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View Large Image | Download PowerPoint SlideAs readers of TREE are undoubtedly aware, William (Bill) Hamilton was one of the most influential evolutionary biologists of the second half of the 20th century. Ullica Segerstrale's Nature's Oracle is the first full-length biography to appear since Hamilton's untimely death early in 2000, and provides a mass of details about both his professional and personal lives. It conveys a vivid impression of a brilliant but flawed person, who had a very strong sense of what he wanted to achieve, and a lack of social skills that seems unusual even by the low standards of many scientists.From a very early age, Hamilton had a deep curiosity about the living world, and an intense interest in understanding it in terms of evolution by natural selection. As an undergraduate, he soon discovered Fisher's The Genetical Theory of Natural Selection [1xThe Genetical Theory of Natural Selection. Fisher, R.A. See all References][1]. This inspired much of his future work; the problems of altruism, sex ratio evolution, selection in relation to age, sexual selection, and the evolution of sex and recombination, were all discussed by Fisher. He decided to work on the problem of altruism during his final year at Cambridge University. He was fortunate to be taken on by the London School of Economics and the Galton Laboratory at University College London, and allowed to pursue this goal under light supervision. Hamilton clearly felt isolated and misunderstood during his PhD work, and the letters from this period that are quoted convey feelings of self-pity that seem to have persisted throughout his life. He complained that he was never invited to give a presentation on his work, but from my own experience this was quite normal at the time; PhD students were then largely to be seen and not heard.Segerstrale makes it clear that, from the start of his career, Hamilton was unusually sensitive to what he saw as a lack of due recognition. At times, he displayed an almost paranoid view of some of his colleagues. The most notorious example of this was his reaction to John Maynard Smith's 1975 review of E.O. Wilson's Sociobiology [2xSociobiology: The New Synthesis. Wilson, E.O. See all References][2] in the New Scientist [3xSurvival through suicide. Maynard Smith, J. New Sci. 1975; 28: 496–497See all References][3], which is covered in considerable detail. To be brief, John mentioned that J.B.S. Haldane had made a remark in a London pub conversation to the effect that ‘he was prepared to lay down his life for eight cousins or two brothers’. Hamilton refused to accept this as true, even after it had been pointed out that Haldane had published something very similar in 1955, in an article in the popular science publication Penguin New Biology [4xPopulation genetics. Haldane, J.B.S. Penguin New Biol. 1955; 18: 34–51See all References][4]. Hamilton all but accused John of having invented the story in an attempt to minimise the importance of his contributions. This lead to several years in which he was deeply hostile to John, and even refused to attend scientific meetings at which John was present. In reality, John was always ready to express his admiration for Hamilton's work on kin selection, and I remember his expressing this very clearly in a lecture to a Cambridge undergraduate society in 1965. It was only when H.J. Eysenck confirmed that he too had heard Haldane's remarks that Hamilton relented, in a letter to John in 1980 quoted by Segerstrale.These examples illustrate the major strength of the book: it provides revealing details of how Hamilton worked and thought, and how he interacted with his peers. One of its weaknesses is that Segerstrale does not seem to have a broad knowledge of evolutionary biology, and so does not do a very good job of putting Hamilton's work into the context of developments in the field as whole. Although the areas in which Hamilton worked were indeed very significant growth points, and were driven forward by his insights, there were several others that were also advancing rapidly over this period, to which Hamilton made little or no contribution. For example, no mention is made of molecular evolution, a hugely important area of modern evolutionary biology that was largely ignored by him. In discussing Hamilton's visit to Japan in 1986, Segerstrale implies that there was then no important Japanese evolutionary biologist, at a time when Motoo Kimura had helped to create the field of molecular evolution. Similar, she fails to give a clear account of how Hamilton's work on the role of host–parasite interactions in the evolution of sex and recombination relates to the work of others at the same time; he was not alone in proposing this idea.The last phase of Hamilton's career mainly concerned the origin of human HIV, resulting in his final trip to Africa and tragic death from a gastrointestinal haemorrhage following a malarial infection. It is not entirely clear from Segerstrale's account why he got involved in this topic, and became a supporter of Edward Hooper's theory of the transmission of HIV-1 from chimpanzees during the development of a polio vaccine in the Congo in the 1950s. She does not explain the nature of the evidence that was needed to ascertain the truth and led to the downfall of this hypothesis, which may confuse nonspecialists.Overall, the book gives enough information about Hamilton's career to enable the reader to see him warts and all, despite a tendency towards hero worship. He comes over as an exceptionally single-minded person with a large ego, despite a shy and unassuming manner. He was a poor lecturer to undergraduates, and frequently also to his peers in seminars and conferences. He published relatively few papers. Nonetheless, he did work of enormous importance. This is, of course, because of Hamilton's great abilities, but some credit should probably be given to the rather ramshackle British academic system of the 1960s, for allowing such a singular person to establish a career. One is led to wonder whether someone like this could survive beyond the first few years of their career, in the modern era of pressure from the top to teach, publish in ‘high-impact’ journals, bring in juicy research grants, and devote time to filling out endless electronic forms. We may be in danger of losing the most creative minds from science.

The proximate and evolutionary causes of the levelling of mortality rates at late ages, observed in several species, remain obscure. To investigate the causes of mortality levelling late in life in Drosophila melanogaster, we examined the effect of reproduction on mortality patterns, by conducting population cage experiments with a total of more than 45,000 individuals. Several different genotypes of reproducing and non-reproducing males from F(1) crosses among isogenic lines were studied. Our results suggest that significant mortality levelling can occur even in non-reproducing males, but that reproduction also significantly affects mortality patterns. The results show that mortality levelling is strongly affected by the Gompertz initial mortality rate and exponential rate of increase parameters, probably through the effects of heterogeneity in mortality risks.

The net rate of mutation to deleterious but nonlethal alleles and the sizes of effects of these mutations are of great significance for many evolutionary questions. Here we describe three replicate experiments in which mutations have been accumulated on chromosome 3 of Drosophila melanogaster by means of single-male backcrosses of heterozygotes for a wild-type third chromosome. Egg-to-adult viability was assayed for nonlethal homozygous chromosomes. The rates of decline in mean and increase in variance (DM and DV, respectively) were estimated. Scaled up to the diploid whole genome, the mean DM for homozygous detrimental mutations over the three experiments was between 0.8 and 1.8%. The corresponding DV estimate was ∼0.11%. Overall, the results suggest a lower bound estimate of at least 12% for the diploid per genome mutation rate for detrimentals. The upper bound estimates for the mean selection coefficient were between 2 and 10%, depending on the method used. Mutations with selection coefficients of at least a few percent must be the major contributors to the effects detected here and are likely to be caused mostly by transposable element insertions or indels.

We have investigated the pattern of DNA sequence variation at the exuperantia2 locus in Drosophila pseudoobscura. This adds to the increasing dataset of genetic variation in D. pseudoobscura, a useful model species for evolutionary genetic studies. The level of silent site nucleotide diversity and the divergence from an outgroup Drosophila miranda are comparable with those for other X-linked loci. One peculiar pattern at the exu2 locus of D. pseudoobscura is a complete linkage disequilibrium between two SNPs, one of which is a replacement site. As a result, there are two distinct haplotype groups in our dataset. Based upon the comparisons with the outgroup sequences from D. miranda and Drosophila persimilis, we show that the newly derived haplotype group has lower diversity than the ancestral haplotype group. The pattern of protein evolution at exu2 shows some deviation from the neutral model. Together, these and other characteristics of the exu2 locus suggest the action of selection on the pattern of SNP variation, consistent with a partial selective sweep associated with the newly derived haplotype.

Less than 150 years ago, the view that living species were the result of special creation by God was still dominant. The recognition by Charles Darwin and Alfred Russel Wallace of the mechanism of evolution by natural selection has completely transformed our understanding of the living world, including our own origins. Evolution: A Very Short Introduction provides a summary of the process of evolution by natural selection, highlighting the wide range of evidence, and explains how natural selection gives rise to adaptations and eventually, over many generations, to new species. It introduces the central concepts of the field of evolutionary biology and discusses some of the remaining questions regarding evolutionary processes.

Brian Charlesworth reviews Steve Jones' new book for non-specialists on human maleness and sexual reproduction.

Specialized genes in lower eukaryotes prevent fusion between gametes of identical mating type; their molecular characterization has revealed features that may shed light on the evolutionary origin of mating types.

A fast-timescale approximation is applied to the coalescent process in a single population, which is demographically structured by sex and/or age. This provides a general expression for the probability that a pair of alleles sampled from the population coalesce in the previous time interval. The effective population size is defined as the reciprocal of twice the product of generation time and the coalescence probability. Biologically explicit formulas for effective population size with discrete generations and separate sexes are derived for a variety of different modes of inheritance. The method is also applied to a nuclear gene in a population of partially self-fertilizing hermaphrodites. The effects of population subdivision on a demographically structured population are analyzed, using a matrix of net rates of movement of genes between different local populations. This involves weighting the migration probabilities of individuals of a given age/sex class by the contribution of this class to the leading left eigenvector of the matrix describing the movements of genes between age/sex classes. The effects of sex-specific migration and nonrandom distributions of offspring number on levels of genetic variability and among-population differentiation are described for different modes of inheritance in an island model. Data on DNA sequence variability in human and plant populations are discussed in the light of the results.

Senescence is the post-maturation decline in survivorship and fecundity that accompanies advancing age. Two main evolutionary theories have been proposed to account for senescence. (1) The mutation-accumulation theory. Deleterious mutations exerting their effects only late in life would tend to accumulate, because of their minimal effects on fitness. More precisely, exclusively late-acting deleterious mutations will attain higher equilibrium frequencies under mutation-selection balance than will mutations that act early, resulting in lower mean values for fitness components late in life (ref. 3 , p. 218). Medawar emphasized the possibility that this effect would be enhanced by selection of modifiers that postpone the age of onset of genetic diseases. (2) The pleiotropy theory. Williams suggested that many of the genes with beneficial effects on early fitness components have pleiotropy deleterious effects on late fitness components, but are nevertheless favoured by natural selection. (These theories are based on the decline with age in the effect of age-specific fitness-component changes on total fitness (ref. 3 , pp. 206-214 and refs 4, 5 ). Either or both of these theories could apply in any particular population.) Selection experiments in Drosophila and Tribolium support the pleiotropy theory, although one such experiment gave results that only bordered on significance, but the mutation-accumulation theory has never been tested. The present results provide evidence for the pleiotropy theory, but do not support the mutation-accumulation theory. Reproduced by permission. Michael Rose, Brian Charlesworth, A Test of Evolutionary Theories of Senescence. Nature 287 , 141-142 (1980).

There is a great diversity of sex determination mechanisms, with evidence for numerous evolutionary transitions between different systems. For example, environmental sex determination is widespread in lower vertebrates, and genetic sex determination has probably evolved from it several times. This requires the establishment of genes that override environmental cues. Close linkage between male and female determining loci is favoured by selection, and represents the first step towards the evolution of highly differentiated sex chromosomes. Once crossing over between primitive sex chromosomes has been suppressed, the primitive Y (W) chromosome is vulnerable to the operation of forces that lead to a reduction in its effective population size. This reduces the ability of natural selection to maintain the functionality of genes on the proto-Y, so that it gradually degenerates. Primitive sex chromosome systems, and systems of neo-X and neo-Y chromosomes formed by translocations involving autosomes and sex chromosomes, provide an opportunity to test evolutionary models of the degeneration of Y chromosomes and to determine the time-scales involved. Recent data confirm that newly-evolving Y or neo-Y chromosomes experience a sharp reduction in effective population size, and indicate that degeneration can occur over a few million generations.

Sex chromosomes are generally believed to have descended from a pair of homologous autosomes. Suppression of recombination between the ancestral sex chromosomes led to the genetic degeneration of the Y chromosome1. In response, the X chromosome may become dosage-compensated1,2. Most proposed mechanisms for the degeneration of Y chromosomes involve the rapid fixation of deleterious mutations on the Y1. Alternatively, Y-chromosome degeneration might be a response to a slower rate of adaptive evolution, caused by its lack of recombination3. Here we report patterns of DNA polymorphism and divergence at four genes located on the neo-sex chromosomes of Drosophila miranda. We show that a higher rate of protein sequence evolution of the neo- X-linked copy of Cyclin B relative to the neo-Y copy is driven by positive selection, which is consistent with the adaptive hypothesis for the evolution of the Y chromosome3. In contrast, the neo- Y-linked copies of even-skipped and roundabout show an elevated rate of protein evolution relative to their neo-X homologues, probably reflecting the reduced effectiveness of selection against deleterious mutations in a non-recombining genome1.Our results provide evidence for the importance of sexual recombination for increasing and maintaining the level of adaptation of a population.

The evolutionary significance of sexual reproduction and genetic recombination is a long-standing puzzle. Some recent experiments on Drosophila show that a lack of recombination can impede adaptive evolution.

Formulae for the effective population sizes of autosomal, X-linked, Y-linked and maternally transmitted loci in age-structured populations are developed. The approximations used here predict both asymptotic rates of increase in probabilities of identity, and equilibrium levels of neutral nucleotide site diversity under the infinite-sites model. The applications of the results to the interpretation of data on DNA sequence variation in Drosophila, plant, and human populations are discussed. It is concluded that sex differences in demographic parameters such as adult mortality rates generally have small effects on the relative effective population sizes of loci with different modes of inheritance, whereas differences between the sexes in variance in reproductive success can have major effects, either increasing or reducing the effective population size for X-linked loci relative to autosomal or Y-linked loci. These effects need to be accounted for when trying to understand data on patterns of sequence variation for genes with different transmission modes.

A general quantitative genetic model of mutations with age-specific deleterious effects is developed. It is shown that, for the simplest case of a species with age-independent reproductive rates and extrinsic adult mortality rates, and no pleiotropic effects of age-specific mutations, exponential increases with age of both the mean and additive genetic variance of age-specific mortality rates are expected. Models where age-specific mutations have pleiotropic effects on mortality that extend either throughout adult life, or are confined to juvenile stages, produce equilibria with exponential increases in the mean and additive variance of mortality rates during much of adult life. However, the rates of increase diminish late in life, and can even become zero. Predictions concerning the additive genetic correlations in mortality rates between different ages are also developed. The predictions of the models are compared with data on humans and Drosophila.

We analyze genetic variation at fused1, a locus that is close to the centromere of the X chromosome-autosome (X/4) fusion in Drosophila americana. In contrast to other X-linked and autosomal genes, for which a lack of population subdivision in D. americana has been observed at the DNA level, we find strong haplotype structure associated with the alternative chromosomal arrangements. There are several derived fixed differences at fused1 (including one amino acid replacement) between two haplotype classes of this locus. From these results, we obtain an estimate of an age of ∼0.61 million years for the origin of the two haplotypes of the fused1 gene. Haplotypes associated with the X/4 fusion have less DNA sequence variation at fused1 than haplotypes associated with the ancestral chromosome arrangement. The X/4 haplotypes also exhibit clinal variation for the allele frequencies of the three most common amino acid replacement polymorphisms, but not for adjacent silent polymorphisms. These patterns of variation are best explained as a result of selection acting on amino acid substitutions, with geographic variation in selection pressures.

Evolutionary change often involves what geneticists call quantitative traits—traits such as height, weight, or skin color that are determined by more than one gene and vary “continuously” or “semicontinuously” within a population (when graphed, the variation in the trait often resembles a bell-shaped curve). Quantitative traits are involved in many human diseases and in breeding economically important plants and animals; as a result, researchers are interested in understanding the underlying causes of their variation. Geneticists are getting ever closer to pinpointing the locations of the genetic variants that cause variability in quantitative traits, thanks to increasingly detailed studies of genomes that identify naturally occurring variants at individual chromosomal sites, especially differences at single-nucleotide sites in the DNA sequence (single-nucleotide polymorphisms, or SNPs) ( 1 ). There has been every reason to suppose that quantitative trait variation is subject to the same evolutionary forces that affect other types of DNA sequence variability, primarily by effects on the genes concerned through selection on a specific trait. On page 372 of this issue, Rockman et al. ( 2 ) test this idea and find that evolutionary mechanisms that target larger regions of the genome are more prominent than expected.

The mutation rate per genome for local affecting fitness is crucial in theories of the evolution of sex and recombination and of outbreeding mechanisms. Mutational variation in fitness may also be important in the evolution of mate choice in animals. No information is available on the rate at which spontaneous mutations with small effects on fitness arise, although viability (probability of survival to adulthood) has been studied in Drosophila melanogaster. These experiments involved the accumulation of spontaneous mutations in the virtual absence of natural selection, in a set of independently maintained lines with a common origin. The rates of decline in mean and increase in variance among lines permit estimation of limits to the mean number of new mutations arising per generation (U) and the average homozygous effect of a new mutation of minor effect(s). For the second chromosome of D. melanogaster, the value of U is at least 0.17 (ref. 7), and (1-h)s is less than 0.02, where hs is the average decline in fitness of heterozygotes. As the second chromosome is about 40% of the genome, these data indicate a mutation rate per haploid genome of at least 0.42 for viability. Here we present similar data on the effects of homozygous spontaneous mutations on a measure of fitness in D. melanogaster.

Many species persist as a metapopulation under a balance between the local extinction of subpopulations or demes and their recolonization through dispersal from occupied patches. Here we review the growing body of literature dealing with the genetic consequences of such population turnover. We focus our attention principally on theoretical studies of a classical metapopulation with a ‘finite–island’ model of population structure, rather than on ‘continent–island’ models or ‘source–sink’ models. In particular, we concern ourselves with the subset of geographically subdivided population models in which it is assumed that all demes are liable to extinction from time to time and that all demes receive immigrants. Early studies of the genetic effects of population turnover focused on population differentiation, such as measured byFST. A key advantage ofFSTover absolute measures of diversity is its relative independence of the mutation process, so that different genes in the same species may be compared. Another advantage is thatFSTwill usually equilibrate more quickly following perturbations than will absolute levels of diversity. However, becauseFSTis a ratio of between–population differentiation to total diversity, the genetic effects of metapopulation processes may be difficult to interpret in terms ofFSTon its own, so that the analysis of absolute measures of diversity in addition is likely to be informative. While population turnover may either increase or decreaseFST, depending on the mode of colonization, recurrent extinction and recolonization is expected always to reduce levels of both within–population and specieswide diversity (πSand πT, respectively). One corollary of this is that πScannot be used as an unbiased estimate of the scaled mutation rate, θ, as it can, with some assumptions about the migration process, in species whose demes do not fluctuate in size. The reduction of π in response to population turnover reflects shortened mean coalescent times, although the distribution of coalescence times under extinction–colonization equilibrium is not yet known. Finally, we review current understanding of the effect of metapopulation dynamics on the effective population size.

Background: In many species, sex is determined by a system involving X and Y chromosomes, the latter having lost much of their genetic activity. Sex chromosomes have evolved independently many times, and several different mechanisms responsible for the degeneration of the Y chromosome have been proposed. Here, we have taken advantage of the secondary sex chromosome pair in Drosophila miranda to test for the effects of evolutionary forces involved in the early stages of Y-chromosome degeneration. Because of a fusion of one of the autosomes to the Y chromosome, a neo-Y chromosome and a neo-X chromosome have been formed, resulting in the transmission of formerly autosomal genes in association with the sex chromosomes. Results: We found a 25-fold lower level of variation at microsatellites located on the neo-Y chromosome compared with homologous loci on the neo-X chromosome, or with autosomal and X-linked microsatellites. Sequence analyses of the region flanking the microsatellites suggested that the neo-sex chromosomes originated about 1 million years ago. Conclusions: Variability of the neo-Y chromosome of D. miranda is substantially reduced below expectations at mutation-drift equilibrium. Such a reduction is predicted by theories of the degeneration of the Y chromosome. Another possibility is that there is little or no mutation at microsatellite loci on a non-recombining chromosome such as the neo-Y, but this seems inconsistent with other data.

Associations between selected alleles and the genetic backgrounds on which they are found can reduce the efficacy of selection. We consider the extent to which such interference, known as the Hill-Robertson effect, acting between weakly selected alleles, can restrict molecular adaptation and affect patterns of polymorphism and divergence. In particular, we focus on synonymous-site mutations, considering the fate of novel variants in a two-locus model and the equilibrium effects of interference with multiple loci and reversible mutation. We find that weak selection Hill-Robertson (wsHR) interference can considerably reduce adaptation, e.g., codon bias, and, to a lesser extent, levels of polymorphism, particularly in regions of low recombination. Interference causes the frequency distribution of segregating sites to resemble that expected from more weakly selected mutations and also generates specific patterns of linkage disequilibrium. While the selection coefficients involved are small, the fitness consequences of wsHR interference across the genome can be considerable. We suggest that wsHR interference is an important force in the evolution of nonrecombining genomes and may explain the unexpected constancy of codon bias across species of very different census population sizes, as well as several unusual features of codon usage in Drosophila.

In organisms with chromosomal sex determination, sex is determined by a set of dimorphic sex chromosomes that are thought to have evolved from a set of originally homologous chromosomes. The chromosome inherited only through the heterogametic sex (the Y chromosome in the case of male heterogamety) often exhibits loss of genetic activity for most of the genes carried on its homolog and is hence referred to as degenerate. The process by which the proto-Y chromosome loses its genetic activity has long been the subject of much speculation. We present a DNA sequence variation analysis of marker genes on the evolving sex chromosomes (neo-sex chromosomes) of Drosophila miranda. Due to its relatively recent origin, the neo-Y chromosome of this species is presumed to be still experiencing the forces responsible for the loss of its genetic activity. Indeed, several previous studies have confirmed the presence of some active loci on this chromosome. The genes on the neo-Y chromosome surveyed in the current study show generally lower levels of variation compared with their counterparts on the neo-X chromosome or an X-linked gene. This is in accord with a reduced effective population size of the neo-Y chromosome. Interestingly, the rate of replacement nucleotide substitutions for the neo-Y linked genes is significantly higher than that for the neo-X linked genes. This is not expected under a model where the faster evolution of the X chromosome is postulated to be the main force driving the degeneration of the Y chromosome.

The accumulation of deleterious mutations due to the process known as Muller's ratchet can lead to the degeneration of nonrecombining populations. We present an analytical approximation for the rate at which this process is expected to occur in a haploid population. The approximation is based on a diffusion equation and is valid when N exp(−u/s) ⪢ 1, where N is the population size, u is the rate at which deleterious mutations occur, and s is the effect of each mutation on fitness. Simulation results are presented to show that the approximation estimates the rate of the process better than previous approximations for values of mutation rates and selection coefficients that are compatible with the biological data. Under certain conditions, the ratchet can turn at a biologically significant rate when the deterministic equilibrium number of individuals free of mutations is substantially >100. The relevance of this process for the degeneration of Y or neo-Y chromosomes is discussed.

A multilocus stochastic model is developed to simulate the dynamics of mutational load in small populations of various sizes. Old mutations sampled from a large ancestral population at mutation–selection balance and new mutations arising each generation are considered jointly, using biologically plausible lethal and deleterious mutation parameters. The results show that inbreeding depression and the number of lethal equivalents due to partially recessive mutations can be partly purged from the population by inbreeding, and that this purging mainly involves lethals or detrimentals of large effect. However, fitness decreases continuously with inbreeding, due to increased fixation and homozygosity of mildly deleterious mutants, resulting in extinctions of very small populations with low reproductive rates. No optimum inbreeding rate or population size exists for purging with respect to fitness (viability) changes, but there is an optimum inbreeding rate at a given final level of inbreeding for reducing inbreeding depression or the number of lethal equivalents. The interaction between selection against partially recessive mutations and genetic drift in small populations also influences the rate of decay of neutral variation. Weak selection against mutants relative to genetic drift results in apparent overdominance and thus an increase in effective size (Ne) at neutral loci, and strong selection relative to drift leads to a decrease in Ne due to the increased variance in family size. The simulation results and their implications are discussed in the context of biological conservation and tests for purging.

Most of the familiar features of living organisms show clear signs of adaptation of structure to function. There is overwhelming evidence that this is the outcome of evolution by natural selection. It is, accordingly, tempting to assume that the same applies to the more subtle aspects of biological organisation uncovered by the past century of research in genetics, cell biology and molecular biology. No doubt in many cases this assumption is true. In this wide-ranging and ambitious book, Michael Lynch sets out to challenge the view that natural selection rules supreme at the level of the organisation of the genome.

ESTIMATES of the rate of mutation to mildly deleterious alleles are fundamental to the testing of theories of the maintenance of sexual reproduction1 and recombination2,3. There are, however, few estimates of this parameter4,5. We suggest that data on inbreeding depression in highly self-fertilizing populations might provide such estimates. The effect of inbreeding in reducing genetic load and inbreeding depression is well known6,7, but little attention has been paid to the magnitude of these quantities in highly inbred natural populations. Modelling of mutational load shows that highly self-fertilizing populations should still have some genetic load and inbreeding depression8–10. In such populations, inbreeding depression is the converse of heterosis and its magnitude can be estimated from the increase in fitness-related characteristics in individuals produced by intercrossing different strains. Here we derive the inbreeding depression expected in completely inbred populations, and use it to estimate mutation rates per genome for some plant species.

Dosage compensation of some X-linked genes varies among mammals. Inactivation of an X-linked copy of a gene in females appears to correlate with lack of an active homologue on the Y chromosome, implying that dosage compensation evolves in response to the loss of function of genes on the Y.

Associations between heterozygosities at different loci are generated by inbreeding. This can cause a fusion or translocation involving a sex chromosome and an autosome to have a selective advantage, when there is selection in favour of heterozygotes. Population genetic models of Y-autosome and X-autosome rearrangments in populations mating by a mixture of full sib-matings and random mating are described, in which the rearrangements cause an autosomal locus with heterozygote advantage to become linked to the true sex chromosomes. Such rearrangements gain a selective advantage under a wide range of conditions. If they can invade, Y-autosome rearrangements always spread to fixation, whereas X-autosome rearrangements may be maintained as stable polymorphisms. The results are discussed in relation to data on breeding systems and karyotypic evolution in termites.

The magnitude of inbreeding depression in Drosophila melanogaster appears too large to be accounted for by mutational load with multiplicative fitness interactions among loci, if current estimates of mutation and selection parameters are valid. One possible explanation for this discrepancy is synergistic epistasis among the fitness effects of deleterious mutations. A simple model of the effect of synergistic epistasis on the inbreeding load is developed. This model is used to show that deleterious mutations could account for the Drosophila data on the effects of inbreeding on components of fitness such as viability.

Although wild-type alleles are generally dominant over mutant alleles, recently established alleles for pesticide resistance are rarely recessive in combination with their progenitors. This seems to be caused by a combination of a ‘selective sieve' favouring non-recessive mutations, and the biochemical basis of resistance.

Most mutations with observable phenotypic effects are deleterious. Studies of Drosophila and inbred plant populations suggest that a new individual may have a mean number of new deleterious mutations that exceeds one-half. Most of these have relatively small homozygous effects and reduce fitness by 1–2% when heterozygous. Several striking features of present-day organisms have apparently evolved in response to the constant input of deleterious alleles by recurrent mutation. For example, the adaptations of hermaphroditic organisms for outcrossing have been widely interpreted in terms of the benefits of avoiding the reduced fitness of inbred progeny, which is partly due to deleterious mutations. Population genetic models of modifiers of the breeding system in the presence of genome-wide deleterious mutation are reviewed and their predictions related to genetic and comparative data. The evolution of degenerate Y chromosomes is a phenomenon that may be caused by the accumulation of deleterious mutations. The population genetic mechanisms that can drive this degeneration are reviewed and their significance assessed in the light of available data.

Theoretical arguments are presented which suggest that each advance of Muller's ratchet in a haploid asexual population causes the fixation of a deleterious mutation at a single locus. A similar process operates in a diploid, fully asexual population under a wide range of parameter values, with respect to fixation within one of the two haploid genomes. Fixations of deleterious mutations in asexual species can thus be greatly accelerated in comparison with a freely recombining genome, if the ratchet is operating. In a diploid with segregation of a single chromosome, but no crossing over within the chromosome, the advance of the ratchet can be decoupled from fixation if mutations are sufficiently close to recessivity. A new analytical approximation for the rate of advance of the ratchet is proposed. Simulation results are presented that validate the assertions about fixation. The simulations show that none of the analytical approximations for the rate of advance of the ratchet are satisfactory when population size is large. The relevance of these results for evolutionary processes such as Y chromosome degeneration is discussed.

The extent of genetic degeneration of the nec-Y chromosome of Drosophila americana americana has been investigated. Three loci, coding for the enzymes enolase, phosphoglycerate kinase and alcohol dehydrogenase, have been localized to chromosome 4 of D. a. americana, which forms the neo-Y and neo-X chromosomes. Crosses between D. a. americana, and D. virilis or D. montana showed that the loci coding for these enzymes carry active alleles on the neo-Y chromosome in all wild-derived strains of americana that were tested. Intercrosses between a genetically marked stock of virilis and strains of americana were carried out, creating F3 males that were homozygous for sections of the neo-Y chromosome. The sex ratios in the F3 generation of the intercrosses showed that no lethal alleles have accumulated on any of the neo-Y chromosomes tested. There was evidence for more minor reductions in fitness, but this seems to be mainly caused by deleterious alleles that are specific to each strain. A similar picture was provided by examination of the segregation ratios of two marker genes among the F3 progeny. Overall, the data suggest that the neo-Y chromosome has undergone very little degeneration, certainly not to the extent of having lost the functions of vital genes. This is consistent with the recent origin of the neo-Y and neo-X chromosomes, and the slow rates at which the forces that cause Y chromosome degeneration are likely to work.

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The Plausibility of Life . Resolving Darwin's Dilemma. By Marc W. Kirschner and John C. Gerhart . Yale University Press, New Haven, CT, 2005. 330 pp. $30, £18.95. ISBN 0-300-10865-6. The authors hold that the accumulation of small genetic mutations over time does not explain the variety and complexity of life. Instead, they propose "facilitated variation" to account for the conversion of random genetic change into complex innovations.

Many long-lived avian species adopt life strategies that involve a gregarious way of life at juvenile and sub-adult stages and territoriality during adulthood. However, the potential associated costs of these life styles, such as stress, are poorly understood. We examined the effects of group living, sex and parasite load on the baseline concentration of faecal stress hormone (corticosterone) metabolites in a wild population of common ravens ( Corvus corax ). Corticosterone concentrations were significantly higher in non-breeding gregarious ravens than in territorial adults. Among territorial birds, males showed higher stress levels than their mates. Parasite burdens did not affect hormone levels. Our results suggest a key role of the social context in the stress profiles of the two population fractions, and that group living may be more energetically demanding than maintaining a territory. These findings have implications for understanding hormonal mechanisms under different life styles and may inspire further research on the link between hormone levels and selective pressures modulating gregarious and territorial strategies in long-lived birds.

SummaryTheoretical models of the effects of selection against deleterious mutations on variation at linked neutral sites (background selection) are used to predict the relations between chromosomal location and genetic variability at the DNA level, inDrosophila melanogaster. The sensitivity of the predictions to variation in the mutation, selection and recombination parameters on which they are based is examined. It is shown that many features of the observed relations between chromosomal location and level of genetic diversity inD. melanogastercan be explained by background selection, especially if the weak selective forces acting on transposable elements are taken into account. In particular, the gradient in diversity in the distal portion of the X chromosome, and the lack of diversity on chromosome 4 and at the bases of the major chromosomes, can be fully accounted for. There are, however, discrepancies between predicted and observed values for some loci inD. melanogaster, which may reflect the effects of forces other than background selection.

Two major theories of the evolution of senescence (mutation accumulation and antagonistic pleiotropy) make different predictions about the relationships between age, inbreeding effects, and the magnitude of genetic variance components of life-history components. We show that, under mutation accumulation, inbreeding decline and three major components of genetic variance are expected to increase with age in randomly mating populations. Under the simplest version of the antagonistic pleiotropy model, no changes in the severity of inbreeding decline, dominance variance, or the genetic variance of chromosomal homozygotes are expected, but additive genetic variance may increase with age. Age-specific survival rates and mating success were measured on virgin males, using lines extracted from a population of Drosophila melanogaster. For both traits, inbreeding decline and several components of genetic variance increase with age. The results are consistent with the mutation accumulation model, but can only be explained by antagonistic pleiotropy if there is a general tendency for an increase with age in the size of allelic effects on these life-history traits.