Quorum sensing as a mechanism to harness the wisdom of the crowds.

Bacteria release and sense small molecules called autoinducers in a process known as quorum sensing. The prevailing interpretation of quorum sensing is that by sensing autoinducer concentrations, bacteria estimate population density to regulate the expression of functions that are only beneficial when carried out by a sufficiently large number of cells. However, a major challenge to this interpretation is that the concentration of autoinducers strongly depends on the environment, often rendering autoinducer-based estimates of cell density unreliable. Here we propose an alternative interpretation of quorum sensing, where bacteria, by releasing and sensing autoinducers, harness social interactions to sense the environment as a collective. Using a computational model we show that this functionality can explain the evolution of quorum sensing and arises from individuals improving their estimation accuracy by pooling many imperfect estimates - analogous to the 'wisdom of the crowds' in decision theory. Importantly, our model reconciles the observed dependence of quorum sensing on both population density and the environment and explains why several quorum sensing systems regulate the production of private goods.

The impact of failure: unsuccessful bacterial invasions steer the soil microbial community away from the invader's niche.

Although many environments like soils are constantly subjected to invasion by alien microbes, invaders usually fail to succeed, succumbing to the robust diversity often found in nature. So far, only successful invasions have been explored, and it remains unknown to what extent an unsuccessful invasion can impact resident communities. Here we hypothesized that unsuccessful invasions can cause impacts to soil functioning by decreasing the diversity and niche breadth of resident bacterial communities, which could cause shifts to community composition and niche structure-an effect that is likely exacerbated when diversity is compromised. To examine this question, diversity gradients of soil microbial communities were subjected to invasion by the frequent, yet oft-unsuccessful soil invader, Escherichia coli, and evaluated for changes to diversity, bacterial community composition, niche breadth, and niche structure. Contrary to expectations, diversity and niche breadth increased across treatments upon invasion. Community composition and niche structure were also altered, with shifts of niche structure revealing an escape by the resident community away from the invader's resources. Importantly, the extent of the escape varied in response to the community's diversity, where less diverse communities experienced larger shifts. Thus, although transient and unsuccessful, the invader competed for resources with resident species and caused tangible impacts that modified both the diversity and functioning of resident communities, which can likely generate a legacy effect that influences future invasion attempts.

Evolutionary transitions between sex-determining mechanisms: a review of theory.

The extraordinary diversity of sex-determining mechanisms found in nature is thought to have arisen by the addition, modification or replacement of regulators at the upstream end of the sex-determining pathway. The spread of a novel regulator of sex determination can manifest itself by an evolutionary transition between environmental and genetic sex determination, for example, or between male and female heterogamety. Both kinds of transition have occurred frequently in the course of evolution. In this paper, various evolutionary forces acting on sex-determining mutations that can bias transitions in one direction or the other are reviewed. Furthermore, the adaptive significance of the main modes of sex determination are discussed, and the common principle underlying ultimate explanations for environmental sex determination, genetic sex determination and maternal control over sex determination in the offspring are highlighted. Most of the current theory concentrates on the population-genetic aspects of sex determination transitions, using models that do not reflect the developmental mechanisms involved in sex determination. However, the increasing availability of molecular data creates opportunities for the future development of mechanistic models that will further clarify how selection and developmental architecture interact to direct the evolution of sex determination genes.

Turnover of sex chromosomes induced by sexual conflict.

Sex-determination genes are among the most fluid features of the genome in many groups of animals. In some taxa the master sex-determining gene moves frequently between chromosomes, whereas in other taxa different genes have been recruited to determine the sex of the zygotes. There is a well developed theory for the origin of stable and highly dimorphic sex chromosomes seen in groups such as the eutherian mammals. In contrast, the evolutionary lability of genetic sex determination in other groups remains largely unexplained. In this theoretical study, we show that an autosomal gene under sexually antagonistic selection can cause the spread of a new sex-determining gene linked to it. The mechanism can account for the origin of new sex-determining loci, the transposition of an ancestral sex-determining gene to an autosome, and the maintenance of multiple sex-determining factors in species that lack heteromorphic sex chromosomes.

Sexual selection at the protein level drives the extraordinary divergence of sex-related genes during sympatric speciation.

An increasing number of molecular studies are indicating that, in a wide variety of species, genes directly related to fertilization evolve at extraordinarily high rates. We try to gain insight into the dynamics of this rapid evolution and its underlying mechanisms by means of a simple theoretical model. In the model, sexual selection and sympatric speciation act together in order to drive rapid divergence of gamete recognition proteins. In this process, intraspecific competition for fertilizations enlarges male gamete protein variation by means of evolutionary branching, which initiates sympatric speciation. In addition, avoidance of competition for fertilizations between the incipient species drives the rapid evolution of gamete recognition proteins. This mechanism can account for both strong stabilizing selection on gamete recognition proteins within species and rapid divergence between species. Moreover, it can explain the empirical finding that the rate of divergence of fertilization genes is not constant, but highest between closely related species.

On the stall force for growing microtubules.

The assembly of microtubules generates forces that play a role in cellular motility processes such as the motion of chromosomes during mitosis. Recently, Mogilner and Oster proposed a model for the growth of microtubules that agrees quantitatively with the force-velocity relation measured for individual microtubules. In addition, the authors predicted that the stall force for any polymer consisting of N independently growing protofilaments should increase as the square root of N. We simulated this model and found that the stall force increases linearly with N, and is in fact consistent with the maximum force predicted by thermodynamic arguments. We show that this discrepancy can be explained by a more careful treatment of the "off-term" in the Mogilner-Oster model.