Abstracts (coauthor)


Signal blind mutants are naturally occurring bacterial strains that are defective for cell to cell signalling. These mutants can produce signal but do not respond to it, so they have reduced expression of quorum sensing regulated genes. Public goods are often regulated by quorum sensing and so signal blind mutants act as defectors, exploiting signal competent co-operators. Critically, signal blind strains are unable to increase their signal output in line with co-operators, because signal production is increased in response to signal, via a positive feedback loop. Therefore signal concentration in the environment is expected to be reduced when signal blind defectors are common. When public goods are regulated by quorum sensing, lower signal concentrations may reduce the production of public goods, minimising exploitation. Using knock-out strains of Pseudomonas aeruginosa we demonstrate that signal in the environment decreases as signal competent co-operators become rare. We show that this translates to a reduced co-operator output of secreted protease. Using competition experiments we then demonstrate that this can lead to negative frequency dependence of co-operator fitness, because co-operators behave as phenotypic defectors when rare. Frequency dependence has important implications as socio-microbiology is applied to new fields, notably the emergence of drug resistance.


The majority of emergent human pathogens are zoonotic in origin. Understanding the factors underlying the evolution of pathogen host range is therefore of critical importance in protecting human health. Classical evolutionary theory predicts that the evolution of generalism in pathogens will be subject to trade-offs, and hence reduced within-host fitness compared to specialists, as pathogens evolve to tolerate multiple host environments. Here we show that rather than passively reacting to host environments, bacteria can use niche construction via cooperative secretions to achieve host generalism. We use an epidemiological framework to show that cooperative niche construction strategies can outcompete both specialists and classical generalists under a wide range of realistic conditions. We then use a phylogenetic comparative analysis of 191 bacterial pathogens to show that larger secretome sizes are associated with a greater probability of zoonosis, in agreement with our theoretical predictions. Our results suggest that cooperative behaviour is a key factor in the evolution of generalism in bacteria, and that monitoring programmes focusing on the horizontal transfer of secreted proteins could help identify future emerging human pathogens.


Polymicrobial communities usually form surface-attached and spatially structured consortia such as biofilms. These communities display a broad range of metabolic interactions, thereby setting the stage for the emergence of diverse ecological outcomes, spanning competition, exploitation, or mutualism. Our understanding, however, of how the mechanistic nature of interspecific interaction shapes spatial structure within these communities is still limited. Using an individual-based model of a two-species community growing on a surface and where resources are traded for detoxification, we explore the relationship between mechanism of interspecific interaction and emergence of spatial structure within the community. We show that both abiotic and biotic factors can affect the spatial organization of species within these polymicrobial communities, and in a manner that reflects the balance between the costs (interspecific competition) and benefits (need for help) of association. Understanding the mechanisms that shape the emergence of spatial structuring within multi-species communities may provide new insights into how to maintain beneficial polymicrobial communities (e.g. microbiota) and combat polymicrobial infections.


Many bacterial exoproducts yield population-level benefits. Such ‘public goods’ (PG) include key virulence factors, and therapies designed to block their production are attracting increasing attention nowadays. The disruption of cell-to-cell communication (quorum sensing, QS), is considered especially promising because it could block production of multiple exoproducts, yet should prompt weaker selection for resistance than conventional antimicrobials. However, initial enthusiasm for this approach (‘quorum quenching’, QQ) has been tempered by claims that resistance in fact evolves readily, for example by improving pumps to eject QQ compounds from cells. Here, we focus on a different strategy, in which PGs (siderophores) are quenched outside producer cells. We show that adding gallium (Ga) to iron-limited Pseudomonas aeruginosa cultures suppresses growth in a dose-dependent manner by (a) deactivating siderophores and thereby choking the supply of iron, and (b) inducing costly production of further siderophores. In experimental infections of moth larvae (Galleria mellonella), Ga suppressed bacterial growth and extended larval survival. Crucially, moderate levels of Ga reduced virulence below those of infections with siderophore-defective mutant strains, which suggests that Ga also induces siderophore overproduction in vivo, imposing extra metabolic burden on bacteria without generating benefits. We argue that strategies that quenching secreted PGs extracellularly should be more effective than those that inhibit synthesis in the cell, since PG production costs remain or even increase. With Ga-mediated PG-quenching, resistance is particularly unlikely to evolve because (a) extracellular quenching is impervious to typical within-cell resistance traits; (b) avoiding siderophore production is maladaptive (non-producing ‘cheats’ could not spread in our experiments); and (c) evolving siderophores with reduced susceptibility to Ga appears to be biochemically unfeasible.


Chairman: Octávio S. Paulo
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XIV Congress of the European Society for Evolutionary Biology

Organization Team
Department of Animal Biology (DBA)
Faculty of Sciences of the University of Lisbon
P-1749-016 Lisbon


Computational Biology & Population Genomics Group