Et Tu, E. Coli? MCDB scientists uncover a new way that bacteria lay siege to neighboring cells by hijacking two factors involved in protein synthesis
So they can’t use smartphones or WiFi, but bacteria have evolved some seriously complex strategies to communicate with one another. And the resulting interactions are a delicate balance of cooperation and, in some cases, competition. These intraspecies exchanges take place within contact-dependent growth inhibition (CDI) systems, which regulate cellular activities via cell-to-cell contact and are found in a wide variety of gram-negative bacteria, including important human pathogens such as Escherichia coli. New research by MCDB scientists examines how a particular pathogenic strain of E. coli — EC869, which causes diarrhea or hemorrhagic colitis in humans — destroys its neighbors by transferring toxins that inhibit their cell growth. Previous work by other UCSB researchers had shown that a different variation of E. coli required a “permissive factor” for toxin activation. The authors of the new paper, which appears in the Proceedings of the National Academy of Sciences, wondered whether EC869 also needed to bind protein in the target cell to activate its toxin. The answer is yes, with a twist.