James J. Bull

Combining data in phylogenetic analysis.

Systematists have access to multiple sources of character information in phylogenetic analysis. For example, it is not unusual to have nucleotide sequences from several different genes, or to have molecular and morphological data. How should diverse data be analyzed in phylogenetic analysis? Several methods have been proposed for the treatment of partitioned data: the total evidence, separate analysis, and conditional combination approaches. Here, we review some of the advantages and disadvantages of the different approaches, with special concentration on which methods help us to discern the evolutionary process and provide the most accurate estimates of phylogeny.

The Evolution of Cooperation

Darwin recognized that natural selection could not favor a trait in one species solely for the benefit of another species. The modern, selfish‐gene view of the world suggests that cooperation between individuals, whether of the same species or different species, should be especially vulnerable to the evolution of noncooperators. Yet, cooperation is prevalent in nature both within and between species. What special circumstances or mechanisms thus favor cooperation? Currently, evolutionary biology offers a set of disparate explanations, and a general framework for this breadth of models has not emerged. Here, we offer a tripartite structure that links previously disconnected views of cooperation. We distinguish three general models by which cooperation can evolve and be maintained: (i) directed reciprocation—cooperation with individuals who give in return; (ii) shared genes—cooperation with relatives (e.g., kin selection); and (iii) byproduct benefits—cooperation as an incidental consequence of selfish action. Each general model is further subdivided. Several renowned examples of cooperation that have lacked explanation until recently—plant‐rhizobium symbioses and bacteria‐squid light organs—fit squarely within this framework. Natural systems of cooperation often involve more than one model, and a fruitful direction for future research is to understand how these models interact to maintain cooperation in the long term.

Sex Determination in Reptiles

Two factors in reptile sex determination have been studied: (1) the presence or absence of heteromorphic sex chromosomes, and (2) the influence of temperature. Recognizable sex chromosomes are common in snakes and lizards, but are apparently rare in turtles and absent in crocodilians and the tuatara. Temperature-dependent sex determination (TSD) is common in turtles and has been reported in two lizards and alligators; however, data on TSD are available for few non-turtle species. Present findings on TSD suggest that (1) temperature actually determines sex rather than simply causing differential mortality, and (2) temperature controls sex determination in nature as well as in the laboratory. Only one study, however, has convincingly demonstrated the latter. Sex determination by nest temperature is proposed to interfere with the evolution of sex chromosomes and live-bearing (ovoviviparity); a negative correlation should thus be observed between TSD and sex chromosomes/live-bearing. Present evidence is consistent with these predictions. Possible selective advantages and disadvantages of the different sex-determined mechanisms are discussed, and an attempt is made to deduce their ancestries.

Population and evolutionary dynamics of phage therapy

Following a sixty-year hiatus in western medicine, bacteriophages (phages) are again being advocated for treating and preventing bacterial infections. Are attempts to use phages for clinical and environmental applications more likely to succeed now than in the past? Will phage therapy and prophylaxis suffer the same fates as antibiotics — treatment failure due to acquired resistance and ever-increasing frequencies of resistant pathogens? Here, the population and evolutionary dynamics of bacterial–phage interactions that are relevant to phage therapy and prophylaxis are reviewed and illustrated with computer simulations.

Fighting change with change: adaptive variation in an uncertain world

Organisms live in an ever-changing world. Most of evolutionary theory considers one solution to this problem: population-level adaptation. In fact, empirical studies have revealed an enormous variety of mechanisms to cope with environmental fluctuations. Some organisms use behavioral or physiological modifications that leave no permanent trace in the genes of future generations. Others withstand environmental change through the regular production of diverse offspring, in which the diversity can be either genetic or nongenetic. Evolutionary theorists now have the opportunity to catch up with the empirical evolutionary biology, and to integrate the diverse forms of ‘adaptive variation’ into a single conceptual framework. Here, we propose a classification according to the level at which the adaptive variation occurs and discuss some of the mechanisms underlying the variation. This perspective unites independent lines of research in molecular biology, microbiology, macroevolution, ecology, immunology and neurobiology, and suggests directions for a more comprehensive theory of adaptive variation.

SELECTION OF BENEVOLENCE IN A HOST-PARASITE SYSTEM

A paradigm for the evolution of cooperation between parasites and their hosts argues that the mode of parasite transmission is critical to the long‐term maintenance of cooperation. Cooperation is not expected to be maintained whenever the chief mode of transmission is horizontal: a parasites progeny infect hosts unrelated to their parents host. Cooperation is expected to be maintained if the chief mode of transmission is vertical: a parasites progeny infect only the parents host or descendants of that host. This paradigm was tested using bacteria and filamentous bacteriophage (f1). When cells harboring different variants of these phage were cultured so that no infectious spread was allowed, ensuring that all parasite transmission was vertical, selection favored the variants that were most benevolent to the host—those that least harmed host growth rate. By changing the culture conditions so that horizontal spread of the phage was allowed, the selective advantage of the benevolent forms was lost. These experiments thus support the theoretical arguments that mode of transmission is a major determinant in the evolution of cooperation between a parasite and its host.

A Model of Population Growth, Dispersal and Evolution in a Changing Environment

The climatic and biotic conditions at any geographic location will change through time, for example, because of the advance of glaciers. If it is to avoid extinction, a species adapted to a moving habitat must either track its habitat spatially, or adapt genetically to the new environmental conditions. These processes of migration and evolution are important in determining continental biogeographic patterns. We develop a model to explore the relative contributions of adaptation and dispersal as alternative mechanisms whereby a population can respond to changing environmental conditions. In our model the environment to which the species is adapted moves across the landscape at a constant velocity, and a quantitative trait determines each individuals fitness as a function of the local environmental conditions. Local populations are allowed to adapt genetically to the environmental conditions at each point in space, so that a cline develops in the quantitative character. We find that if the rate of environmental movement is slow, the species will track its environment across space, otherwise it will go extinct. Additionally, the higher the genetic variance in the character, the easier it is for the species to maintain itself in a moving environment. Our results generalize previous models that predict a critical patch size of suitable habitat necessary for population persistence.

Short-sighted evolution and the virulence of pathogenic microorganisms

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.

Challenging the trade-off model for the evolution of virulence: is virulence management feasible?

Progress in understanding the evolution of infectious diseases has inspired proposals to manage the evolution of pathogen (including parasite) virulence. A common view is that social interventions that lower pathogen transmission will indirectly select lower virulence because of a trade-off between transmission and virulence. Here, we argue that there is little theoretical justification and no empirical evidence for this plan. Although a trade-off model might apply to some pathogens, the mechanism appears too weak for rapid selection of substantial changes in virulence. Direct selection against virulence itself might be a more rewarding approach to managing the evolution of virulence.

Evolution of phenotypic variance.

A cornerstone of evolutionary theory is that the phenotypic variance of a population may be partitioned into genetic and environmental (nonheritable) components. The traditional motivation for this distinction is that the rate of evolution under natural selection depends on the (relative) magnitudes of certain genetic components of variance. The components of variation are also interesting from another perspective, as illustrated here. Phenotypic variation may be selectively maintained in a population according to its components: selection may favor the maintenance of only the environmental components, only the genetic components, or be indifferent to the composition of the variance. Even when selection is shown to favor phenotypic variation regardless of its components, the possibility exists that environmental variance will evolve to displace the genetic components or vice versa. Environmental and genetic factors may thus compete to produce a given selected level of phenotypic variance. A test of some of these models is provided from the example of seed dormancy: the prediction that variation in seed germination time should be purely environmental is supported by the demonstration of low heritability of germination time in the two available studies.