Researchers at McMaster University have discovered a previously unknown bacteria-killing toxin that could pave the way for a new generation of antibiotics.
The study, led by John Whitney at the Michael G. DeGroote Institute for Infectious Disease Research, shows that the bacterial pathogen Pseudomonas aeruginosaknown to cause nosocomial infections such as pneumonia, secretes a toxin that has evolved to kill other species of bacteria.
For Whitney, the key aspect of his discovery is not just that this toxin kills bacteria, but how it does it.
“This research is important because it shows that the toxin targets essential RNA molecules from other bacteria, effectively rendering them non-functional,” said Whitney, an associate professor in the Department of Biochemistry and Biomedical Sciences.
“Like humans, bacteria need properly functioning RNA to live.”
“It’s an all-out assault on the cell because of the number of essential pathways that depend on functional RNAs,” said study first author Nathan Bullen, a graduate student in McMaster’s Department of Biochemistry and Biomedical Sciences.
“This toxin penetrates its target, hijacks an essential molecule needed for life, and then uses that molecule to disrupt normal processes.”
Whitney and Bullen, together with colleagues from Imperial College London and the University of Manitoba, studied this toxin for almost three years to understand exactly how it works at the molecular level.
The breakthrough, published in molecular cellwas made by Bullen following rigorous experimentation on common toxin targets, such as proteins and DNA molecules, before finally testing the toxin against RNA.
This finding breaks well-established precedents set by toxins targeting proteins secreted by other bacteria, such as those that cause cholera and diphtheria.
The researchers say this development holds great potential for future research that could eventually lead to new innovations that fight infection-causing bacteria.
Whitney says the newly discovered vulnerability can be exploited for future antibiotic development.