An
international research collaboration has discovered a new bacteria-killing
toxin that shows promise of impacting superbug infectious diseases.
The
discovery of this growth-inhibiting toxin, which bacteria inject into rival
bacteria to gain a competitive advantage is the result of teamwork by co-senior
authors John Whitney, assistant professor of the Department of Biochemistry and
Biomedical Sciences at McMaster University, and Mike Laub, professor of biology
at the Massachusetts Institute of Technology (MIT).
Whitney
and his PhD student Shehryar Ahmad at McMaster's Michael G. DeGroote Institute
for Infectious Disease Research were studying how bacteria secrete
antibacterial molecules when they came across a new toxin. This toxin was an
antibacterial enzyme, one the researchers had never seen before.
After determining
the molecular structure of this toxin, Whitney and Ahmad realized that it
resembles enzymes that synthesize a well-known bacterial signalling molecule
called (p)ppGpp. This molecule normally helps bacteria survive under stressful
conditions, such as exposure to antibiotics.
Boyuan
Wang, a postdoctoral researcher in the Laub lab who specializes in (p)ppGpp
signaling, examined the activity of the newly discovered enzyme. He soon
realized that rather than making (p)ppGpp, this enzyme instead produced a
poorly understood but related molecule called (p)ppApp. Somehow, the production
of (p)ppApp was harmful to bacteria.
The
researchers determined that the rapid production of (p)ppApp by this enzyme
toxin depletes cells of a molecule called ATP. ATP is often referred to as the
'energy currency of the cell' so when the supply of ATP is exhausted, essential
cellular processes are compromised and the bacteria die.
"I
find it absolutely fascinating that evolution has essentially
"repurposed" an enzyme that normally helps bacteria survive
antibiotic treatment and, instead, has deployed it for use as an antibacterial
weapon," said Whitney.
The
research conducted at McMaster University was funded by the Canadian Institutes
for Health Research and is affiliated with the CIHR Institute for Infection and
Immunity (CIHR-III) hosted at McMaster University with additional funding from
the David Braley Centre for Antibiotic Discovery. The research at MIT was
supported by the Howard Hughes Medical Institute and the U.S. National
Institutes of Health.
See:
Posted by Dr. Tim Sandle, Pharmaceutical Microbiology Resources (http://www.pharmamicroresources.com/)
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