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Balancing Offense and Defense in Oral Biofilm

In the oral biofilm, the polymicrobial communities that inhabit our mouths, oral microbes benefit greatly from their strength in numbers. But as space grows tighter and the benefits of symbiosis become stressed, certain bacteria shoot noxious biochemicals called bacteriocins into the channel-like extracellular spaces to stop the growth of their competitors. Those that receive this biochemical attack shift into defensive mode. They take up pieces of free-floating DNA in the biofilm, a biological process called competence, and use the extra base pairs to repair the damage from a well-timed bacteriocin and, hopefully for them, just keep going.
A few years ago, a team of National Institute of Dental and Craniofacial Research (NIDCR)-supported researchers who study the oral bacterium Streptococcus mutans had an idea that was already mildly suggested in the scientific literature. They hypothesized that as a biofilm reaches a critical mass on a tooth surface, S mutans likely clicks on a specialized network of genes that regulate the production of bacteriocins. If the scientists could piece together the network, they could assemble a list of possible molecular targets to inhibit a behavior that this leading cause of tooth decay needs to survive. Their hunch led to the discovery of a 2-gene operon that they named hdrRM. An operon is a cluster of genes controlled by a single regulatory signal and which coordinates their expression for a specific cellular response. The researchers published 3 papers on hdrRM, establishing that its coordinated response involved bacteriocin production to some extent but primarily regulated competence. Then, while studying the global changes in gene expression that hdrRM activation induces in S mutans, the researchers stumbled onto an interesting find.
As reported in the December 2010 issue of Molecular Microbiology, the research group discovered another completely novel 2-gene operon. They named it brsRM, and it acts as a complementary mirror image of hdrRM. That is, when one operon is active, the other will click on too. But unlike its partner, brsRM has only modest regulatory control over the competence system. Its regulatory role is tilted heavily toward bacteriocin production. Although each operon seems to coregulate the other, ie, shifting from an offensive (bacteriocin) to a defensive mode (competence), the scientists found that if the 2 systems are fully activated simultaneously, the combination is lethal to S mutans. The scientists are now attempting to work out how the operons work and interact.

(Source: NIDCR, Science News in Brief, January 28, 2011)


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