Recombination-defective meiotic mutants and mutagen-sensitive mutants of D. melanogaster have been examined for their effects on meiotic chromosome behavior, sensitivity to killing by mutagens, somatic chromosome integrity, and DNA repair processes. Several loci have been identified that specify functions that are necessary for both meiotic recombination and DNA repair processes, whereas mutants at other loci appear to be defective in only one pathway of DNA processing. Mutational analyses of prokaryotic systems have established that DNA replication, repair, and recombination are, in part, under common genic control (1-3). Although there are strong theoretical grounds for extending this conclusion to eukaryotes in general (4-7), direct experimental evidence for an interrelation of the various pathways of DNA metabolism in organisms that undergo meiosis comes primarily from studies of fungi (8, 9). Recombination-defective and repair-defective mutants have been reported in other eukaryotes (9, 10), although in most instances it is not known whether these mutants affect more than one pathway of DNA processing.In Drosophila melanogaster two classes of mutants with potential effects on DNA metabolism have been reported. First, substantial numbers of meiotic mutants are available, which were recognized because they produce genetically detectable abnormal meiotic chromosome behavior (for reviews see refs. 9, 11-14). Mutants at 12 loci are defective in processes essential for normal exchange (frequency and/or distribution along the chromosome) and are thus recombination-defective mutants. Watson (15,16) presented evidence that one of these recombination-defective mutants, c(3)G 17, is more susceptible than wild type to the induction of mutants and rearrangements during meiosis, and on this basis has suggested that the product of c(3)G + functions in both repair and recombination. Second, mutagen-sensitive mutants have been isolated on the basis of hypersensitivity to killing by methylmethanesulfonate (MMS) (17, 18,t). The characterization of meiotic mutants and mutagen-sensitive mutants (18, 19, ¶) by three separate groups using a variety of approaches has led to the realization that overlapping sets of mutants are being examined. In this preliminary communication we coordinate the results of the three groups and outline the conclusions concerning the relation between the genic controls of DNA repair processes and meiotic recombination in Drosophila. We focus here primarily on studies of several selected X-linked mutagen-sensitive and meiotic mutants. The detailed data on the arrays of mutants from which our conclusions have been derived will be published elsewhere.Known X-linked recombination-defective and/or mutagen-sensitive loci Recombination-defective mutants are known at 5 X chromosomal loci; mei-9, nmwi-218, me i-41, mei-352, and mei-251 (20, 21). In addition to decreasing the frequency and/or altering the distribution of exchanges along the chromosomes during female meiosis, these mutants all produce el...