Biomedical subjects

Stephen R Proulx

Publications and source records attributed to Stephen R Proulx.

7 recordsLinked to original sources

PubMed2006

The role of life cycle and migration in selection for variance in offspring number.

For two genotypes that have the same mean number of offspring but differ in the variance in offspring number, naturalselection will favor the genotype with lower variance. In such cases, the average growth rate is not sufficient as a measure of fitness or as a predictor of fixation probability. However, the effect of variance in offspring number on the fixationprobability of mutant strategies has been calculated under several scenarios with the general conclusion that variance in offspring number reduces fitness in proportion to the inverse of the population size [Gillespie, J., Genetics 76:601-606, 1974; Proulx, S.R., Theor. Popul. Biol. 58:33-47, 2000]. This relationship becomes more complicated under a metapopulation scenario where the "effective" population size depends on migration rate, population structure, and lifecycle. It is shown that in a life cycle where reproduction and migration (the birth-migration-regulation life cycle, or BMR)occur prior to density regulation within every deme, the fitness of a strategy depends on migration rate. When migration rates are near zero, the fitness of the strategy is determined by the size of individual demes, so that the strategy favoredin small populations tends to be fixed. As migration rate increases and approaches panmixis between demes, the fitness ofa reproductive strategy approaches what its value would be in a single, panmictic deme with a population size correspondingtothe census size of the metapopulation. Interestingly, when the life cycle is characterized by having density regulation in each deme prior to migration (the BRM life cycle) the fixation probability of a strategy is independent of migration rate. These results are found to be qualitatively consistent with the individual-based simulation results in Shpak [Theor. Biosci.124:65-85, 2005].

Alleles↗

PubMed2006

Allelic divergence precedes and promotes gene duplication.

One of the striking observations from recent whole-genome comparisons is that changes in the number of specialized genes in existing gene families, as opposed to novel taxon-specific gene families, are responsible for the majority of the difference in genome composition between major taxa. Previous models of duplicate gene evolution focused primarily on the role that neutral processes can play in evolutionary divergence after the duplicates are already fixed in the population. By instead including the entire cycle of duplication and divergence, we show that specialized functions are most likely to evolve through strong selection acting on segregating alleles at a single locus, even before the duplicate arises. We show that the fitness relationships that allow divergent alleles to evolve at a single locus largely overlap with the conditions that allow divergence of previously duplicated genes. Thus, a solution to the paradox of the origin of organismal complexity via the expansion of gene families exists in the form of the deterministic spread of novel duplicates via natural selection.

Computer Simulation↗

PubMed2005

Network thinking in ecology and evolution.

Although pairwise interactions have always had a key role in ecology and evolutionary biology, the recent increase in the amount and availability of biological data has placed a new focus on the complex networks embedded in biological systems. The increased availability of computational tools to store and retrieve biological data has facilitated wide access to these data, not just by biologists but also by specialists from the social sciences, computer science, physics and mathematics. This fusion of interests has led to a burst of research on the properties and consequences of network structure in biological systems. Although traditional measures of network structure and function have started us off on the right foot, an important next step is to create biologically realistic models of network formation, evolution, and function. Here, we review recent applications of network thinking to the evolution of networks at the gene and protein level and to the dynamics and stability of communities. These studies have provided new insights into the organization and function of biological systems by applying existing techniques of network analysis. The current challenge is to recognize the commonalities in evolutionary and ecological applications of network thinking to create a predictive science of biological networks.

Journal Article↗

PubMed2004

The opportunity for canalization and the evolution of genetic networks.

There has been a recent revival of interest in how genetic interactions evolve, spurred on by an increase in our knowledge of genetic interactions at the molecular level. Empirical work on genetic networks has revealed a surprising amount of robustness to perturbations, suggesting that robustness is an evolved feature of genetic networks. Here, we derive a general model for the evolution of canalization that can incorporate any form of perturbation. We establish an upper bound to the strength of selection on canalization that is approximately equal to the fitness load in the system. This method makes it possible to compare different forms of perturbation, including genetic, developmental, and environmental effects. In general, load that arises from mutational processes is low because the mutation rate is itself low. Mutation load can create selection for canalization in a small network that can be achieved through dominance evolution or gene duplication, and in each case selection for canalization is weak at best. In larger genetic networks, selection on genetic canalization can be reasonably strong because larger networks have higher mutational load. Because load induced through migration, segregation, developmental noise, and environmental variance is not mutation limited, each can cause strong selection for canalization.

Evolution, Molecular↗

PubMed2004

Does sex age you?

The evolution of aging and longevity has typically been considered to be a resolution of the conflicting demands on an organism to grow, reproduce, and survive. When social or environmental factors change the opportunities for reproduction in a way that affects differently aged individuals, there will be an evolutionary response in the schedule of senescence. This means that social dynamics can have an important effect on aging. A recent study by Berec and Boukal has shown that the dynamics of mating and divorce can also affect observed life spans through their effect on population dynamics. If females cannot find and maintain mating pairs for long enough to replace themselves, the population will become extinct. This puts a lower limit on the levels of longevity that will be observed in nature.

Aging↗

PubMed2004

A general theory for the evolutionary dynamics of virulence.

Most theory on the evolution of virulence is based on a game-theoretic approach. One potential shortcoming of this approach is that it does not allow the prediction of the evolutionary dynamics of virulence. Such dynamics are of interest for several reasons: for experimental tests of theory, for the development of useful virulence management protocols, and for understanding virulence evolution in situations where the epidemiological dynamics never reach equilibrium and/or when evolutionary change occurs on a timescale comparable to that of the epidemiological dynamics. Here we present a general theory similar to that of quantitative genetics in evolutionary biology that allows for the easy construction of models that include both within-host mutation as well as superinfection and that is capable of predicting both the short- and long-term evolution of virulence. We illustrate the generality and intuitive appeal of the theory through a series of examples showing how it can lead to transparent interpretations of the selective forces governing virulence evolution. It also leads to novel predictions that are not possible using the game-theoretic approach. The general theory can be used to model the evolution of other pathogen traits as well.

Animals↗

PubMed2002

Older males signal more reliably.

The hypothesis that females prefer older males because they have higher mean fitness than younger males has been the centre of recent controversy. These discussions have focused on the success of a female who prefers males of a particular age class when age cues, but not quality cues, are available. Thus, if the distribution of male quality changes with age, such that older males have on average genotypes with higher fitness than younger males, then a female who mates with older males has fitter offspring, which allows the female preference to spread through a genetic correlation. We develop a general model for male display in a species with multiple reproductive bouts that allows us to identify the conditions that promote reliable signalling within an age class. Because males have opportunities for future reproduction, they will reduce their levels of advertising compared with a semelparous species. In addition, because higher-quality males have more future reproduction, they will reduce their advertising more than low-quality males. Thus, the conditions for reliable signalling in a semelparous organism are generally not sufficient to produce reliable signalling in species with multiple reproductive bouts. This result is due to the possibility of future reproduction so that, as individuals age and the opportunities for future reproduction fade, signalling becomes more reliable. This provides a novel rationale for female preference for older mates; older males reveal more information in their sexual displays.

Age Factors↗