By Morgan Nwanguma
Bacteria are exploiting a repurposed version of their own virus-defense machinery to burst open and exchange DNA, a process that may accelerate the spread of antibiotic resistance.
Researchers at the John Innes Centre have uncovered new details about how bacteria transfer genes between cells, including genes linked to antimicrobial resistance (AMR), one of the world’s fastest-growing health threats. Their work focused on unusual virus-like structures known as gene transfer agents, or GTAs.
GTAs resemble bacteriophages – viruses that infect bacteria, but they no longer behave as harmful invaders. Instead, scientists believe they originated from ancient viruses that bacteria gradually adapted for their own use.
These microscopic particles function as DNA delivery systems, carrying genetic material from one bacterial cell to another nearby. Through this process, called horizontal gene transfer, bacteria can rapidly share beneficial traits, including the ability to survive antibiotic treatment.
For GTAs to spread, however, the host bacterial cell must first rupture in a process known as cell lysis. Until now, researchers did not fully understand how bacteria controlled this step.
In a study published in Nature Microbiology, scientists used deep sequencing techniques to investigate GTA activity in the model bacterium Caulobacter crescentus. Their analysis identified a three-gene cluster called LypABC as the central regulator of cell lysis.
The researchers found that deleting the lypABC genes prevented bacterial cells from breaking open and releasing GTA particles. In contrast, over stimulating the system caused widespread cell destruction, confirming that LypABC acts as a key control hub for GTA-mediated DNA transfer.
One of the study’s most unexpected findings was that LypABC closely resembles an anti-phage immune system normally used by bacteria to defend themselves against viral attacks. Instead of protecting the cell, however, this system appears to have been repurposed to promote GTA release and gene exchange.
The research, conducted in collaboration with the University of York and the Rowland Institute at Harvard, highlights the remarkable adaptability of bacterial biology.
Scientists also identified a regulatory protein responsible for tightly controlling GTA activation and cell lysis. This regulation appears essential because improper activation of LypABC is highly toxic to bacterial cells.
By revealing how bacteria can recycle and adapt existing biological systems for new purposes, the study provides important insight into how genes, including antibiotic resistance genes, spread through microbial populations.
Head of the research team Dr. Emma Banks, a Royal Commission for the Exhibition of 1851 Research Fellow, said: “What’s particularly interesting is that LypABC looks like an immune system, yet bacteria are using it to release GTA particles. It suggests that immune systems can be repurposed to help bacteria share DNA with each other — a process that can contribute to the spread of antibiotic resistance.”
The subsequent stage for the study is to find out how the LypABC control hub is activated as well as how it works to take charge of the rupture of bacterial cells and release of GTA particles.
“A bacterial CARD-NLR-like immune system controls the release of gene transfer agents,” appears in Nature Microbiology.
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