FEMS microbiology reviews最新文献

Bacteria and ectomycorrhizal fungi (EcMF) represent two of the most dominant plant root-associated microbial groups on Earth, and their interactions continue to gain recognition as significant factors that shape forest health and resilience. Yet, we currently lack a focused review that explains the state of bacteria-EcMF interaction research in the context of experimental approaches and technological advancements. To these ends, we illustrate the utility of studying bacteria-EcMF interactions, detail outstanding questions, outline research priorities in the field, and provide a suite of approaches that can be used to promote experimental reproducibility, field advancement, and collaboration. Though this review centers on the ecology of bacteria, EcMF, and trees, it by default offers experimental and conceptual insights that can be adapted to various subfields of microbiology and microbial ecology.

Metabolic engineering is a key enabling technology for rewiring cellular metabolism to enhance production of chemicals, biofuels, and materials from renewable resources. However, how to make cells into efficient factories is still challenging due to its robust metabolic networks. To open this door, metabolic engineering has realized great breakthroughs through three waves of technological research and innovations, especially the third wave. To understand the third wave of metabolic engineering better, we discuss its mainstream strategies and examples of its application at five hierarchies, including part, pathway, network, genome, and cell level, and provide insights as to how to rewire cellular metabolism in the context of maximizing product titer, yield, and productivity. Finally, we highlight future perspectives on metabolic engineering for the successful development of cell factories.

African swine fever (ASF), caused by the highly contagious African swine fever virus (ASFV), poses a significant threat to domestic and wild pigs worldwide. Despite its limited host range and lack of zoonotic potential, ASF has severe socio-economic and environmental consequences. Current control strategies primarily rely on early detection and culling of infected animals, but these measures are insufficient given the rapid spread of the disease. Developing effective therapeutics against ASFV is crucial to prevent further spread and mitigate economic losses. Although vaccination remains critical, recent vaccine approvals in Vietnam have raised safety and efficacy concerns. Moreover, as challenges persist in vaccine development and deployment, particularly in complex field conditions, antiviral agents have emerged as a critical complementary approach. These agents have the potential to mitigate side effects and control viral spread when vaccines alone are insufficient or when animals face simultaneous exposure to vaccine strains and wild-type viruses. However, advancing them from proof-of-concept to widespread practical application entails a significant interdisciplinary effort, given the logistical and economic constraints of in vivo testing. In this review, we examine emerging antiviral approaches and highlight key ASFV replication mechanisms and therapeutic targets to guide rational drug design amidst an evolving viral landscape.

Aromatic compounds serve pivotal roles in plant physiology and exhibit antioxidative and antimicrobial properties, leading to their widespread application, such as in food preservation and pharmaceuticals. However, direct plant extraction and petrochemical synthesis often struggle to meet current needs due to low yield or facing economic and environmental hurdles. In the past decades, systems metabolic engineering enabled eco-friendly production of various aromatic compounds, with some reaching industrial levels. In this review, we highlight monocyclic aromatic chemicals, which have relatively simple structures and are currently the primary focus of microbial synthesis research. We then discuss systems metabolic engineering at the enzyme, pathway, cellular, and bioprocess levels to improve the production of these chemicals. Finally, we overview the current limitations and potential resolution strategies, aiming to provide reference for future studies on the biosynthesis of aromatic products.

Understanding plant-microbe interactions is vital for developing sustainable agricultural practices and mitigating the consequences of climate change on food security. Plant-microbe interactions can improve nutrient acquisition, reduce dependency on chemical fertilizers, affect plant health, growth, and yield, and impact plants' resistance to biotic and abiotic stresses. These interactions are largely driven by metabolic exchanges and can thus be understood through metabolic network modelling. Recent developments in genomics, metagenomics, phenotyping, and synthetic biology now enable researchers to harness the potential of metabolic modelling at the genome scale. Here, we review studies that utilize genome-scale metabolic modelling to study plant-microbe interactions in symbiotic, pathogenic, and microbial community systems. This review catalogues how metabolic modelling has advanced our understanding of the plant host and its associated microorganisms as a holobiont. We showcase how these models can contextualize heterogeneous datasets and serve as valuable tools to dissect and quantify underlying mechanisms. Finally, we consider studies that employ metabolic models as a testbed for in silico design of synthetic microbial communities with predefined traits. We conclude by discussing broader implications of the presented studies, future perspectives, and outstanding challenges.

Host-mediated natural competence for transformation of DNA and mobile genetic element (MGE)-driven conjugation and transduction are key modes of horizontal gene transfer. While these mechanisms are traditionally believed to shape bacterial evolution by enabling the acquisition of new genetic traits, numerous studies have elucidated an antagonistic relationship between natural transformation and MGEs. A new role of natural transformation as a chromosome-curing mechanism has now been proposed. Experimental data, along with mathematical models, suggest that transformation can eliminate deleterious MGEs. Supporting this hypothesis, MGEs have been shown to use various mechanisms to decrease or block transformability, such as disrupting competence genes, regulating the development of competence, hindering DNA uptake machinery, producing DNases that target the exogenous (transforming) DNA, and causing lysis of competent cells. A few examples of synergistic relationships between natural transformation and MGEs have also been reported, with natural transformation facilitating MGE transfer and phages enhancing transformation by supplying extracellular DNA through lysis and promoting competence via kin discrimination. Given the complexity of the relationships between natural transformation and MGEs, the balance between antagonism and synergy likely depends on specific selection pressures in a given context. The evidence collected here indicates a continuous conflict over horizontal gene transfer in bacteria, with semiautonomous MGEs attempting to disrupt host-controlled DNA acquisition, while host competence mechanisms work to resist MGE interference.

Targeted degradation is emerging as a new therapeutic approach in the treatment of different diseases. It allows hijacking the cellular pathways deputed to protein or nucleic acid homeostasis to degrade a target macromolecule of interest involved in a pathogenic process. In the last decades, targeted protein degradation has been widely applied for the treatment of cancer or neurodegenerative disorders and some of such therapies are already in clinical use. More recently, therapeutic degraders such as PROTACs, LYTACs, HyTs, BacPROTACs, and others have also been explored in the field of antimicrobial and antiviral drug discovery. The peculiar mechanism of action, along with the opportunity to degrade both microbial and host targets, holds great promise for overcoming some limitations of classic antimicrobials, e.g. drug resistance, as well as for increasing the potency of current therapies. With a focus on the antimicrobial field, this Review aims at providing a comprehensive, state-of-the-art description of targeted degradation mechanisms and strategies developed so far, as well as to discuss advantages, disadvantages, and caveats of this innovative approach for combating infectious diseases.

The genus Enterococcus comprises a diverse group of species, many of which are commensal members of the gut microbiota of humans and animals. The two most prominent species associated with humans, Enterococcus faecalis and Enterococcus faecium, have also emerged as prominent opportunistic pathogens causing a range of infections in hospitalized patients, including urinary tract infections, bloodstream infections, and endocarditis. The rise of antibiotic resistance in enterococci undermines the efficacy of the treatment of infections, thus posing a significant public health risk. Enterococci readily acquire resistance to antibiotics through chromosomal mutations and the horizontal gene transfer of antibiotic resistance genes. This review offers a comprehensive examination of the mechanisms of antibiotic resistance among enterococci, with an emphasis on resistance to last-line antibiotics, including to glycopeptide antibiotics like vancomycin and teicoplanin, oxazolidinones (primarily linezolid), and daptomycin. Furthermore, we evaluate relevant candidates in the current development pipeline for antibiotics and discuss alternative strategies (phage therapy and immunotherapeutics) for the treatment and prevention of infections with multidrug-resistant enterococci. As enterococci rapidly adapt to novel conditions, including by developing resistance to new drugs and therapies, sustained research efforts are required to ensure the continuous development of treatment options for these important opportunistic pathogens.

Group A Streptococcus (GAS) has recently reemerged as a leading cause of both mild and severe invasive infections worldwide, with recent upsurges in invasive disease among children and adults. Notwithstanding a partial synchronicity with the COVID-19 pandemic, this rapid global dissemination of more virulent GAS lineages has been promptly detected, as well as the molecular shifts underlying the observed changes in clinical patterns. Whole-genome sequencing (WGS)-based genomic epidemiology allowed us to gain relevant insights into this upsurge as it was happening. This review integrates the canonical research publication-based approach with genomic data and metadata and identifies a subset of genomic clusters playing a major role in invasive GAS (iGAS) infections worldwide, which were named as Global Pathogenic Lineages (GPLs). The four GPLs broadly coincide with five sequence types (STs): GPL1 with ST28, GPL2 with ST15 and ST315, GPL3 with ST52, and GPL4 with ST39. While non-GPLs clusters maintain a baseline reservoir of antimicrobial-resistance and virulence genes, GPLs show varying but noteworthy resistance profiles and are frequent causes of iGAS. The integration of WGS into routine diagnostics procedures is a forthcoming improvement, aimed not only at informing tailored therapy and implementing infection control strategies, but also to perform continuous surveillance. Ongoing WGS in clinical microbiology, as a matter of fact, will provide unparalleled insights into lineage emergence, transmission dynamics, and the geographic clustering of virulence and resistance determinants.