A bacterial quorum is not unlike the human variety — as soon as enough individuals are gathered together, decisions can be made. For bacteria, these decisions result from the production of signals that switch on genes involved in processes such as virulence. But a report by Lian-Hui Zhang and colleagues in Nature now shows that such decisions can be reversed by 'quenching' these quorum signals.

Bacterial quorum sensing, as it's called, is a response to increased population density that is often associated with a shift from a free-living to host-associated lifestyle. Individual bacteria produce quorum-sensing signals such as N-acyl homoserine lactones (AHLs) and, once the concentration of these signals reaches a certain threshold, the AHLs interact with transcription factors to activate gene expression. Different bacterial species may produce different AHLs, which vary in the length and substitution of the acyl chain, but maintain the same homoserine lactone moiety.

Last year, Zhang and colleagues showed that the aiiA (for 'autoinducer inactivation') gene from Bacillus sp. encodes a factor that can inactivate AHLs, suggesting that it might be possible to control bacterial infection by paralysing the quorum-sensing system. The authors have now further characterized AiiA by using it to digest several AHLs. In each case they found the molecular mass of the AHL to be increased by 18 after the enzymatic digestion, indicating the addition of a water molecule. This is consistent with hydrolysis of the ester bond of the homoserine lactone ring, leading the authors to conclude that AiiA is an AHL-lactonase.

The authors next investigated the effect of this enzyme on bacterial infection by introducing the aiiA gene into tobacco and potato plants. They then inoculated these transgenic plants with Erwinia carotovora, a bacterial pathogen that causes wilts and soft rots in crop plants. And the results were dramatic — there was a strong correlation between resistance to disease and the levels of the AHL-lactonase. This resistance also correlated with the population density of the Erwinia, such that high levels of the pathogen caused extensive tissue damage to controls, and even to some of the transgenic plants. Nonetheless, the transgenic plants were able to resolve the infection over time.

As Zhang and colleagues point out, their results show that enzymatic quenching of AHL quorum-sensing signals — an effect that they call 'quorum quenching' — is a feasible approach for preventing bacterial infection. And, as quorum sensing is a common strategy adopted by many pathogens, this approach could be widely applicable.