Biology subjects

Booth, S. C.

Publications and source records attributed to Booth, S. C..

4 recordsLinked to original sources

bioRxiv2026

Similar weapons play different roles in bacterial competition

Bacteria are aggressive organisms that inhibit and kill their competitors using a diverse range of molecular weapon systems. Surprisingly, strains commonly carry multiple similar weapons that appear to perform the same function. Here we investigate the evolutionary benefits of this apparent functional duplication using the heavily-armed opportunistic pathogen, Pseudomonas aeruginosa as a model species. We first use genomics to ask whether carrying multiple similar bacteriocins (S pyocins) increases the probability of inhibiting other strains. However, simply carrying a single uncommon S pyocin is typically as effective as carrying several. We then combine genome-editing with competition experiments to study the effects of S pyocins alone and in combinations. S pyocins sometimes function better together than alone, which helps to explain their co-carriage. However, we also find evidence of specialisation: pyocin S5 is much more effective than S2 in iron limited conditions, and vice-versa when iron is available. We test the generality of our findings using a second class of weapon carried by P. aeruginosa, contact-dependent inhibition, which again reveals differing effectiveness as conditions change. Our work shows how similar weapons are specialised for combat under different environmental conditions. We argue that functional specialisation is key to understanding why bacteria carry so many weapons.

microbiology↗

bioRxiv2023

Cell motility greatly empowers bacterial contact weapons

Many bacteria kill competitors using short-range weapons, such as the Type VI Secretion System (T6SS) and Contact Dependent Inhibition (CDI). While these can deliver powerful toxins, they rely on direct contact between attacker and target cells. We hypothesised that movement enables attackers to contact more targets and thus greatly empower their weapons. To explore this, we developed individual-based and continuum models to show that motility greatly improves contact-dependent toxin delivery through two underlying processes. First, genotypic mixing increases the inter-strain contact probability of attacker and sensitive cells. Second, target switching ensures attackers constantly attack new cells, instead of repeatedly hitting the same cell. We test our predictions with the pathogen Pseudomonas aeruginosa, using genetically engineered strains to study the interaction between CDI and twitching motility. As predicted, we find that motility massively improves the effectiveness of CDI, in some cases up to 10,000-fold. Moreover, we demonstrate that both mixing processes occur using timelapse single-cell microscopy and quantify their relative importance by combining experimental data with our models. Our work shows how bacteria combine cell movement with contact-based weapons to launch powerful attacks on their competitors.

microbiology↗

bioRxiv2022

Bows and swords: why bacteria carry short and long-range weapons

Bacteria possess a diverse range of mechanisms for inhibiting competitors, including bacteriocins, tailocins, the type VI secretion system, and contact-dependent inhibition. Why bacteria have evolved such a wide array of weapon systems remains a mystery. Here we develop an agent-based model to compare short-range weapons that require cell-cell contact, with long-range weapons that rely on diffusion. Our models predict that contact weapons are useful when an attacking strain is outnumbered, facilitating invasion and establishment. By contrast, ranged weapons tend to only be effective when attackers are abundant. We test our predictions with the opportunistic pathogen Pseudomonas aeruginosa, which naturally carries multiple weapons, including contact-dependent inhibition (CDI) and diffusing tailocins. As predicted, short-range CDI functions better at low frequency, while long-range tailocins require high frequency and cell density to function effectively. Head-to-head competitions between the two weapon types further support our predictions: a tailocin attacker only defeats CDI when it is numerically dominant, but then we find it can be devastating. Finally, we show that the two weapons work well together when one strain employs both. We conclude that short and long-range weapons serve different functions and allow bacteria to fight both as individuals and as a group.

microbiology↗

bioRxiv2021

Suicidal chemotaxis in bacteria

Bacteria commonly live in communities on surfaces where steep gradients of antibiotics and other chemical compounds routinely occur. While many species of bacteria can move on surfaces, we know surprisingly little about how such antibiotic gradients affect cell motility. Here we study the behaviour of the opportunistic pathogen Pseudomonas aeruginosa in stable spatial gradients of a range of antibiotics by tracking thousands of cells in microfluidic devices as they form biofilms. Unexpectedly, these experiments reveal that individual bacteria use pili-based ( twitching) motility to actively navigate towards regions with higher antibiotic concentrations. Our analyses suggest that this biased migration is driven, at least in part, by a direct response to the antibiotics. Migrating cells can reach antibiotic concentrations hundreds of times higher than their minimum inhibitory concentration in a few hours and remain highly motile. However, isolating these cells - using fluid-walled microfluidic devices that can be reconfigured in situ - suggests that these bacteria are terminal and not able to reproduce. In spite of moving towards their death, we show that migrating cells are capable of entering a suicidal program to release bacteriocins that are used to kill other bacteria. Our work suggests that bacteria respond to antibiotics as if they come from a competing colony growing in the neighbourhood, inducing them to invade and attack. As a result, clinical antibiotics have the potential to serve as a bait that lures bacteria to their death.

microbiology↗