The Daily Bulletin Archive

Please join the Biology Department for the seminar "Bacterial Pathogens: Bacterial Diseases as a Response to Protist Predation," presented by Gerald B. Koudelka, Ph.D., professor and chair of the Department of Biological Sciences at the University at Buffalo, on Monday, November 10, from 3:30 to 4:30 p.m. in Technology Building 160.

All faculty, staff, and students are welcome.

Seminar Abstract
With approximately 10³¹ individuals, bacteriophages (bacterial viruses) are likely the most abundant organism on the planet. Bacteriophages often bear genes encoding exotoxins (e.g., Shiga toxin, diphtheria toxin, cholera toxin, and botulinum toxin), which cause disease in mammals. While these phage-encoded toxins harm mammals, these phages can be prevalent where mammals are not found. Predation by phagocytic predators is a major source of bacterial mortality, a possible explanation for the prevalence of exotoxin-encoding phage and bacteria; i.e., exotoxins are antipredator defense molecules.

Phagocytic protozoan bacterial predators have "prey detection" mechanisms that are similar to those of mammalian phagocytes. Therefore, the evolution and refinement of anti-protozoan strategies apparently selects for traits that also allow bacteria to ward off attack by human phagocytes, meaning the bacterial response to predation is an important driving force in pathogen evolution. Thus, humans may not be the original nor primary "targets" of exotoxins. Moreover, while exotoxins allow bacteria to ward off attack by human phagocytes, humans may be just innocent bystanders in the ongoing evolutionary arms race between bacterivorous protozoan predators and their bacterial prey.

I will discuss our evidence indicating the phage-encoded exotoxins evolved as a bacterial anti-predator defense strategy. I will also describe our work that has uncovered uncanny similarities between the molecular mechanisms of prey recognition by protists and phagocytic mammalian cells, along with novel aspects of how the exotoxins enter the predator and how bacteria and toxin-encoding phage may be evolving together to better target humans.