Bacteria destroy themselves to ... survive

Like firefighters fighting the fire, researchers at the University of Illinois and the University of Massachusetts at Amherst have discovered a way to trick the evolutionary mechanism of bacteria into self-programming 'death'.

Gerard Wong, professor of materials science and biotechnology at U. of I, said: 'The basic idea is that an antimicrobial drug targets a place for bacteria, if desired. against, need to kill yourself through a suicide mutation '.

Wong is the author of the article published in the Proceedings of the National Academy of Sciences. This article will be posted on the magazine's website this week.

The researchers showed that a synthetic antimicrobial drug was based on the presence of phosphoethanolamine, a negative gram-negative conical lipid in the bacterial membrane.Although PE lipids are instructed to kill bacteria, but not having this kind of lipids, bacteria cannot survive.

Wong said: 'It's Catch-22. Some variations of bacteria can be ignored, and others are not to be missed. In this case, the bacteria must undergo a mutation that will destroy itself, against the anti-microbial drugs'.

Picture 1 of Bacteria destroy themselves to ... survive Researcher Gerard Wong has led the research team to find ways to trick bacteria's evolutionary mechanism into self-programming death. (Photo: Brian Stauffer) In the study, scientists compared the survivability of Escherichia coli with a mutation of E. coli lacking PE lipid in its membrane. The type of mutant bacteria lacking in fragile PE has a higher survival rate than the normal healthy bacteria when exposed to this new synthetic anti-bacterial drug.

However, the opposite happens when both of the above bacteria are exposed to tobramycin, a common metabolic antibiotic that attacks the bacterial ribosomal structure.

The researchers reported on compounds that functioned as 'punched' molecules last year in the American Chemical Society. Their latest research sheds light on this mechanism.

"This new antimicrobial drug recycles PE lipids into holes in the bacterial membrane," said Wong, a researcher at Beckman Academy. The ruptured membrane is the cause of killing bacteria '.

Finding new therapies for pathogens that are most resistant to antibiotics is a very important issue in the future. Wong said: 'Now that we understand the behavior of' perforated 'molecules, we can look for similar methods to create anti-microbial drugs that bacteria cannot evolve to become. Should be immune '.

In addition to Wong, co-authors include graduate student at U. of I Lihua Yang, Dallas professor of materials science R. Trinkle, microbiology professor John E. Cronan Jr., and polymer science professor. at Massachusetts University Gregory N. Tew.

The research was funded by the National Science Foundation, the National Institutes of Health and the Naval Research Office.