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Sean C Booth

Publications and source records attributed to Sean C Booth.

2 recordsLinked to original sources

Implications of proteome allocation constraints for understanding interbacterial antagonism.

Bacteria live in dense communities where competition influences the composition and, therefore, the function of these communities. Beyond competing for resources, bacteria engage in antagonism by deploying a range of molecular weapon systems to inhibit and kill other bacteria. Investing in antagonism is expected to incur a fitness trade-off, but the nature of this trade-off at the level of molecular physiology remains underexplained. Applying recent advances about the physiological constraints faced by bacterial cells may help us better understand existing studies and design new investigations into interbacterial antagonism. Bacterial cells face two important constraints: a finite amount of protein and a maximum translation speed for ribosomes. As a result, the only way for a cell to grow faster is to allocate more of its finite proteome to synthesizing ribosomes. A cell choosing to attack competitors must therefore allocate some of its limited proteome budget to antagonistic proteins instead of other functions. Conversely, being attacked and resisting the effects of such attacks also require an investment of proteomic resources. The extent to which proteome allocation constraints influence bacterial physiology is not fully understood; consequently, how these constraints influence interbacterial antagonism has not been investigated. Here, I will discuss how proteome allocation constraints can re-contextualize our existing understanding of the costs of both deploying and resisting attacks and how investigation of these constraints may further our understanding of interbacterial antagonism.

Proteome

Role of AprA and pyocyanin from Pseudomonas aeruginosa on Staphylococcus aureus tolerance to silver.

The opportunistic pathogens Staphylococcus aureus and Pseudomonas aeruginosa are often found together causing persistent infections where they exhibit complex interactions that affect their virulence and resistance to treatment. We sought to clarify how interactions between these organisms affect their resistance to the antimicrobial metal silver (AgNO3). As previous work showed that cell-free supernatant from P. aeruginosa enhances the resistance of S. aureus, we aimed to identify the exact factor(s) responsible for this increase. Using molecular weight cutoff filters and proteomics, we identified the protein AprA and pyocyanin as the responsible factors. Transposon-mediated disruption of aprA led to the production of supernatant which could not enhance the silver tolerance of S. aureus. These findings suggest that the protease AprA from P. aeruginosa plays an important role in increasing the tolerance of S. aureus to AgNO3 via in part by mediating the levels of pyocyanin which in turn reduces Ag2+ to detoxify it.

Pseudomonas aeruginosa