Horizontal gene transfer (HGT) is a key mechanism driving microbial evolution, enabling diverse lineages to rapidly acquire adaptive traits. However, the forces governing the retention and functional impact of transferred genes remain poorly understood, particularly in natural communities where gene exchange is frequent but strongly shaped by environmental selection. In extreme environments, high stress and nutrient limitation amplifies the role of HGT in microbial adaptation and community structure. Here, we synthesise evidence that HGT is strongly environment-dependent and often enriched for genes involved in core metabolic functions. We propose that genome streamlining, metabolic plasticity and mobile genetic element enrichment are hallmarks of frequent HGT in microbial communities inhabiting extreme environments. These traits contribute to metabolic interdependence that collectively shapes community-level gene-sharing networks. However, current metagenomic and phylogenetic approaches have limited resolution to capture the diversity and dynamics of HGT in extreme environments. We propose that integrating ecological and evolutionary perspectives is essential to better understand how HGT drives functional innovation and microbial adaptation in these ecosystems.
Free-living amoebae (FLA), including Acanthamoeba species, Balamuthia, Naegleria and Sappinia, can cause severe human infections. In addition to their direct pathogenicity, they play a role as intracellular reservoirs that protect bacteria, viruses, fungi and protozoa from environmental stress, promoting persistence, virulence, antimicrobial resistance (AMR) and horizontal gene transfer (HGT). Hospitals and aging water systems may provide an ideal environment for these interactions, and increase the risk of emerging healthcare-associated pathogens. In the context of climate change and microbial resilience, integrating FLA into surveillance, genomic monitoring, infection-control policy and AMR research is important to prevent future environmental and clinical threats.
Antimicrobial resistance (AMR) is driven not only by antimicrobial use but also by the horizontal transfer of resistance genes between bacteria. Conjugative plasmids are key drivers of this process, facilitating the dissemination of antibiotic resistance genes across diverse bacterial populations. While efforts to address AMR have largely focused on developing new antimicrobials, strategies to restrict gene flow remain comparatively underexplored. Mobile genetic elements frequently compete for host occupancy, and exclusion mechanisms that limit their coexistence are widespread. These interactions suggest an opportunity to exploit natural competition between elements as a means to restrict horizontal gene transfer. In particular, bacteriophage–plasmid interactions provide a compelling model. For example, the bacteriophage B3 exclusion system strongly inhibits IncP plasmid transfer in Pseudomonas aeruginosa, demonstrating how phage mediated interference can act as a barrier to gene exchange. Harnessing such interactions may provide a complementary approach to limiting the spread of antimicrobial resistance. More broadly, understanding and leveraging natural barriers on gene flow could open new avenues for AMR control beyond conventional therapeutics.
Clostridium perfringens is a Gram-positive anaerobe responsible for a wide spectrum of diseases in humans and animals, driven by an expanding arsenal of toxins. Notably, many of these virulence factors are encoded on mobile genetic elements, particularly conjugative plasmids, positioning mobile DNA at the centre of C. perfringens pathogenicity. Over the past decade, the pace of discovery has accelerated, with at least 11 new putative toxin-encoding genes identified, revealing an increasingly complex and dynamic toxin landscape. Here, we review advances in our understanding of toxin diversity and plasmid biology in C. perfringens, highlighting the remarkable plasticity of its mobile genome. We discuss how plasmid-encoded virulence, horizontal gene transfer and the emergence of novel plasmid families are reshaping current models of pathogenesis and evolution. We also consider key gaps in knowledge, including plasmid function, mobility and ecological context, and outline priorities for future genomic and functional studies. Together, these advances position C. perfringens as a compelling model to understand how mobile genetic elements drive virulence, adaptation and disease in bacterial pathogens.
Antimicrobial resistance (AMR) is a natural and ancient bacterial defence strategy that has been heavily manipulated by human use of antibiotics. While our understanding of AMR in the environment (microbial habitats outside of human or animal hosts) is rapidly developing, there remains a disconnect between descriptions of the abundance and distribution of AMR determinants in environmental reservoirs and our ability to interpret meaningful risks to health. Here we discuss the missing knowledge that limits our ability to link environmental AMR to a measure of risk, and thus to actionable solutions: (1) an understanding of baseline or ‘natural’ AMR in different environments; (2) the co-occurrence of pathogens with mobile antibiotic resistance genes as an overlooked component of risk; and (3) a comprehensive understanding of the factors that drive selection, persistence and transmission of AMR and resistant pathogens from the environment into other settings. Research focus on these areas will assist our understanding of what components of environmental AMR are relevant, crucial to monitor, and indicative of emerging risk.
