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Optimality models have been used to predict evolution of many properties of organisms. They typically neglect genetic details, whether by necessity or design. This omission is a common source of criticism, and although this limitation of optimality is widely acknowledged, it has mostly been defended rather than evaluated for its impact. Experimental adaptation of model organisms provides a new arena for testing optimality models and for simultaneously integrating genetics. First, an experimental context with a well-researched organism allows dissection of the evolutionary process to identify causes of model failure--whether the model is wrong about genetics or selection. Second, optimality models provide a meaningful context for the process and mechanics of evolution, and thus may be used to elicit realistic genetic bases of adaptation--an especially useful augmentation to well-researched genetic systems. A few studies of microbes have begun to pioneer this new direction. Incompatibility between the assumed and actual genetics has been demonstrated to be the cause of model failure in some cases. More interestingly, evolution at the phenotypic level has sometimes matched prediction even though the adaptive mutations defy mechanisms established by decades of classic genetic studies. Integration of experimental evolutionary tests with genetics heralds a new wave for optimality models and their extensions that does not merely emphasize the forces driving evolution.

Komodo dragons, the world's largest lizard, dispatch their large ungulate prey by biting and tearing flesh. If a prey escapes, oral bacteria inoculated into the wound reputedly induce a sepsis that augments later prey capture by the same or other lizards. However, the ecological and evolutionary basis of sepsis in Komodo prey acquisition is controversial. Two models have been proposed. The "bacteria as venom" model postulates that the oral flora directly benefits the lizard in prey capture irrespective of any benefit to the bacteria. The "passive acquisition" model is that the oral flora of lizards reflects the bacteria found in carrion and sick prey, with no relevance to the ability to induce sepsis in subsequent prey. A third model is proposed and analyzed here, the "lizard-lizard epidemic" model. In this model, bacteria are spread indirectly from one lizard mouth to another. Prey escaping an initial attack act as vectors in infecting new lizards. This model requires specific life history characteristics and ways to refute the model based on these characteristics are proposed and tested. Dragon life histories (some details of which are reported here) prove remarkably consistent with the model, especially that multiple, unrelated lizards feed communally on large carcasses and that escaping, wounded prey are ultimately fed on by other lizards. The identities and evolutionary histories of bacteria in the oral flora may yield the most useful additional insights for further testing the epidemic model and can now be obtained with new technologies.

A wealth of molecular biology has been exploited in designing and interpreting experimental evolution studies with bacteriophage T7. The modest size of its genome (40 kb dsDNA) and the ease of making genetic constructs, combined with the many genetic resources for its host (Escherichia coli), have enabled comprehensive and detailed studies of experimental adaptations. In several studies, the genome was specifically altered (gene knockouts, gene replacements, reordering of genetic elements) such that a priori knowledge of genetics and biochemistry of the phage could be used to predict the pathways of compensatory evolution when the modified phage is adapted to recover fitness. In other work, the phage has been adapted to specific environmental conditions chosen to select phenotypic outcomes with a quantitative basis, and the molecular bases of that evolution have been explored. Predicting the outcomes of these adaptations has been challenging. In hindsight, one-third to one-half of the compensatory nucleotide changes observed during the adaptation can be rationalized based on T7 biology. This rationalization usually only applies at the genetic level-a gene product may be known to be involved in the affected pathway, but it usually remains unknown how the observed change affects activity. The progress is encouraging, but the prediction of experimental evolution pathways remains far from complete, and is still sometimes confounded by observation when an adaptation yields a completely unexpected outcome.

A cornerstone of evolutionary ecology is that population density affects adaptation: r and K selection is the obvious example. The reverse is also appreciated: adaptation impacts population density. Yet, empirically demonstrating a direct connection between population density and adaptation is challenging. Here, we address both evolution and ecology of population density in models of viral (bacteriophage) chemostats. Chemostats supply nutrients for host cell growth, and the hosts are prey for viral reproduction. Two different chemostat designs have profoundly different consequences for viral evolution. If host and virus are confined to the same chamber, as in a predator-prey system, viral regulation of hosts feeds back to maintain low viral density (measured as infections per cell). Viral adaptation impacts host density but has a small effect on equilibrium viral density. More interesting are chemostats that supply the viral population with hosts from a virus-free refuge. Here, a type of evolutionary succession operates: adaptation at low viral density leads to higher density, but high density then favors competitive ability. Experiments support these models with both phenotypic and molecular data. Parallels to these designs exist in many natural systems, so these experimental systems may yield insights to the evolution and regulation of natural populations.

For some microorganisms, virulence may be an inadvertent consequence of mutation and selection in the parasite population, occurring within a host during the course of an infection. This type of virulence is short-sighted, in that it engenders no advantage to the pathogen beyond the afflicted host. Bacterial meningitis, poliomyelitis and AIDS are three candidates for this model of the evolution of virulence.

The occurrence of rare or novel alleles has been documented in at least 23 different hybrid zones spanning vertebrate and invertebrate taxa. As most novel alleles either occur at high frequencies in hybrid populations or are exclusively restricted to hybrids, it has seemed probable that hybridization has a role in their origin; however, the molecular nature of these novel alleles and the mechanisms responsible for their origin remain obscure. We examined the complete coding sequences of six alleles of alcohol dehydrogenase in a mammalian hybrid zone between two species of pocket gophers (Geomys). One of these sequences encodes a novel electromorph that had been identified in earlier allozyme studies; this novel allele differs from one of the parental alleles by a single base substitution. This substitution generates an amino acid replacement that affects the net charge of the translated protein. This resultant charge change is congruent with the observed allozyme mobility patterns. Our data thus provide evidence for simple DNA substitution as a mechanism for the origin of this novel hybrid-zone allele.

The existence of co-operation between species has been cast as a problem to the selfish-gene view of evolution: why does co-operation persist, when it would seem that individual selection should favor the unco-operative individual who exploits the co-operative tendencies of its partner and gives nothing in return? The recent literature has emphasized one type of model as underlying the evolution and stability of interspecific co-operation, which we term the "partner-fidelity" model, and which is typified by the game theory model known as the iterated Prisoner's Dilemma game. Under this mechanism, individuals are associated with the same partner(s) during an indefinite sequence of interactions. Individuals who at any time fail to co-operate with their partner can be penalized by those same partners in subsequent trials, hence the co-operation can be evolutionarily stable. Many examples of biological co-operation that have been offered appear to conform to this model. However, a few examples appear instead to fit a different and unrecognized mechanism, termed "partner-choice". Under partner-choice, individuals are associated for just one interaction, but an asymmetry enables one member to differentially reward co-operative vs. unco-operative partners in advance of any possible exploitation. Possible examples of co-operation maintained through partner-choice mechanisms are provided by the yucca/yucca moth system and the fig/fig wasp system.

The ESS primary sex ratio (male/female) under environmental sex determination (ESD) is shown to be equal to the ratio of the average fertility of a female to the average fertility of a male. Thus, depending upon how male and female fertility change over the environmental variable causing ESD, the primary sex ratio may be either male or female biased, or neither. The primary sex ratio thus contains information as to how male and female fertilities change with the environment.

Theories on the evolution of sex determining mechanisms are reviewed for male and female heterogamety, environmental sex determination, and briefly, haplo-diploidy and hermaphroditism. Because of their discrete and well-defined nature, sex determining mechanisms lend themselves to three types of evolutionary questions: what variety occurs and might be expected but does not occur, how do changes occur from one mechanism to another, and why do certain changes occur? All three approaches were illustrated for these different sex determining mechanisms. A generality emerging from these studies is that, at the level of selection of the sex ratio, there are no intrinsic problems in evolving from one sex determining mechanism to another: straightforward transitions between different mechanisms exist under various conditions.

Theories on the evolution of sex determining mechanisms are reviewed for male and female heterogamety, environmental sex determination, and briefly, haplodiploidy and hermaphroditism. Because of their discrete and well-defined nature, sex determining mechanisms lend themselves to three types of evolutionary questions: what variety occurs and might be expected but does not occur, how do changes occur from one mechanism to another, and why do certain changes occur? All three approaches are illustrated for these different sex determining mechanisms. A generality emerging from these studies is that, at the level of selection on the sex ratio, there are no intrinsic problems in evolving from one sex determining mechanism to another: straightforward transitions between different mechanisms exist under various conditions.

Some lemmings have a large proportion of XY females in the population, as well as XX females and XY males. In this paper we first review the biological literature on XY females in mammals, with particular emphasis on the genetics and cytogenetics of this trait. We then consider population genetics models of the behaviour of this trait, and we show that there are serious discrepancies between predictions and observations regarding the sex ratio and the frequency of XY females; in several lemming populations the reported sex ratio is lower and XY females are more common than expected. Finally we consider evolutionary models to understand why XY females persist in these populations and how selection might act on other parts of the reproductive biology to modify the system.

Beneficial mutations are the driving force of evolution by natural selection. Yet, relatively little is known about the distribution of the fitness effects of beneficial mutations in populations. Recent work of Gillespie and Orr suggested some of the first generalizations for the distributions of beneficial fitness effects and, surprisingly, they depend only weakly on biological details. In particular, the theory suggests that beneficial mutations obey an exponential distribution of fitness effects, with the same exponential parameter across different regions of genotype space, provided only that few possible beneficial mutations are available to that genotype. Here we tested this hypothesis with a quasi-empirical model of RNA evolution in which fitness is based on the secondary structures of molecules and their thermodynamic stabilities. The fitnesses of randomly selected genotypes appeared to follow a Gumbel-type distribution and thus conform to a basic assumption of adaptation theory. However, the observed distributions of beneficial fitness effects conflict with specific predictions of the theory. In particular, the distributions of beneficial fitness effects appeared exponential only when the vast majority of small-effect beneficial mutations were ignored. Additionally, the distribution of beneficial fitness effects varied with the fitness of the parent genotype. We believe that correlation of the fitness values among similar genotypes is likely the cause of the departure from the predictions of recent adaptation theory. Although in conflict with the current theory, these results suggest that more complex statistical generalizations about beneficial mutations may be possible. [ABSTRACT FROM AUTHOR]

Two lines of the bacteriophage T7 were grown to fix mutations indiscriminately, using a combination of population bottlenecks and mutagenesis. Complete genome sequences revealed 404 and 299 base substitutions in the two lines, the largest number characterized in functional microbial genomes so far. Missense substitutions outnumbered silent substitutions. Silent substitutions occurred at similar rates between essential and nonessential genes, but missense substitutions occurred at a higher rate in nonessential genes than in essential genes, as expected if they were less deleterious in the nonessential genes. Viral fitness declined during this protocol, and subsequent passaging of each mutated line in large population sizes restored some of the lost fitness. Substitution levels during these recoveries were less than 6% of those during the bottleneck phase, and only two changes during recovery were reversions of the original mutations. Exchanges of genomic fragments between the two recovered lines revealed that fitness effects of some substitutions were not additive—that interactions were accumulating which could lead to incompatibility between the diverged genomes. Based on these results, unprecedented high rates of nucleotide and functional divergence in viral genomes should be attainable experimentally by using repeated population bottlenecks at a high mutation rate interspersed with recovery. [ABSTRACT FROM AUTHOR]

We used mathematical models to address several questions concerning the epidemiologic and evolutionary future of HIV/AIDS in human populations. Our analysis suggests that 1) when HIV first enters a human population, and for many subsequent years, the epidemic is driven by early transmissions, possibly occurring before donors have seroconverted to HIV-positive status; 2) new HIV infections in a subpopulation (risk group) may decline or level off due to the saturation of the susceptible hosts rather than to evolution of the virus or to the efficacy of intervention, education, and public health measures; 3) evolution in humans for resistance to HIV infection or for the infection to engender a lower death rate will require thousands of years and will be achieved only after vast numbers of persons die of AIDS; 4) evolution is unlikely to increase the virulence of HIV; and 5) if HIV chemotherapy reduces the transmissibility of the virus, treating individual patients can reduce the frequency of HIV infections and AIDS deaths in the general population. [ABSTRACT FROM AUTHOR]

The literature has regarded migration as both an ecological phenomenon (the mere movement of individuals from one area to another) and a genetic phenomenon (i.e., dispersal, the mixing of individuals between demes or subpopulations). For example, the seasonal movement of birds between a breeding ground and an overwintering ground constitutes ecological migration, whereas the movement of an individual between breeding grounds is genetic migration. Ecological migration does not influence population structure (by definition), and natural selection therefore acts on ecological migration in a simple manner: the migratory habits yielding the highest fecundity are favored. Genetic migration influences population structure, however, and its evolution is not as simple. A model of genetic migration is studied and reveals that genetic migration is selected according to the geometric mean fitness of movements that constitute a "loop," involving gene flow away from and ultimately back to a deme. Since the natural selection of genetic migration is coupled to the fitnesses of multiple movements in a loop, the fitness of any component migration within such a loop may be high or low and cannot itself indicate the nature of selection for that component of migration. The present results are discussed in the context of previous results concerning the evolution of genetic migration. [ABSTRACT FROM AUTHOR]