Evolution of microbial pathogenicity as a consequence of predator-prey interactions
Arnold, Jason W.
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Human pathogens often encode factors that target specific highly conserved pathways common to all eukaryotes. The arms race between predator and prey select for bacteria that avoid predation either by killing predators, or by evading consumption. Bacterially encoded exotoxins are a common cause of human diseases, however we show here that these toxins likely arose as a result of predator-prey interactions. We show that toxins such as STX2 are efficient anti-predator defense molecules, and likely arose to kill predators, not humans. Additionally, our work explores the interactions between our model prey ( E. coli O157:H7) and our model predator ( Acanthamoeba castellanii ) that select for factors which result in disease in humans. The interaction between Acanthamoeba mannose binding protein (aMBP) and lipopolysaccharides allows for recognition of bacterial prey, and consequently selects for individuals within bacterial populations that are unable to be recognized by the predator. Consequently, aMBP has function which is highly similar to the function of mammalian macrophage mannose binding proteins, allowing for evolution of bacteria able to evade mammalian innate immune system as a direct consequence of predation by Acanthamoeba . By better understanding the predator-prey interactions within microbial communities, we can better understand the evolution of emerging microbial pathogens.