Abstract
Over millions of years of evolution, bacteria have developed complex strategies for intra-and interspecies interactions and competition for ecological niches and resources. Contact-dependent growth inhibition systems (CDI) are designed to realize a direct physical contact of one bacterial cell with other cells in proximity via receptor-mediated toxin delivery. These systems are found in many microorganisms including clinically important human pathogens. The main purpose of these systems is to provide competitive advantages for the growth of the population. In addition, non-competitive roles for CDI toxin delivery systems including interbacterial signal transduction and mediators of bacterial collaboration have been suggested. In this review, our goal was to systematize the recent findings on the structure, mechanisms, and purpose of CDI systems in bacterial populations and discuss the potential biological and evolutionary impact of CDI-mediated interbacterial competition and/or cooperation.
Highlights
IntroductionThe inhabitants of the microworld (including bacteria) prefer to form mono-species or more complex multi-species communities
Like most living organisms, the inhabitants of the microworld prefer to form mono-species or more complex multi-species communities
One of the ways a bacterial cell can adapt to its environment is the production of effector molecules (“toxins”), some of which are designed to interact with the host cells, while others are aimed at regulating relationships with other inhabitants of the microbiome
Summary
The inhabitants of the microworld (including bacteria) prefer to form mono-species or more complex multi-species communities. One of the ways a bacterial cell can adapt to its environment is the production of effector molecules (“toxins”), some of which are designed to interact with the host cells, while others are aimed at regulating relationships with other inhabitants of the microbiome These effector molecules, usually proteins, are exported from the cell to the environment, where they diffuse freely until meeting a target cell that is both sensitive to them and has a suitable receptor on its surface. When the outer sheath, which plays the role of a kind of piston, contracts, the “needle” is pushed out, puncturing the membrane of a neighboring cell and releasing toxic effectors into its cytoplasm This mechanism is found in about a quarter of all bacterial species and is described in detail in several excellent reviews [17–20]. We provide an overview of what is currently known about the molecular mechanism and the biological role of CDI mediated competition and cooperation in bacterial species
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