Offense or defense? Quorum sensing has been tied to a number of bacterial functions, many of them involving virulence, but could quorum sensing also be used in defense? In mBio this week, there's new evidence that E. coli uses quorum sensing to trigger an antiphage mechanism that defends against at least two very different types of phage.
In evading phages, timing is everything. There are any number of ways for a bacterium to defend itself, but the benefits of evading an attack have to be weighed against the metabolic costs or readiness, so it makes sense to set up defenses only when they're needed. Since phages are thought to be more abundant and diverse in densely-populated environments with many different bacterial species, the authors reasoned that it would make sense for a bacterium to detect these conditions and turn on antiphage defenses on an as-needed basis.
Is Quorum Sensing The Trigger?
Høyland-Kroghsbo et al. wondered whether bacteria use quorum sensing to specifically upregulate antiphage defenses when confronted with these high-risk conditions. E. coli was a natural test subject for these experiments, since it's not only the best understood genetic system for bacteria, it also possesses a working quorum sensing system but lacks the ability to produce quorum sensing signals.
Using N-acyl-l-homoserine lactone (AHL) quorum-sensing signals and two different phages, λ and χ, they showed that more E. coli cells survive an attack in the presence of AHL than without. Cells apparently survived better because sensing the signal molecule leads to downregulation of receptors on the cell surface, depriving phages of receptor sites. In the case of phage λ, the downregulated receptor is LamB λ. When phage χ, which has a broader host range, attacks, AHLs protect against infection presumably by leading downregulating χ receptors in the flagellum. The AHL receptor is key: mutant cells lacking AHL receptor gene, sdiA, do not fend off phage attack.
And it doesn't take much to keep phages at bay. Cells exposed to AHL that fell under attack by phage λ reduced the number of λ receptors on the cell surface enough to cause a 2-fold reduction in the phage adsorption rate, but it dramatically increased the frequency of uninfected survivor cells.
Since the two phages, χ and λ, use different mechanisms of infection, the authors suggest that quorum sensing may be a general trigger for antiphage strategies in E. coli and other bacteria.
This is the first example of an antiphage mechanism that is controlled by quorum sensing, the authors point out, and it offers bacteria the ability to strike a balance between preparedness and efficiency.
Is it a general phenomenon in microbial communities? Time will tell.