Biology

Bacterial "homing missiles" could unlock new antibiotic treatments

Bacterial "homing missiles" co...
An artist's model of a tailocin, puncturing a bacterial membrane
An artist's model of a tailocin, puncturing a bacterial membrane
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An artist's model of a tailocin, puncturing a bacterial membrane
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An artist's model of a tailocin, puncturing a bacterial membrane

Microscopic wars are constantly raging all around, on and inside us, as bacteria fight for resources and room. They’ve developed some crafty weapons in the process, such as tailocins, which act somewhat like “homing missiles” against their enemies. Now, researchers have investigated just how tailocins work, and how we might use them to our advantage.

Bacteria are very social little critters, for better or worse. While they live in cooperative communities with their own species, they may indiscriminately murder other microbes that dare to try to steal nutrients. They’ll often use specialized toxins, which is where many of our antibiotics come from, but as we’re all too aware bacteria can evolve resistance to these substances, rendering them ineffective.

Another lesser known, but still powerful, weapon are what are known as tailocins. Only recently identified, these protein structures look like the “tails” of bacteriophages, tiny viruses that prey on bacteria. It seems like the bugs have turned these attackers to their advantage, producing tailocins themselves and firing them off against their enemies. Tailocins will latch onto other bacteria, then punch a hole through the cell, killing it.

“Tailocins are extremely strong protein nanomachines made by bacteria,” says Vivek Mutalik, an author of the study. “They look like phages but they don’t have the capsid, which is the ‘head’ of the phage that contains the viral DNA and replication machinery. So, they’re like a spring-powered needle that goes and sits on the target cell, then appears to poke all the way through the cell membrane making a hole to the cytoplasm, so the cell loses its ions and contents and collapses.”

Perhaps the most interesting thing about tailocins is that they’re picky about who they attack. Rather than killing whatever they find, they only target a specific species of bacteria, which has earned them the nickname of bacterial homing missiles.

But there are still unintended casualties. It turns out that producing tailocins is lethal for the individual bacterium, since they have to burst out of the cell in the first place. It’s strange that evolution would allow such self-destructive behavior to persist, but the net benefit to the species must outweigh the cost to the individual.

For the new study, researchers at Lawrence Berkeley National Laboratory investigated what makes tailocins target a particular bacteria species over another. They sampled 12 strains of soil bacteria that produce tailocins, and screened their genomes to look for relevant genes that might make the bugs more or less susceptible to the weapons.

They found that the differences mostly lie in structures called lipopolysaccharides, molecules of fat and sugar that sit on the outer membranes. Tailocins tend to bind to certain configurations of these molecules more so than others, a discovery which could eventually help us develop new antibacterials that are more focused on certain strains and less likely to trigger resistance.

“Once we understand the targeting mechanisms, we can start using these tailocins ourselves,” says Adam Arkin, co-lead author of the study. “The potential for medicine is obviously huge, but it would also be incredible for the kind of science we do, which is studying how environmental microbes interact and the roles of these interactions in important ecological processes, like carbon sequestration and nitrogen processing.”

The research was published in The ISME Journal.

Source: Berkeley Lab

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michael_dowling
Phage therapy has a long history in Russia : https://en.wikipedia.org/wiki/Phage_therapy Maybe reading what they have found would speed the process of applying tailocins to bacterial infection.