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...

In an effort to identify the enzymatic mechanism responsible for the synthesis of reactive oxygen species produced during the hypersensitive response, preparations of rose (Rosa damascena) cell plasma membranes, partially solubilized plasma membrane protein, and cytosol were assayed for the NADH-and NADPH-dependent synthesis of superoxide using assays for the reduction of cytochrome c (Cyt c), assays for the reduction of nitroblue tetrazolium, and assays for the chemiluminescence of N,N-dimethyl-9,9-biacridium dinitrate (lucigenin). Each assay ascribed the highest activity to a different preparation: the Cyt c assay to cytosol, the nitroblue tetrazolium assay to plasma membrane, and the lucigenin assay to the partially solubilized plasma membrane protein (with NADH). This suggests that no two assays measure the same set of enzymes and that none of the assays is suitable for comparisons of superoxide synthesis among different cell fractions. With the plasma membrane preparation, the presence of large amounts of superoxide-dismutase-insensitive Cyt c reductase confounded attempts to use Cyt c to measure superoxide synthesis. With the partially solubilized membrane protein, direct reduction of lucigenin probably contributed to the chemiluminescence. Superoxide synthesis detected with lucigenin should be confirmed by superoxide-dismutase-sensitive Cyt c reduction.In plant systems the synthesis of ROS, including superoxide, hydrogen peroxide, and the hydroxyl radical, occurs as a by-product of normal metabolism. However, excesses of ROS are produced during particular periods of development and in response to various stresses. There has been a recent focus on ROS produced during the hypersensitive response to pathogen infection and to the presence of noninfective elicitors from pathogenic and nonpathogenic microbes.One mechanism for the production of ROS is the singleelectron reduction of O 2 to form superoxide. Dismutation of superoxide forms hydrogen peroxide and in the presence of transition metals, principally ferrous iron, the Fenton reaction produces hydroxyl radicals from the substrate hydrogen peroxide. Thus, the formation of superoxide leads to the other species of ROS. The detection of superoxide and the quantification of superoxide synthesis is a challenge, because traditional spectrophotometric methods are not especially sensitive. A sensitive method that depends on the chemiluminescence of lucigenin has been used extensively; it is considered to be a specific indicator of superoxide because it shows little signal from hydrogen peroxide (Corbisier et al., 1987) and has been used in a large number of studies of ROS production (for refs., see Faulkner and Fridovich, 1993).Using lucigenin, our laboratory (Auh and Murphy, 1995) reported the accumulation of superoxide in suspension cultures of rose (Rosa damascena) cells treated with a cell wall elicitor from Phytophthora cinnamomea. Subsequently, Murphy and Auh (1996) used lucigenin to measure the rate of synthesis of superoxide by enzymes in rose cell plasm...

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