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Hybridization may influence evolution in a variety of ways. If hybrids are less fit, the geographical range of ecologically divergent populations may be limited, and prezygotic reproductive isolation may be reinforced. If some hybrid genotypes are fitter than one or both parents, at least in some environments, then hybridization could make a positive contribution. Single alleles that are at an advantage in the alternative environment and genetic background will introgress readily, although such introgression may be hard to detect. 'Hybrid speciation', in which fit combinations of alleles are established, is more problematic; its likelihood depends on how divergent populations meet, and on the structure of epistasis. These issues are illustrated using Fisher's model of stabilizing selection on multiple traits, under which reproductive isolation evolves as a side-effect of adaptation in allopatry. This confirms a priori arguments that while recombinant hybrids are less fit on average, some gene combinations may be fitter than the parents, even in the parental environment. Fisher's model does predict heterosis in diploid F1s, asymmetric incompatibility in reciprocal backcrosses, and (when dominance is included) Haldane's Rule. However, heterosis arises only when traits are additive, whereas the latter two patterns require dominance. Moreover, because adaptation is via substitutions of small effect, Fisher's model does not generate the strong effects of single chromosome regions often observed in species crosses.

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SummaryA general representation of multilocus selection is extended to allow recombination to depend on genotype. The equations simplify if modifier alleles have small effects on recombination. The evolution of such modifiers only depends on how they alter recombination between the selected loci, and does not involve dominance in modifier effects. The net selection on modifiers can be found explicitly if epistasis is weak relative to recombination. This analysis shows that recombination can be favoured in two ways: because it impedes the response to epistasis which fluctuates in sign, or because it facilitates the response to directional selection. The first mechanism is implausible, because epistasis must change sign over periods of a few generations: faster or slower fluctuations favour reduced recombination. The second mechanism requires weak negative epistasis between favourable alleles, which may either be increasing, or held in check by mutation. The selection (si) on recombination modifiers depends on the reduction in additive variance of log (fitness) due to linkage disequilibria (υ1 < 0), and on non-additive variance in log (fitness) (V′2, V′3,.. epistasis between 2, 3.. loci). For unlinked loci and pairwise epistasis, si = − (υ1 + 4V2/3)δr, where δr is the average increase in recombination caused by the modifier. The approximations are checked against exact calculations for three loci, and against Charlesworth's analyses of mutation/selection balance (1990), and directional selection (1993). The analysis demonstrates a general relation between selection on recombination and observable components of fitness variation, which is open to experimental test.

Selection on one or more genes inevitably perturbs other genes, even when those genes have no direct effect on fitness. This article reviews the theory of such genetic hitchhiking, concentrating on effects on neutral loci. Maynard Smith and Haigh introduced the classical case where the perturbation is due to a single favourable mutation. This is contrasted with the apparently distinct effects of inherited variation in fitness due to loosely linked loci. A model of fluctuating selection is analysed which bridges these alternative treatments. When alleles sweep between extreme frequencies at a rate lambda, the rate of drift is increased by a factor (1 + E[1/pq]lambda/(2(2lambda + r))), where the recombination rate r is much smaller than the strength of selection. In spatially structured populations, the effects of any one substitution are weaker, and only cause a local increase in the frequency of a neutral allele. This increase depends primarily on the rate of recombination relative to selection (r/s), and more weakly, on the neighbourhood size, Nb = 4(pi rho sigma)2. Spatial subdivision may allow local selective sweeps to occur more frequently than is indicated by the overall rate of molecular evolution. However, it seems unlikely that such sweeps can be sufficiently frequent to increase significantly the drift of neutral alleles.

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We review the various factors that limit adaptation by natural selection. Recent discussion of constraints on selection and, conversely, of the factors that enhance "evolvability", have concentrated on the kinds of variation that can be produced. Here, we emphasise that adaptation depends on how the various evolutionary processes shape variation in populations. We survey the limits that population genetics places on adaptive evolution, and discuss the relationship between disparate literatures.

Evolutionary explanations of ageing fall into two classes. Organisms might have evolved the optimal life history, in which survival and fertility late in life are sacrificed for the sake of early reproduction and survival. Alternatively, the life history might be depressed below this optimal compromise by deleterious mutations: because selection against late-acting mutations is weaker, these will impose a greater load on late life. Evidence for the importance of both is emerging, and unravelling their relative importance presents experimentalists with a major challenge.