Abstract
Summary Radiation-sensitive mutations of yeast in multiple-mutant combinations interact with one another to affect survival. From these interactions, and from the effects of these mutations on other genetic events such as recombination or mutation, it is possible to deduce a scheme representing the pathways by which repair is effected. The biochemical roles of these pathways can be determined by simple assay systems. For example, one pathway controlled by 4 loci is concerned with the early stages of excision of pyrimidine dialers. Some of the loci used in this investigation affect the rate and duality of UV-induced mutation and so indicate what part repair might play in this process.
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