FEMS microbiology reviews最新文献

Ambrosia gall midges (AGMs) represent an intriguing group within the Cecidomyiidae, one of the most diversified dipteran families. AGMs form galls on plants, where they cultivate and consume fungal symbionts (phytomycetophagy). This mutualistic relationship may play a critical role in larval nutrition, gall morphogenesis, and protection against natural enemies. Although most other fungus-farming taxa have been intensively studied, AGMs have largely been neglected. This review synthesizes current knowledge on the diversity, biology, and ecological interactions of AGM, highlighting the intricate relationships with their fungal symbionts. The implications for adaptive radiation and speciation are critically considered, including how fungal associations may have facilitated ecological flexibility and diversification. We also tackle the processes of coevolution, not only between AGM and their fungal symbionts but also involving plants and parasitoids. We identify the most pressing issues and discrepancies in the current understanding the AGM-fungi interactions. Key areas of future research should include elucidating fungal acquisition and transmission mechanisms, determining the specificity and diversity of AGM-associated fungal communities, understanding the evolutionary pathways leading to phytomycetophagy, and addressing taxonomic challenges within the AGM group, where species identification has been complicated by reliance on gall morphology and host specificity.

Bacterial vaginosis (BV) is a complex polymicrobial vaginal infection that affects a large percentage of women during different stages of life including the reproductive age. In a healthy vaginal environment, the epithelium is colonized by protective Lactobacillus species that make up 90%-95% of the total vaginal microbiota. BV is characterized by a reduction of lactobacilli and a concurrent increase in diverse anaerobic bacteria, including Gardnerella vaginalis, Prevotella bivia, Hoylesella timonensis, and Fannyhessea vaginae. BV is associated with an increased risk of infertility, preterm birth, and a higher susceptibility to sexually transmitted infections (STIs), including Human Immunodeficiency Virus type-1 (HIV-1). This review examines the contribution of individual pathogenic bacteria to the development of BV and the resulting effects on susceptibility to STI. The impact of the different key bacterial virulence factors, such as secreted proteins, biofilm formation, and inflammatory potential on subsequent viral infection are discussed. While antibiotics are commonly prescribed to treat BV, recurrence rates are high, and antimicrobial resistance among BV-associated bacteria is increasingly reported. Understanding the mechanisms underlying BV and the impact of specific bacteria and their virulence factors on viral infections can improve preventive strategies and open up novel therapeutic applications.

Microbial functional ecology is expanding as we can now measure the traits of wild microbes that affect ecosystem functioning. Here, we review techniques and advances that could be the bedrock for a unified framework to study microbial functions. These include our newfound access to environmental microbial genomes, collections of microbial traits, but also our ability to study microbes' distribution and expression. We then explore the technical, ecological, and evolutionary processes that could explain environmental patterns of microbial functional diversity and redundancy. Next, we suggest reconciling microbiology with biodiversity-ecosystem functioning studies by experimentally testing the significance of microbial functional diversity and redundancy for the efficiency, resistance, and resilience of ecosystem processes. Such advances will aid in identifying state shifts and tipping points in microbiomes, enhancing our understanding of how and where will microbes guide Earth's biomes in the context of a changing planet.

Phenotypic heterogeneity in genetically clonal populations facilitates cellular adaptation to adverse environmental conditions while enabling a return to the basal physiological state. It also plays a crucial role in pathogenicity and the acquisition of drug resistance in unicellular organisms and cancer cells, yet the exact contributing factors remain elusive. In this review, we outline the current state of understanding concerning the contribution of phenotypic heterogeneity to fungal pathogenesis and antifungal drug resistance.

The adaptive mechanisms of Burkholderiales during the catabolism of aromatic compounds and abiotic stress are crucial for their fitness and performance. The aims of this report are to review the bacterial adaptation mechanisms to aromatic compounds, oxidative stress, and environmental stressful conditions, focusing on the model aromatic-degrading Paraburkholderia xenovorans LB400, other Burkholderiales, and relevant degrading bacteria. These mechanisms include (i) the stress response during aromatic degradation, (ii) the oxidative stress response to aromatic compounds, (iii) the metabolic adaptation to oxidative stress, (iv) the osmoadaptation to saline stress, (v) the synthesis of siderophore during iron limitation, (vi) the proteostasis network, which plays a crucial role in cellular function maintenance, and (vii) the modification of cellular membranes, morphology, and bacterial lifestyle. Remarkably, we include, for the first time, novel genomic analyses on proteostasis networks, carbon metabolism modulation, and the synthesis of stress-related molecules in P. xenovorans. We analyzed these metabolic features in silico to gain insights into the adaptive strategies of P. xenovorans to challenging environmental conditions. Understanding how to enhance bacterial stress responses can lead to the selection of more robust strains capable of thriving in polluted environments, which is critical for improving biodegradation and bioremediation strategies.

The gut microbiota (GM) is a dynamic ecosystem intricately linked to human health, including metabolic, immune, endocrine, and gastrointestinal functions. Exercise is recognized as a significant modifier of this microbial ecosystem, yet the complexities of this relationship are underexplored. Here, we delve into the multifaceted interactions between structured physical activity and the GM, emphasizing the role of exercise-induced stressors in shaping microbial composition and function. Unique to our review, we discuss the acute effects of different forms of exercise-induced stress on the GM and explore how these responses may influence long-term adaptability, stability, and resilience. Furthermore, we address critical junctures in microbial dynamics leading to shifts between different stable states. Finally, we explore the implications of host-controlled factors such as diet, exercise training, and nutritional supplementation in modulating the microbial community in the gut to optimize athletic performance. We conclude that while the potential to harness the synergistic effects of exercise-induced stressors, dietary interventions, and microbial adaptations appears promising, current evidence remains preliminary, highlighting the need for additional targeted research to guide future strategies that manipulate the GM for optimal health and athletic performance.

The Bacterial Locomotion And Signal Transduction (BLAST) conference was founded in 1991 and has been held biennially thereafter. While BLAST meetings have typically covered two-component and chemotactic signaling, as well as aspects of motor and flagellum, this year's program broadened its scope and included emerging areas of research, such as microbial signal perception, cellular signal processing, downstream physiological impacts of bacterial signaling, microbe interactions and communities, integrative approaches, and technology innovations. This review summarizes the oral presentations from BLAST XVIII, held in January 2025 in Cancun, Mexico.

Escherichia coli and Bacillus subtilis provide well-studied models for understanding how bacteria manage DNA replication stress (RS). These bacteria employ various strategies to detect and stabilize stalled replication forks (RFs), circumvent or bypass lesions, resolve replication-transcription conflicts (RTCs), and resume replication. While central features of responses to RS are broadly conserved, distinct mechanisms have evolved to adapt to their complex environments. In this review, we compare the RS sensors, regulators, and molecular players of these two phylogenetically distant bacteria. The differing roles of the RecA recombinase are used as the touchstone of the distinct strategies each bacterium employs to overcome RS, provided that the fork does not collapse. In E. coli, RecA mainly assembles at locations distal from replisomes, promotes global responses, and contributes to circumvent or bypass lesions. RecA assembles less frequently at stalled RFs, and its role in lesion skipping, fork remodeling, RTC resolution, and replication restart remains poorly defined. In contrast, in B. subtilis, RecA assembles at stalled forks, fine-tunes damage signaling, and, in concert with RecA-interacting proteins, may facilitate fork remodeling or lesion bypass, overcome RTCs, and contribute to replication restart.

Histone-like nucleoid structuring protein H-NS plays a pivotal role in orchestrating bacterial chromatin and regulating horizontal gene transfer (HGT) elements. In response to environmental signals, H-NS undergoes dynamic post-translational modifications (PTMs) that resemble the epigenetic codes of eukaryotic histones. This review explores how environmental cues regulate PTMs at specific sites within distinct domains of H-NS, thereby modulating its oligomerization and DNA-binding capabilities to reprogram bacterial responses. Notably, HGT elements commonly encode counter-silencing factors, including PTM-modifying enzymes, that counteract H-NS repression. We propose that combinatorial PTM patterns on H-NS form the bacterial histone-like epigenetic code, regulating the expression of HGT elements. Collectively, these interactions establish a sophisticated network of silencing and counter-silencing mechanisms that drive bacterial genome evolution.

Helicobacter pylori is a widespread pathogen responsible for chronic gastritis, peptic ulcers, and an elevated risk of gastric cancer. Lipopolysaccharide (LPS), localized exclusively in the outer leaflet of the outer membrane, is essential for maintaining bacterial integrity. Recent advances have deepened our understanding of H. pylori LPS structure, particularly lipid A modifications and the redefinition of the core oligosaccharide and O-antigen regions. The complete set of enzymes involved in LPS biosynthesis has been identified in the reference strain G27, and comparative genomics has revealed a notable regional difference (the absence of the heptan domain in East Asian strains). Here, we summarize recent insights into the structure and function of H. pylori LPS, emphasizing its role in bacterial persistence and its promise as a target for LPS-based glycoconjugate vaccine development.