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Balancing Offense and Defense

January 28, 2011

Deferred antagonism assayThe Museum of Modern Art in New York City launched an exhibit two years ago featuring the Lewis Carroll-meets-Gary Larson drawings of the popular Hollywood director Tim Burton.  As ticketholders moved from frame to frame and wall to wall, a recurring artistic theme was strength in numbers.  Burton often lumped oddly shaped life forms, like herds of buffalo, to make the larger point that the whole of a community is greater than the individual parts. 

Ironically, this point was easily lost on the daily afternoon mass of humanity that mobbed the Burton exhibit. One could stand off to the side and watch the initial bemusement of ticketholders morph within minutes into red-cheeked irritation and lead-with-your-elbows discomfort at the constant jostling for space.  For those on the receiving end of the elbows, they shifted into defensive mode. They absorbed the nudges and learned just to keep going.

The same phenomenon occurs 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 lead with their elbows.  In this case, shooting noxious biochemicals called bacteriocins into the channel-like extracellular spaces to stop the growth of its competitors.  Those that receive the biochemical elbows 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 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 two-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 three 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 issue of the journal Molecular Microbiology, the group discovered another completely novel two-gene operon.  They call their find the brsRM operon, 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, i.e., shifting from an offensive (bacteriocin) to a defensive mode (competence), the scientists found that if the two systems are fully activated simultaneously, the combination is lethal to S. mutans.  The scientists are now attempting to work out further how the operons work and interact. Future results should prove interesting.

  • Xie Z, Okinaga T, Niu G, Qi F, and Merritt J, Identification of a novel bacteriocin regulatory system in Streptococcus mutans, Mol Microbiol. 2010 Dec;78(6):1431-47

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This page last updated: February 26, 2014