Microbiology and Molecular Biology Reviews最新文献

SUMMARYBacteroides fragilis occupies a dynamic position within the human gut. Though it comprises a relatively minor fraction of the gut microbiota, it is disproportionately enriched at extraintestinal sites of infection. This ability to survive in contrasting host environments pivots on a regulatory framework that is both modular and highly plastic. Rather than deploying a suite of hierarchical global regulators, B. fragilis employs numerous operon-embedded transcriptional switches, including site-specific DNA inversions, phase-variable epigenetic systems, extracytoplasmic function sigma/anti-sigma factor pairs, and hybrid two-component systems. These networks are further complemented by cis-regulatory elongation checkpoints and post-transcriptional control by small RNAs. This review explores the full spectrum of these regulatory mechanisms, highlighting how they facilitate niche adaptation, surface variation, immune evasion, and metabolic prioritization. It also explores intraspecies variation focusing on glycan metabolism, antibiotic resistance, and virulence. Additionally, it outlines recombination-driven regulation, alongside extracytoplasmic function sigma factor diversification, flexible promoter architecture, and elongation checkpoints, each contributing to the evolution of transcriptional control in B. fragilis. Finally, it outlines unanswered questions, including the largely unexplored sRNA regulon, the coordination of DNA inversions, elongation control, and phase-variable methylation, and proposes experimental strategies to investigate the integration of these regulatory systems during environmental transitions. Taken together, B. fragilis emerges as a model bacterium for studying decentralized gene regulation in complex microbial ecosystems, with implications for both microbial ecology and therapeutic targeting of the gut microbiota.

SUMMARYThere is growing recognition in both the experimental and modeling literature of the importance of spatial structure to the dynamics of viral infections within the host. Aided by the evolution of computing power and motivated by recent biological insights, there has been an explosion of new, spatially explicit models for within-host viral dynamics in recent years. This development has only been accelerated in the wake of the COVID-19 pandemic. Spatially structured models offer improved biological realism and can account for dynamics that cannot be well-described by conventional, mean-field approaches. However, despite their growing popularity, spatially structured models of viral dynamics are underused in biological applications. One major obstacle to the wider application of such models is the huge variety in approaches taken, with little consensus as to which features should be included and how they should be implemented for a given biological context. Previous reviews of the field have focused on specific modeling frameworks or on models for particular viral species. Here, we instead apply a scoping review approach to the literature of spatially structured viral dynamics models as a whole to provide an exhaustive update of the state of the field. Our analysis is structured along two axes, methodology and viral species, in order to examine the breadth of techniques used and the requirements of different biological applications. We then discuss the contributions of mathematical and computational modeling to our understanding of key spatially structured aspects of viral dynamics and suggest key themes for future model development to improve robustness and biological utility.

SUMMARYSynthetic polymers have transformed modern life, giving rise to a wide spectrum of versatile materials commonly known as plastics. They are essential to industries including packaging, medical devices, automotive, textiles, and many consumer goods. However, significant environmental challenges have emerged because of the same properties that make plastics so useful. Of the estimated 400-450 million tons (Mt) of plastics produced each year, nearly 80 percent end up in the environment. Many of these plastics will persist in nature for hundreds or even thousands of years because they are mostly not biodegradable or poorly biodegradable. The identification of polymer-active microorganisms and enzymes that target most fossil fuel-based plastics is one of the greatest challenges microbiologists are facing today. Currently, more than 255 functionally verified plastic-active enzymes from more than 11 microbial phyla are known. Here, we summarize current knowledge on the microbial pathways and enzymes involved in the degradation of polyethylene terephthalate (PET), polyamide (PA) oligomers, ester-based polyurethane (PUR), and polycarbonates (PC), as well as some of the most widely used bioplastics. We also highlight the challenges microbiologists face in identifying microorganisms acting on highly persistent commodity polymers such as polyethylene (PE), polypropylene (PP), polyvinyl chloride (PVC), ether-based PUR, PA, polystyrene (PS), epoxy resins, and synthetic rubber (SR), for which no truly efficient degraders are currently known. We highlight methods used to discover novel microorganisms and enzymes involved in biodegradation and measure and quantify their activities. Finally, we will review the biotechnological applications of microbial-driven plastics recycling.

SUMMARYAs microbial communities are increasingly recognized as central to animal development and health, simplified animal models have become valuable tools for exploring the complex dynamics of these interactions. The mutualism between siphonfish (Siphamia spp.) and the bioluminescent bacterium Photobacterium mandapamensis offers a naturally occurring, binary, gut-associated symbiosis within a vertebrate host that is a promising system for investigating host-microbe interactions. Over the past decade, the application of genomic, ecological, and microbiological approaches has revealed high levels of strain-level variation within this highly specific and stable symbiosis, highlighting its value for exploring host control and microbial diversity in vertebrate systems. These discoveries demonstrate the potential of the Siphamia-P. mandapamensis system as a powerful model for investigating how vertebrate hosts regulate and maintain long-term bacterial associations, particularly within gut-associated partnerships, as well as the eco-evolutionary processes that shape these relationships. This review aims to consolidate recent findings, evaluate their broader implications for vertebrate-microbe interactions, and propose future directions for research using this association as a model system.

SUMMARYY-box binding proteins (YBXs) are abundant and conserved nucleic acid-binding proteins that interact with cellular and viral RNAs to modify their stability, localization, and translation. In this review, we summarize the biochemical activities and biological functions of the three human YBX paralogs. Furthermore, we highlight features of RNAs bound by YBXs, including sequence motifs, modifications, and secondary structures. We hypothesize how these features are cooperatively used by YBXs for paralog-specific recognition of RNA targets. Furthermore, we discuss the interactions of YBXs with cellular non-coding RNAs known to be associated with autoimmune diseases. We postulate on how YBXs may interact with these RNAs to maintain cellular homeostasis and prevent aberrant immune activation. Finally, we summarize the roles of YBXs in the life cycles of pathogenic RNA viruses and propose the use of RNA viruses as a valuable tool to dissect unresolved questions in YBX biology.

SUMMARYMost known chemicals originate from humans, thousands enter industrial usage annually, and new chemicals pose a continuous challenge to microbial evolution. The evolution of microbes to biodegrade new chemicals is crucial in protecting human and ecosystem health. New chemical biodegradation requires the evolution of new enzymes and metabolic pathways to meet the challenge. The rate of this process is determined by the structures of the new chemicals and preexisting enzymes, and the available metabolic pathways of the host microbe. Existing metabolism evolved over billions of years in response to naturally occurring chemicals. Natural petroleum is one example. Its diverse chemical structures have provided a training ground for microbial evolution. Similarly, studies on the biodegradation of petroleum have elucidated mechanisms that microbes have recruited to degrade industrial chemicals. Such studies have also led to the concepts of co-oxidation, co-metabolism, and enzyme promiscuity, which underlie new enzyme evolution. The focus of the present review is on evolutionary adaptations leading to the microbial biodegradation of non-polymeric industrial organic molecules. The greatest challenges to microbes and evolution are chemicals synthesized to resist biodegradation. A major current example is for per- and polyfluorinated alkyl substances, often known as PFAS. Most recently, directed evolution and artificial intelligence are being applied to the problems posed by highly resistant chemicals.

SUMMARYPhenazines are small, redox-active secondary metabolites produced by various bacterial species. These compounds participate in electron-transfer reactions, aiding microbes in surviving stressful or oxygen-limited environments. In this review, we examine the extensive structural diversity of phenazines and trace the evolutionary history of their biosynthetic pathways, which often move between distantly related species through horizontal gene transfer. We also explore how environmental factors such as nutrient levels and cell-to-cell signaling regulate phenazine production. Beyond their roles in microbial physiology, phenazines influence interactions among organisms, acting as antimicrobial agents, signaling molecules, and factors that shape microbiome dynamics in soils, plant roots, and other habitats. A better understanding of phenazine biology reveals how microbes adapt and thrive in diverse environments and emphasizes the potential applications of these compounds in agriculture and human health.

SUMMARYGap junctions (GJs) are specialized intercellular channels that mediate the direct exchange of ions, metabolites, and signaling molecules between adjacent cells, playing essential roles in tissue homeostasis and immune coordination. Their function is tightly controlled by connexin isoform composition, trafficking and turnover, and post-translational modifications, particularly phosphorylation and ubiquitination. This review synthesizes current knowledge on the diverse strategies employed by DNA and RNA viruses, including members of the Herpesviridae, Adenoviridae, Papillomaviridae, Polyomaviridae, Retroviridae, Flaviviridae, Coronaviridae, Orthomyxoviridae, Bornaviridae, Peribunyaviridae, and Picornaviridae families, to modulate gap junctional intercellular communication (GJIC) and the constituent connexin proteins. We highlight mechanisms such as phosphorylation-induced GJ closure and degradation, subcellular mislocalization, and transcriptional and post-transcriptional regulation of connexin expression. Viral modulation of GJIC serves a variety of purposes, including promoting viral spread, suppressing innate immune responses mediated by the cGAMP/STING pathway, and facilitating oncogenic transformation. Downregulation and/or selective reprogramming of GJIC during viral transformation mirrors changes seen in non-viral cancers, indicating that GJIC manipulation represents a shared mechanism underpinning both viral and non-viral cellular transformation in solid tumors. By integrating findings across diverse virus families, this review underscores GJIC modulation as a central virus-host interaction axis and identifies potential therapeutic targets for modulating GJIC in viral infections.

SUMMARYAntibodies neutralize the infectivity of viruses, but they can also, on the contrary, enhance the infection by these agents. This harmful effect of antibodies has been described in vitro and/or in vivo and concerns both DNA and RNA viruses. The dengue virus, belonging to the Flaviviridae family, has been particularly studied, as well as members of other families of enveloped viruses but also of non-enveloped viruses, in particular viruses of the genus Enterovirus of the Picornaviridae family. Antibodies can enhance the infection of Fcγ receptor (FcγR)-bearing cells as well as cells that do not possess FcγR. Enhancement of infection is achieved because antibodies directed against viruses increase the entry of these agents into cells or inhibit the antiviral immune response. The enhancing activity of antibodies is improved by several factors, such as antibody afucosylation, low antibody affinity, or epitope accessibility, but is also inhibited by specific geometrical arrangements of antibody-virus complexes. The enhancement of viral infection by antibodies may play a role in the pathophysiology of viral diseases and virus-associated chronic pathologies, as well as in the occurrence of epidemics, which was analyzed using mathematical models. In addition, the existence of these enhancing antibodies is considered in the design of active or passive antiviral immunotherapy to fight viruses. This review addresses the issue of enhancement of viral infections by antibodies and their relevance through a critical examination of available arguments provided by in vivo and in vitro studies.