Current opinion in microbiology最新文献

Legionella species are Gram-negative intracellular bacteria that evolved in soil and freshwater environments, where they infect and replicate within various unicellular protozoa. The primary virulence factor of Legionella is the expression of a type IV secretion system (T4SS), which contributes to the translocation of effector proteins that subvert biological processes of the host cells. Because of its evolution in unicellular organisms, T4SS effector proteins are not adapted to subvert specific mammalian signaling pathways and immunity. Consequently, Legionella pneumophila has emerged as an interesting infection model for investigating immune responses against pathogenic bacteria in multicellular organisms. This review highlights recent advances in our understanding of mammalian innate immunity derived from studies involving L. pneumophila. This includes recent insights into inflammasome-mediated mechanisms restricting bacterial replication in macrophages, mechanisms inducing cell death in response to infection, induction of effector-triggered immunity, activation of specific pulmonary cell types in mammalian lungs, and the protective role of recruiting monocyte-derived cells to infected lungs.

Bacterial microcompartments (BMCs) are polyhedral structures that segregate enzymatic cargo from the cytosol via encapsulation within a protein shell. Unlike other biological polyhedra, such as viral capsids and encapsulins, BMC shells can exhibit a highly advantageous structural and functional plasticity, conforming to a variety of anabolic (CO₂ fixation in carboxysomes) and catabolic (nutrient assimilation in metabolosomes) roles. Consequently, understanding the subunit properties and associated protein–protein interaction processes that guide shell assembly and function is a necessary step to fully harness BMCs as modular, biotechnological nanomachines. Here, we describe the recent insights into the dynamics of structural features of the key BMC domain (Pfam00936)-containing proteins, which serve as a structural template for BMC-H and BMC-T shell building blocks.

Symbiotic interactions between fungi and bacteria range from positive to negative. They are ubiquitous in free-living as well as host-associated microbial communities worldwide. Yet, the impact of fungal–bacterial symbioses on the organization and dynamics of microbial communities is uncertain. There are two reasons for this uncertainty: (1) knowledge gaps in the understanding of the genetic mechanisms underpinning fungal–bacterial symbioses and (2) prevailing interpretations of ecological theory that favor antagonistic interactions as drivers stabilizing biological communities despite the existence of models emphasizing contributions of positive interactions. This review synthesizes information on fungal–bacterial symbioses common in the free-living microbial communities of the soil as well as in host-associated polymicrobial biofilms. The interdomain partnerships are considered in the context of the relevant community ecology models, which are discussed critically.

Myxococcus relies on motility to efficiently invade and predate a prey colony. Upon contact with prey, Myxococcus temporarily halts its motility and initiates prey cell lysis, which involves two contact-dependent predatory machineries, the Kil system and the needleless T3SS*. Predatory cells grow as they invade and feed on prey cells. When dividing, Myxococcus cells systematically pause their movements before division. This highlights a high level of co-ordination between motility and contact-dependent killing but also with cell division. In this review, we give an overview of the different nanomachines used by Myxococcus to move on surfaces, kill by contact, and divide, and we discuss the potential regulatory mechanisms at play during these different processes.

Candida albicans is a ubiquitous fungus of humans. It is not only a component of the oral and intestinal microbiota of most healthy adults but also a major cause of mucosal disorders and life-threatening disseminated infections. Until recently, research on the biology and pathogenesis of the fungus was largely based on a single clinical isolate. We review investigations that have started to dissect a diverse set of C. albicans strains. Using different approaches to leverage the species’ phenotypic and/or genetic diversity, these studies illuminate the wide range of interactions between fungus and host. While connecting genetic variants to phenotypes of interest remains challenging, research on C. albicans’ natural diversity is central to understand fungal commensalism and pathogenesis.

Hybridisation is the crossing of two divergent lineages that give rise to offspring carrying an admixture of both parental genomes. Genome sequencing has revealed that this process is common in the Saccharomycotina, where a growing number of hybrid strains or species, including many pathogenic ones, have been recently described. Hybrids can display unique traits that may drive adaptation to new niches, and some pathogenic hybrids have been shown to have higher prevalence over their parents in human and environmental niches, suggesting a higher fitness and potential to colonise humans. Here, we discuss how hybridisation and its genomic and phenotypic outcomes can shape the evolution of fungal species and may play a role in the emergence of new pathogens.

Animals harbor a diverse array of symbiotic micro-organisms that coexist in communities across different body sites. These microbes maintain host homeostasis and respond to environmental insults to impact host physiological processes. Trillions of indigenous microbes reside in the gastrointestinal tract and engage with the host central nervous system (microbiota–gut–brain axis) by modulating immune responses, interacting with gut intrinsic and extrinsic nervous system, and regulating neuromodulators and biochemicals. These gut microbiota to brain signaling pathways are constantly informed by each other and are hypothesized to mediate brain health across the lifespan. In this review, we will examine the crosstalk of gut microbiota to brain communications in neurological pathologies, with an emphasis on microbial metabolites and neuromodulators, and provide a discussion of recent advances that help elucidate the microbiota as a therapeutic target for treating brain and behavioral disorders.

In this review, we explore the regulation of septal peptidoglycan (sPG) synthesis in bacterial cell division, a critical process for cell viability and proper morphology. Recent single-molecule imaging studies have revealed the processive movement of the FtsW:bPBP synthase complex along the septum, shedding light on the spatiotemporal dynamics of sPG synthases and their regulators. In diderm bacteria (E. coli and C. crescentus), the movement occurs at two distinct speeds, reflecting active synthesis or inactivity driven by FtsZ-treadmilling. In monoderm bacteria (B. subtilis, S. pneumoniae, and S. aureus), however, these enzymes exhibit only the active sPG-track-coupled processive movement. By comparing the dynamics of sPG synthases in these organisms and that of class-A penicillin-binding proteins in vivo and in vitro, we propose a unifying model for septal cell wall synthesis regulation across species, highlighting the roles of the sPG- and Z-tracks in orchestrating a robust bacterial cell wall constriction process.

Carbon dioxide supplies carbon for photosynthetic species and is a major product of respiration for all life forms. Inside the human body where CO₂ is a by-product of the tricarboxylic acid cycle, its level reaches 5% or higher. In the ambient atmosphere, ∼.04% of the air is CO₂. Different organisms can tolerate different CO₂ levels to various degrees, and experiencing higher CO₂ is toxic and can lead to death. The fungal kingdom shows great variations in response to CO₂ that has been documented by different researchers at different time periods. This literature review aims to connect these studies, highlight mechanisms underlying tolerance to high levels of CO₂, and emphasize the effects of CO₂ on fungal metabolism and morphogenesis.

Sulfur is an essential macronutrient for life, and consequently, all living organisms must acquire it from external sources to thrive and grow. Sulfur is a constituent of a multitude of crucial molecules, such as the S-containing proteinogenic amino acids cysteine and methionine; cofactors and prosthetic groups, such as coenzyme-A and iron–sulfur (Fe–S) clusters; and other essential organic molecules, such as glutathione or S-adenosylmethionine. Additionally, sulfur in cysteine thiols is an active redox group that plays paramount roles in protein stability, enzyme catalysis, and redox homeostasis. Furthermore, H₂S is gaining more attention as a crucial signaling molecule that influences metabolism and physiological functions. Given its importance, it is not surprising that sulfur plays key roles in the host–pathogen interaction. However, in contrast to its well-recognized involvement in the plant–pathogen interaction, the specific contributions of sulfur to the human–fungal interaction are much less understood. In this short review, I highlight some of the most important known mechanisms and propose directions for further research.