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Although theory indicates that indirect genetic benefits through mate choice should be widespread, empirical work has often either failed to detect such benefits or shown a net cost to the presence of sexual selection. In this dissertation, I test whether sexual selection facilitates adaptation in populations of Drosophila melanogaster by using an experimental evolution approach where mating system is manipulated. In chapter two, I tested whether sexual selection increases the speed with which a conditionally deleterious allele is removed from a laboratory population of Drosophila melanogaster. Loss of the deleterious allele was more rapid when sexual selection was allowed to act. I also quantified the strength of both nonsexual and sexual selection against the deleterious allele using maximum likelihood estimation. In contrast to recent experiments employing monogamy/polygamy designs, our results demonstrate a population-level benefit to sexual selection that is consistent with the operation of good-genes female choice. If most mutations are deleterious to both overall fitness and condition-dependent traits affecting mating success, sexual selection will purge mutation load and increase nonsexual fitness. In chapter three, I explored this possibility with populations of Drosophila melanogaster exhibiting artificially-elevated levels of deleterious variation and evolving in the presence or absence of sexual selection. After 60 generations of experimental evolution, monogamous populations exhibited higher total reproductive output than polygamous populations. Parental environment also affected fitness measures—flies that evolved in the presence of sexual conflict exhibited reduced nonsexual fitness when their parents experienced a polygamous environment, indicating trans-generational effects of male harassment and highlighting the importance of a common garden design. This cost of parental promiscuity was nearly absent in monogamous lines, evidence for the evolution of reduced sexual antagonism. There was no evidence for an overall difference in egg-to-adult viability between treatments. If mutation load was reduced by the action of sexual selection in this experiment, the resultant gain in fitness was not sufficient to overcome the costs of sexual antagonism. In chapter four, I examined the transcription profiles of these long-term monogamous and polygamous populations. In particular, I looked at two broad classes of sexually-selected genes: those encoding male seminal fluid proteins (Sfps) and female proteases. There is evidence for rapid evolution and sexual conflict in both of these sets of genes. In monogamous populations, Sfps show reduced expression overall, consistent with the idea that they either represent a wasteful use of resources in monogamous populations, due to the absence of male-male competition, and/or harm females. The regulatory response in mated females is in line with these results, as polygamous females upregulate expression of proteases while monogamous females downregulate expression. Expression patterns in virgin females, however, show a conflicting pattern as females from monogamous populations express proteases at a higher basal level. The results of these projects address a major question about the adaptive value of sexual selection. Clearly, sexual selection can accelerate adaptation by purging deleterious alleles. On balance, however, sexual selection depresses nonsexual fitness in polygamous populations when compared to monogamous populations that do not experience sexual conflict, and there is evidence that this decline is due to antagonism between the sexes.