Recessive deleterious mutations are common, causing many genetic disorders in humans and producing inbreeding depression in the majority of sexually reproducing diploids. The abundance of recessive deleterious mutations in natural populations suggests they are likely to be present on a chromosome when a new adaptive mutation occurs, yet the dynamics of recessive deleterious hitchhikers and their impact on adaptation remains poorly understood. Here we model how a recessive deleterious mutation impacts the fate of a genetically linked dominant beneficial mutation. The frequency trajectory of the adaptive mutation in this case is dramatically altered and results in what we have termed a "staggered sweep." It is named for its threephased trajectory: (i) Initially, the two linked mutations have a selective advantage while rare and will increase in frequency together, then (ii), at higher frequencies, the recessive hitchhiker is exposed to selection and can cause a balanced state via heterozygote advantage (the staggered phase), and (iii) finally, if recombination unlinks the two mutations, then the beneficial mutation can complete the sweep to fixation. Using both analytics and simulations, we show that strongly deleterious recessive mutations can substantially decrease the probability of fixation for nearby beneficial mutations, thus creating zones in the genome where adaptation is suppressed. These mutations can also significantly prolong the number of generations a beneficial mutation takes to sweep to fixation, and cause the genomic signature of selection to resemble that of soft or partial sweeps. We show that recessive deleterious variation could impact adaptation in humans and Drosophila.I n diploids, the fitness effect of having a single copy of a mutation depends not only on the mutation's selective effect, s, but also on its heterozygous effect, h. A fully recessive mutation (h = 0) is hidden in the heterozygote (hs = 0), and a fully dominant mutation (h = 1) is completely exposed (hs = s). Although it is generally agreed that beneficial mutations that reach fixation tend to be dominant (i.e., h ≥ 0.5) (1, 2), both empirical data and theoretical models (3-6) suggest that many strongly and even moderately deleterious mutations are likely to be recessive (i.e., h < 0.5). For example, studies of de novo mutations from both mutation accumulation and mutagenesis experiments in Drosophila melanogaster, Saccharomyces cerevisiae, and Caenorhabditis elegans have repeatedly found that strongly deleterious mutations tend to be completely recessive (h ≈ 0) and more weakly deleterious mutations tend to be partially recessive (h ≈ 0.1) (7-13). Furthermore, studies of natural populations have found that inbreeding depression is pervasive across sexually reproducing diploids and is mainly caused by recessive deleterious variation (reviewed in ref. 14). For example, in natural populations of Drosophila, approximately 30% of chromosomes carry a recessive lethal, and chromosomes that do not carry a recessive lethal suffer fro...