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Redundancy reveals drugs in action

Nature Genetics volume 21, pages 245–246 (1999)Cite this article

In most parts of the world, mention the word "redundancy" to academic scientists over the age of 50 and they will reach for the file marked "pension plan" with a worried frown on their faces. However, what Ron Davies and his team of molecular biologists at Stanford University (see the article by Guri Giaever et al. on page 278 of this issue) have realized is that genetic redundancy in the brewers' and bakers' yeast, Saccharomyces cerevisiae, may be exploited to discover the sites of action of drugs and toxins1.

It is usually accepted that deletion of one member of any pair of homologous genes in a diploid cell will be a recessive mutation, having no obvious effect on phenotype. However, this is only universally true if phenotype is measured qualitatively. If, instead, quantitative measures are used, then certain genes will reveal a phenotype when one member of a homologous pair is deleted. This phenomenon is known as haploinsufficiency; it is due to an insufficient concentration of the gene product in the cell to permit growth and division to occur at a normal rate. Adherents of the theory of metabolic control analysis (MCA; ref. 6) would say that genes displaying haploinsufficiency exert a high level of control over the pathways in which their products function. Indeed, Henrich Kacser believed that MCA explains why most mutations are recessive in their effect7.

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  1. Department of Biomolecular Sciences, UMIST, Post Office Box 88, Manchester, M60 1QD, UK

    Stephen Oliver

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Oliver, S. Redundancy reveals drugs in action. Nat Genet 21, 245–246 (1999). https://doi.org/10.1038/6748

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