AUXIN BINDING PROTEIN1: the outsider

AUXIN BINDING PROTEIN1 (ABP1) is one of the first characterized proteins that bind auxin and has been implied as a receptor for a number of auxin responses. Early studies characterized its auxin binding properties and focused on rapid electrophysiological and cell expansion responses, while subsequent work indicated a role in cell cycle and cell division control. Very recently, ABP1 has been ascribed a role in modulating endocytic events at the plasma membrane and RHO OF PLANTS-mediated cytoskeletal rearrangements during asymmetric cell expansion. The exact molecular function of ABP1 is still unresolved, but its main activity apparently lies in influencing events at the plasma membrane. This review aims to connect the novel findings with the more classical literature on ABP1 and to point out the many open questions that still separate us from a comprehensive model of ABP1 action, almost 40 years after the first reports of its existence.     

Constraints on polyploid evolution: a test of the minority cytotype exclusion principle

Polyploid evolution is often considered a mechanism of instant speciation; yet the establishment of rare tetraploids within diploid populations may be constrained by a frequency-dependent mating disadvantage (minority cytotype exclusion principle). I tested this hypothesis using experimental populations of Chamerion angustifolium (Onagraceae) that contained different proportions of tetraploids and diploids. Fitness, measured as total seed production over the entire flowering season, was calculated from a census of flower number and estimates of ovule number per flower and proportion of seed set per fruit. The fitness of tetraploids relative to diploids was frequency dependent, increasing from 0.4, when tetraploids were rare, to 0.7 when at 50% and 1.15 when they were in the majority (67%). This pattern exists because of a negative relationship between tetraploid frequency and seed set per fruit in diploids. Seed set in tetraploids was independent of cytotype frequency. The frequency-independent effect in tetraploids reflects higher assortative mating, partly because of non-random patterns of bee visitation. Bees visited a disproportionately high number of diploid inflorescences; however, the proportion of successive flights between tetraploids increased above random expectations as the frequency of tetraploids decreased. These results provide the first experimental test of frequency-dependent fitness in diploid-polyploid mixtures and suggest an important role for more gradual, population processes governing the evolution of polyploidy in natural populations.     

Resistance evolution can disrupt antibiotic exposure protection through competitive exclusion of the protective species

Antibiotic degrading bacteria can reduce the efficacy of drug treatments by providing antibiotic exposure protection to pathogens. While this has been demonstrated at the ecological timescale, it is unclear how exposure protection might alter and be affected by pathogen antibiotic resistance evolution. Here, we utilised a two-species model cystic fibrosis (CF) community where we evolved the bacterial pathogen Pseudomonas aeruginosa in a range of imipenem concentrations in the absence or presence of Stenotrophomonas maltophilia, which can detoxify the environment by hydrolysing β-lactam antibiotics. We found that P. aeruginosa quickly evolved resistance to imipenem via parallel loss of function mutations in the oprD porin gene. While the level of resistance did not differ between mono- and co-culture treatments, the presence of S. maltophilia increased the rate of imipenem resistance evolution in the four μg/ml imipenem concentration. Unexpectedly, imipenem resistance evolution coincided with the extinction of S. maltophilia due to increased production of pyocyanin, which was cytotoxic to S. maltophilia. Together, our results show that pathogen resistance evolution can disrupt antibiotic exposure protection due to competitive exclusion of the protective species. Such eco-evolutionary feedbacks may help explain changes in the relative abundance of bacterial species within CF communities despite intrinsic resistance to anti-pseudomonal drugs.Subject terms: Microbial ecology, Microbial communities, Antibiotics, Bacterial genetics, Evolution     

The evolution of concerted evolution

Concerted evolution is a consequence of processes that convert copies of a gene in a multigene family into the same copy. Here we ask whether this homogenization may be adaptive. Analysis of a modifier of homogenization reveals (1) that the trait is most likely to spread if interactions between deleterious mutations are not strongly synergistic; (2) that selection on the modifier is of the order of the mutation rate, hence the modifier is most likely to be favoured by selection when the species has a large effective population size and/or if the modifier affects many genes simultaneously; and (3) that linkage between the genes in the family, and between these genes and the modifier, makes invasion of the modifier easier, suggesting that selection may favour multigene families being in clustered arrays. It follows from the first conclusion that genes for which mutations may often be dominant or semi-dominant should undergo concerted evolution more commonly than others. By analysis of the mouse knockout database, we show that mutations affecting growth-related genes are more commonly associated with dominant lethality than expected by chance. We predict then that selection will favour homogenization of such genes, and possibly others that are significantly dosage dependent, more often than it favours homogenization in other genes. The first condition is almost the opposite of that required for the maintenance of sexual reproduction according to the mutation-deterministic theory. The analysis here therefore suggests that sexual organisms can simultaneously minimize both the effects of deleterious, strongly synergistically, interacting mutations and those that interact either weakly synergistically, multiplicatively, or antagonistically, assuming the latter class belong to a multicopy gene family. Recombination and an absence of homogenization are efficient in purging deleterious mutations in the former class, homogenization and an absence of recombination are efficient at minimizing the costs imposed by the latter classes.     

The evolution of cultural evolution

Humans are unique in their range of environments and in the nature and diversity of their behavioral adaptations. While a variety of local genetic adaptations exist within our species, it seems certain that the same basic genetic endowment produces arctic foraging, tropical horticulture, and desert pastoralism, a constellation that represents a greater range of subsistence behavior than the rest of the Primate Order combined. The behavioral adaptations that explain the immense success of our species are cultural in the sense that they are transmitted among individuals by social learning and have accumulated over generations. Understanding how and when such culturally evolved adaptations arise requires understanding of both the evolution of the psychological mechanisms that underlie human social learning and the evolutionary (population) dynamics of cultural systems.     

The lingering enigma of the allelic exclusion mechanism

B lymphocytes produce diverse antibody specificities by "randomly" assembling antibody genes from germline segments. Yet, though each B lymphocyte has multiple allelic loci for the different antibody chains, each clonally derived mature B lymphocyte expresses a single species of antibody with a unique specificity via a process termed allelic exclusion. Despite some progress, the precise mechanism of allelic exclusion remains an enigma.     

The present status of the competitive exclusion principle

Since Darwin accepted the Malthusian population theory to solve the demographic problems he thought to be logically connected with the universal operation of natural selection, the numerical processes in both populations and communities were generally supposed to be governed by competition. For interspecific relations this found expression in the 'competitive exclusion principle'. After it was shown that coexistence rather than exclusion of closely related species is the rule, this principle gradually changed into the 'competitive niche shift principle'. Recently the universality of competition has been increasingly questioned, so that other interspecific relationships (especially predation) are revaluated as possibly governing many natural population and inter-population processes.     

The mechanism of proton exclusion in aquaporin channels

The mechanism of proton exclusion in aquaporin channels is elucidated through free energy calculations of the pathway of proton transport. The second generation multistate empirical valence bond (MS-EVB2) model was applied to simulate the interaction of an excess proton with the channel environment. Jarzynski's equality was employed for rapid convergence of the free energy profile. A barrier sufficiently high to block proton transport is located near the channel center at the NPA motif-a site involved in bi-orientational ordering of the embedded water-wire in absence of the excess proton. A second and lower barrier is observed at the selectivity filter near the periplasmic outlet where the channel is narrowest. This secondary barrier may be essential in filtering other large solutes and cations.     

The impact of exclusion processes on angiogenesis models

Angiogenesis is the process by which new blood vessels form from existing vessels. During angiogenesis, tip cells migrate via diffusion and chemotaxis, new tip cells are introduced through branching, loops form via tip-to-tip and tip-to-sprout anastomosis, and a vessel network forms as endothelial cells, known as stalk cells, follow the paths of tip cells (a process known as the snail-trail). Using a mean-field approximation, we systematically derive one-dimensional non-linear continuum models from a lattice-based cellular automaton model of angiogenesis in the corneal assay, explicitly accounting for cell volume. We compare our continuum models and a well-known phenomenological snail-trail model that is linear in the diffusive, chemotactic and branching terms, with averaged cellular automaton simulation results to distinguish macroscale volume exclusion effects and determine whether linear models can capture them. We conclude that, in general, both linear and non-linear models can be used at low cell densities when single or multi-species exclusion effects are negligible at the macroscale. When cell densities increase, our non-linear model should be used to capture non-linear tip cell behavior that occurs when single-species exclusion effects are pronounced, and alternative models should be derived for non-negligible multi-species exclusion effects.

     

Analytical exclusion chromatography

This review summarizes the development of exclusion chromatography, also termed gel filtration, molecular-sieve chromatography and gel permeation chromatography, for the quantitative characterization of solutes and solute interactions. As well as affording a means of determining molecular mass and molecular mass distribution, the technique offers a convenient way of characterizing solute self-association and solute-ligand interactions in terms of reaction stoichiometry and equilibrium constant. The availability of molecular-sieve media with different selective porosities ensures that very little restriction is imposed on the size of solute amenable to study. Furthermore, access to a diverse array of assay procedures for monitoring the column eluate endows analytical exclusion chromatography with far greater flexibility than other techniques from the viewpoint of solute concentration range that can be examined. In addition to its widely recognized prowess as a means of solute separation and purification, exclusion chromatography thus also possesses considerable potential for investigating the functional roles of the purified solutes.