Researchers at the John Innes Centre have identified a three-gene system that causes bacteria to burst open, releasing virus-like particles that share DNA, including antibiotic resistance genes. The system, called LypABC, resembles a repurposed bacterial immune defense. The findings, published in Nature Microbiology, highlight how bacteria facilitate horizontal gene transfer.
Scientists at the John Innes Centre, in collaboration with the University of York and the Rowland Institute at Harvard, studied gene transfer agents (GTAs) in the bacterium Caulobacter crescentus. These particles, derived from ancient viruses, act as couriers, carrying DNA fragments between bacterial cells to spread useful traits like antibiotic resistance through horizontal gene transfer. A critical step is host cell lysis, where bacteria break open to release the GTAs, but the control mechanism was previously unknown. The team used deep sequencing to pinpoint the LypABC gene cluster, which encodes proteins essential for this lysis. Deleting lypABC prevented cell bursting and GTA release, while overexpressing it caused widespread lysis. A regulatory protein ensures tight control, as misregulation proves toxic to cells. Remarkably, LypABC components mimic a bacterial anti-phage immune system, suggesting bacteria have repurposed defense tools for gene sharing. Dr. Emma Banks, the study's first author and 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 research advances understanding of antimicrobial resistance spread. Future work will explore LypABC activation and its role in cell rupture.
