Bacteria build tiny 'nano-spearguns' to fight back against attacks

Bacterial neighbors can be fierce rivals in their daily scuffle for resources. Some Pseudomonas bacteria species use specialized microscopic membrane devices to fight back against competing bacteria.

According to new research, these cells react to threats by assembling a precise injection tool inside their outer shell.

This work comes from the lab of Professor Marek Basler at the Biozentrum, University of Basel.

Pseudomonas bacteria and nano-spearguns

These weapon-like structures are known as the type VI secretion system (T6SS), and they allow bacteria to inject harmful molecules into rivals.

They have been studied extensively because of their importance in bacterial competition and survival.

“We knew that Pseudomonas aeruginosa bacteria uses its T6SS to fire back when attacked,” said Basler. Scientists had long suspected that external stress might activate these devices in Pseudomonas aeruginosa. 

One survey showed that T6SS genes occur in about a quarter of gram-negative species, highlighting their prevalence as a competitive strategy.

Some bacteria also direct T6SS at eukaryotic targets, affecting plant and animal hosts. This flexibility helps them adapt to diverse situations.

Understanding T6SS genes – the basics

T6SS genes control the Type VI Secretion System (T6SS), an impressive molecular weapon that bacteria use to fight each other and sometimes even mess with host cells.

Think of it as a microscopic harpoon gun – bacteria literally shoot toxic proteins into rival microbes to kill them or weaken their defenses.

Some bacteria also use T6SS to interact with host organisms, either to establish infections or to outcompete other microbes in a shared environment.

This system gives bacteria a serious advantage in the microscopic battlefield, whether they’re battling it out in soil, water, or even inside a host’s gut.

Scientists are fascinated by T6SS because it plays a huge role in bacterial survival, competition, and even virulence.

Some nasty pathogens, like Vibrio cholerae (which causes cholera) and Pseudomonas aeruginosa (a major threat in hospitals), use T6SS to dominate their environments.

Mechanical force as a trigger

“Using AFM, we have been able to mimic a bacterial T6SS attack,” said Yves F Dufrêne, a doctoral researcher at the Swiss Nanoscience Institute.

The team used atomic force microscopy (AFM) to gently push on the bacterial surface with a very fine tip. 

By applying measured force, they found that the outer membrane damage alone could spur this injection tool into action. Once activated, the cells unleashed a burst of toxin-bearing elements to ward off intruders.

Studies from different labs have shown that surfaces with varied stiffness can influence bacterial attachment. However, it was less clear how direct mechanical stress might activate a defensive tool like T6SS.

Laboratories investigating Vibrio species observed T6SS responses to mechanical cues in marine environments.

These clues paved the way for experiments focusing on Pseudomonas under controlled force measurements.

Pseudomonas bacteria attack detection

The scientists discovered that the site of membrane rupture guided the T6SS to assemble at the exact spot of assault. This high precision helps reduce wasted energy and ensures toxins only hit the intended target.

“Our work clearly shows that breaking the outer membrane is necessary and sufficient to trigger T6SS assembly,” said Basler.

Researchers believe this system works thanks to a phosphorylation cascade that springs into action upon sensing disruption. 

Pinpointing the exact trigger site allows minimal resource expenditure while maximizing impact on an aggressor. This specificity keeps the bacterial cell from randomly launching costly attacks.

Scientists are interested in finding the molecular components that link physical membrane disturbance to T6SS initiation. These details could open doors for inhibitors designed to neutralize this response.

Chemical assault on the membrane

Interestingly, certain antibiotics or peptide derivatives also weaken the same barrier. This hints that chemical agents capable of penetrating the membrane can provoke a similar defensive strike.

The findings could be significant when considering multidrug resistance in clinical settings. If a damaged outer membrane leads to a swift T6SS reaction, it might alter how pathogens respond to various medications.

Polymyxin derivatives, often reserved for severe infections, disrupt the outer membrane of Gram-negative bacteria.

This disruption can unintentionally activate T6SS, giving the pathogen a countermeasure against rival organisms.

Understanding this dynamic may help clinicians refine how these drugs are applied in critical care. If T6SS ramps up under partial membrane stress, combination therapies might offer a more thorough strategy.

Next steps for Pseudomonas bacteria study

Much still needs to be clarified, such as how multiple T6SS assemblies are precisely regulated once the membrane is compromised. Different strains may also vary in how sensitive they are to mechanical or chemical cues.

The bigger picture could involve a network of signals that prime bacteria to respond rapidly whenever their boundary is breached.

Exploring these nuances might help researchers develop ways to disrupt this mechanism without harming beneficial microbes.

Researchers suspect that different bacterial species have unique thresholds for activating T6SS when threatened.

This variation might determine which organisms thrive in complex environments like soil or aquatic habitats.

Experts are also investigating the role of protein partners that reset or limit T6SS after activation.

Gaining clarity on the shutdown mechanism could lead to ways of blocking these assemblies and tackling antibiotic-resistant infections in the future.

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Featured image: Pseudomonas bacteria deploy their nano-spearguns when damaged by a sharp tip (15,000 x magnification). Credit: University of Basel, Biozentrum/SNI Nano Imaging Lab

The study is published in the journal Science Advances.

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