Multi-layered genome defences in bacteria.

Bacteria have evolved a variety of defence mechanisms to protect against mobile genetic elements, including restriction-modification systems and CRISPR-Cas. In recent years, dozens of previously unknown defence systems (DSs) have been discovered. Notably, diverse DSs often coexist within the same genome, and some co-occur at frequencies significantly higher than would be expected by chance, implying potential synergistic interactions. Recent studies have provided evidence of defence mechanisms that enhance or complement one another. Here, we review the interactions between DSs at the mechanistic, regulatory, ecological and evolutionary levels.

How do interactions between mobile genetic elements affect horizontal gene transfer?

Horizontal gene transfer is central to bacterial adaptation and is facilitated by mobile genetic elements (MGEs). Increasingly, MGEs are being studied as agents with their own interests and adaptations, and the interactions MGEs have with one another are recognised as having a powerful effect on the flow of traits between microbes. Collaborations and conflicts between MGEs are nuanced and can both promote and inhibit the acquisition of new genetic material, shaping the maintenance of newly acquired genes and the dissemination of important adaptive traits through microbiomes. We review recent studies that shed light on this dynamic and oftentimes interlaced interplay, highlighting the importance of genome defence systems in mediating MGE-MGE conflicts, and outlining the consequences for evolutionary change, that resonate from the molecular to microbiome and ecosystem levels.

Gene mobility promotes the spread of resistance in bacterial populations.

Theory predicts that horizontal gene transfer (HGT) expands the selective conditions under which genes spread in bacterial populations. Whereas vertically inherited genes can only spread by positively selected clonal expansion, mobile genetic elements can drive fixation of genes by infectious HGT. We tested this using populations of Pseudomonas fluorescens and the conjugative mercury resistance (HgR) plasmid pQBR57. HGT expanded the selective conditions allowing the spread of HgR: Chromosomal HgR only increased in frequency under positive selection, whereas plasmid-encoded HgR reached fixation with or without positive selection. Tracking plasmid dynamics over time revealed that the mode of HgR inheritance varied across mercury environments. Under mercury selection, the spread of HgR was driven primarily by clonal expansion while in the absence of mercury HgR dynamics were dominated by infectious transfer. Thus, HGT is most likely to drive the spread of resistance genes in environments where resistance is useless.