Researchers seek to make cavity-causing bacteria sel...(questions that the team will be seeking ...),Health

To help answer these questions, Quiveys team has genetically engineered the first and only mutant form of S. mutans with the FabM gene removed.

This FabM knockdown mutant is a living model that shows the exact impact of the enzyme in live bacteria. Without FabM, the mutant fills its outer membrane with other, smaller fatty acids that are much less acid resistant than those normally created via FabM, but that still provide some protection from acid. Thus, a goal is to design a treatment that would prevent S. mutans from forming both straight chain and smaller chain fatty acids.

As Quivey and others design next-generation antibacterial drugs, they are looking not just for a single way to stop the action of a single disease-causing enzyme, but how to shut down its three or four back-up systems. The process of cutting off genetic escape routes for bacteria applies to every trait central to the ability of the bacteria to survive and cause disease. Beyond acid durability, the team will also look at the genes and proteins that enable S. mutans to stick to teeth enamel like no other, which it does by producing a sugary polymer (plaque). Tooth decay is the result of plaque combined with acid.

Quiveys partners in the grant application were Elizabeth Grayhack, Ph.D., research associate professor of Biochemistry and Biophysics, Robert Marquis, Ph.D., professor of Microbiology and Immunology, and Eric Phizicky, Ph.D., professor of Biochemistry and Biophysics. The grant application succeeded with the NIH, Quivey said, because the team and proposal combined many years of experience in genomic projects (Grayhack and Phizicky) with extensive microbial experience (Marquis and Quivey).

As part of the grant, Grayhack and Phizicky will cr
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