The ability of Streptococcus mutans (S. mutans) to survive in acid is one reason that the species is the main driver of tooth decay worldwide.
Past research has shown that this ability has several components including a bacterial enzyme called fatty acid biosynthase M (FabM), which when shut down,
makes S. mutans almost precisely 10,000 times more vulnerable to acid damage.
Our first goal is to force the major bacterium behind tooth decay to
destroy itself with its own acid as soon as it eats sugar,
said Robert G. Quivey, Ph.D.,
professor of Microbiology & Immunology at the University of Rochester Medical Center and principal investigator for the grant. After that, this line of work
could help lead to new anti-bacterial combination therapies for many infections that have become resistant to antibiotics.
Quivey's partners in the grant application were
Elizabeth Grayhack, Ph.D., research associate professor of Biochemistry & Biophysics,
Robert Marquis, Ph.D., professor of Microbiology & Immunology, and Eric Phizicky, Ph.D., professor of Biochemistry & Biophysics.