To fight antimicrobial resistance (AMR), we must recognize and target all its manifestations. In this review, we briefly summarize the history that led to recognition of the various manifestations of AMR in bacterial pathogens and the ways in which they interrelate. We emphasize the importance of distinguishing between AMR arising from genetic alterations versus induction of endogenous machinery in response to environmental triggers, including - paradoxically - stresses from host immunity and antimicrobial therapy. We present an integrated view of AMR by reframing it as a spectrum of phenotypes within a continuous three-dimensional space defined by the growth rate, prevalence, and kill rate of cells displaying AMR. Finally, we reflect on strategies that may help stem the emergence of AMR.

Multiple eukaryotic cell processes are modulated by calcium ions (Ca2+). As such, Ca2+ is emerging as a crucial regulator of innate immunity in multicellular organisms. In particular, recent studies have identified roles of Ca2+ signalling at the host-bacteria interface. Following microbial exposure, Ca2+ signals mobilised from the extracellular milieu or intracellular stores are transduced into cell physiological responses. However, during infection with host-adapted pathogens, Ca2+ signals are often atypical, due to the activities of virulence factors, with varied consequences for both the pathogen and the host cell. In this review, we describe the Ca2+-dependent host factors regulating antibacterial immunity, in addition to bacterial effectors that promote, inhibit, or co-opt Ca2+-calmodulin signalling to promote infection.

Plants recruit a taxonomically diverse microbial community, collectively termed the plant microbiome, that includes mutualists, pathogens, and commensals. These myriad microorganisms are robustly intertwined with their hosts and can determine plant fate by influencing fitness and growth or offering protection from detrimental bacteria, fungi, and herbivores. Recent studies have revealed significant effects of host genome diversity on plant-microbiome assembly and how host genetics determine microbiome composition, which is crucial for beneficial functions. The few host loci identified through genome-wide association studies suggest that genes involved in plant development, immunity, nutrient uptake, and root exudates regulate plant-microbiome community structure. Elucidating the role of host genetics in plant-microbiome assembly is key to understanding how plant-microbiome interactions are evolving and how to unlock the breeding and engineering potential of the microbiome for sustainable agriculture.

Harnessing the power of beneficial microbes in the rhizosphere to improve crop performance is a key goal of sustainable agriculture. However, the precise management of rhizosphere microbes for crop growth and health remains challenging because we lack a comprehensive understanding of the plant-rhizomicrobiome relationship. In this review, we discuss the latest research progress on root colonisation by representative beneficial microbes (e.g. Bacillus spp. and Pseudomonas spp.). We also highlight the bidirectional chemical communication between microbes and plant roots for precise functional control of beneficial microbes in the rhizosphere, as well as advances in understanding how beneficial microbes overcome the immune system of plants. Finally, we propose future research objectives that will help us better understand the complex network of plant-microbe interactions.

Earth's climate crisis threatens to disrupt ecosystem services and destabilize food security. Microbiome management will be a crucial component of a comprehensive strategy to maintain stable microbinal functions for ecosystems and plants in the face of climate change. Microbiome rescue is the directed, community-level recovery of microbial populations and functions lost after an environmental disturbance. Microbiome rescue aims to propel a resilience trajectory for community functions. Rescue can be achieved via demographic, functional, adaptive, or evolutionary recovery of disturbance-sensitive populations. Various ecological mechanisms support rescue, including dispersal, reactivation from dormancy, functional redundancy, plasticity, and diversification, and these mechanisms can interact. Notably, controlling microbial reactivation from dormancy is a potentially fruitful but underexplored target for rescue.

Salmonella enterica is one of the most widespread bacterial pathogens found worldwide, resulting in approximately 100 million infections and over 200 000 deaths per year. Salmonella isolates, termed 'serovars', can largely be classified as either nontyphoidal or typhoidal Salmonella, which differ in regard to disease manifestation and host tropism. Nontyphoidal Salmonella causes gastroenteritis in many hosts, while typhoidal Salmonella is human-restricted and causes typhoid fever, a systemic disease with a mortality rate of up to 30% without treatment. There has been considerable interest in understanding how different Salmonella serovars cause different diseases, but the molecular details that underlie these infections have not yet been fully characterized, especially in the case of typhoidal Salmonella. In this review, we highlight the current state of research into understanding the pathogenesis of both nontyphoidal and typhoidal Salmonella, with a specific interest in serovar-specific traits that allow human-adapted strains of Salmonella to cause enteric fever. Overall, a more detailed molecular understanding of how different Salmonella isolates infect humans will provide critical insights into how we can eradicate these dangerous enteric pathogens.

Streptococcus pneumoniae is the most common cause of community-acquired pneumonia, and one of the main pathogens responsible for otitis media infections in children. Amoxicillin (AMX) is a broad-spectrum β-lactam antibiotic, used frequently for the treatment of bacterial respiratory tract infections. Here, we discuss the pneumococcal response to AMX, including the mode of action of AMX, the effects on autolysin regulation, and the evolution of resistance through natural transformation. We discuss current knowledge gaps in the synthesis and translocation of peptidoglycan and teichoic acids, major constituents of the pneumococcal cell wall and critical to AMX activity. Furthermore, an outlook of AMX resistance research is presented, including the development of natural competence inhibitors to block evolution via horizontal gene transfer, and the use of high-throughput essentiality screens for the discovery of novel cotherapeutics.