifests its effects during the time that the immature—but seemingly normal—spermatids mature into fully functional sperm. What goes wrong between formation of spermatids by meiosis and their subsequent maturation to sperm? The answer was provided by electron-microscope studies of sperm maturation by Kiyoteru T. Tokuyasu and his colleagues at the University of California, San Diego.
In the course of normal maturation, just before sperm acquire their characteristic elongated cell bodies and their tails, the chromosomes become extremely condensed within the highly compacted sperm nucleus. However, Tokuyasu and his colleagues found that in distorting males the chromosomes in precisely half of the spermatids fail to condense and instead remain dispersed. These spermatids are unable to form mature, viable sperm.
The general interpretation that emerges from these results is that in distorting males, the SD chromosome produces a deleterious effect on its partner chromosome. Spermatids that receive this partner chromosome then fail to mature properly, whereas spermatids that receive the SD chromosome develop normally and carry the SD chromosome into the next generation.
From this perspective, SD chromosomes have managed not merely to cheat the system, but to do it in a diabolical manner worthy perhaps of Shakespeare—they eliminate the competition by fratricide.
In spite of having this general understanding of the basis of distortion, biologists would like to know how, on a molecular level, these events transpire. We would like to know how the specific genes involved—Sd and Rsp—interact. And to understand that, we need to know what products these genes encode. Only when we have answered these questions can we fully unravel the mystery of SD. These are the questions we are now trying to answer in my laboratory.
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