In the study, the researchers also were able to dramatically weaken Staph infections in mice who had large abscesses on their backs caused by the bacteria. The researchers knew they could inhibit virulence. What they didn't know was if these molecules, which have the ability to switch virulence off or on, were doing it to the same class of receptor on the surface of the bacterium. During his medical training, he learned about the pharmacology of drug action and became interested in the process of drug discovery. Lyon worked alternately between Muir's lab and Novick's lab at NYU for a year and a half, learning about the microbiology and genetics of Staphylococcus aureus and the techniques of the new field of chemical biology.
Bacteria use a two-component signaling system to communicate with each other and the outside world.
Initial genetic experiments allowed the researchers to conclude that AgrC was the probable target of both activation and inhibition of the virulence response. There are four different specificity groups of Staphylococcus aureus defined by which type of peptide they produce. A group 1 strain of Staph responds to an extracellular group 1 peptide, and group 2 strain normally is activated by a group 2 peptide. Lyon took the group 1 receptor, AgrC, and the minimal components required for signal transduction in Staph, and put them into a group 1 strain from which he had deleted all of these components, in effect replacing all the components in that strain with group 1 specificity. This strain now responded to group 1 peptide and was inhibited by group 2 peptide.