Evolved resistance against the type 6 secretion system is toxin specific
Smith, W. P. J.; Tejada-Arranz, A.; Tank, R. K. G.; Basler, M.; Brockhurst, M. A.
Show abstract
Across ecosystems, microbes face attacks by competitors armed with lethal weapons, including toxin-injecting Type 6 Secretion Systems (T6SSs). This in turn selects for T6SS resistance, reducing the future effectiveness of T6SS weaponry in competition. However, we have only a limited understanding of how resistance to T6SS attacks evolves de novo. A key challenge is that T6SS-armed bacteria are highly diverse in the number and type of toxins they inject, spanning multiple distinct modes of action. Do functionally distinct T6SS toxins select for different mechanisms of resistance? To address this, we combine genomics, resistance assays and fluorescence microscopy, to characterise evolved resistances against common T6SS toxin classes across spatial scales. We discovered that amidase and lipase toxins select for mutations in distinct sets of genes, resulting in toxin-specific resistance phenotypes and fitness costs. We also discovered resistance trade-offs: lipase-evolved E. coli became less vulnerable to lipase membrane damage, at the cost of increased susceptibility to lysis by amidase toxins. Finally, using single-gene knockout mutants from the Keio collection we confirmed that specific genes not previously linked to T6SS resistance, including inner membrane transporters, osmo-sensing systems and stress response pathways, conferred resistance to specific toxins while generating sensitivity to others. The specificity of resistance, and associated trade-offs observed, are likely to constrain de novo evolution of resistance against T6SS attackers armed with multiple functionally distinct toxins, helping to explain why T6SS systems are so widespread in nature.
Matching journals
The top 4 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- Antibiotic hypersensitivity signatures identify targets for attack in the Acinetobacter baumannii cell envelope 97%
- Necrosignaling: Cell death triggers antibiotic survival pathways in bacterial swarms 97%
- Bacteria evolve macroscopic multicellularity via the canalization of phenotypically plastic cell clustering 96%
Similar papers in this journal
- Competition between phage-resistance mechanisms determines the outcome of bacterial co-existence 97%
- Treatment history shapes the evolution of complex carbapenem-resistant phenotypes in Klebsiella spp. 96%
- Amoxicillin-resistant Streptococcus pneumoniae can be resensitized by targeting the mevalonate pathway as indicated by sCRilecs-seq 96%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.