Annual review of microbiology最新文献

Surprisingly, many single-celled organisms and specialized cell types can achieve speed and acceleration significantly faster than those of multicellular animals. These remarkable cellular machines must integrate energy storage and amplification in actuation, latches for triggered release, and energy dissipation without failure-all implemented in macromolecular assemblies inside a single cell. In this review, we first map the atlas of single cells across the tree of life that use ultrafast motility. We then quantitatively compare extreme acceleration, speed, area strain rate, volume expansion strain rate, and density change rate among single cells. Next, we generalize these ideas by placing various trigger, actuation, and dissipation mechanisms within a unified framework. We conclude with a detailed summary of the diverse functions enabled by ultrafast cellular motility, providing a comprehensive foundation for understanding extreme biophysics and its diverse role at the cellular scale.

The world's citriculture has witnessed large-scale productivity decay due to microbial infections. The specialized metabolites produced during infection by pathogens are an important aspect of complex phytopathogen-host interactions and can be crucial for virulence and disease viability. In this review, we comprehensively explore microbial natural products produced during infection by the following citrus pathogens: Penicillium digitatum, Penicillium italicum, Penicillium citrinum, Aspergillus flavus, Fusarium solani, Alternaria alternata, Alternaria citri, Pseudomonas syringae, Elsinoë fawcettii, and Elsinoë australis. Additionally, we list the major microbial citrus diseases distributed worldwide and highlight the lack of consistent knowledge concerning the specialized metabolites that could play significant roles in some of the most important citrus diseases, such as Huanglongbing, citrus canker, citrus variegated chlorosis, citrus tristeza virus, citrus sudden death, sour rot, anthracnose, and citrus black spot.

Alongside the crisis of antimicrobial-resistant gonorrhea is the threat of bystander selection on commensal Neisseria. As Neisseria species are permissive to gene flow across lineages, their evolutionary fates are irrevocably intertwined. Horizontal gene transfer (HGT) within the genus occurs through transformation and exchange of plasmids through conjugation. Both mechanisms of HGT threaten the long-term efficacy of antimicrobial treatments, with resistance passed between commensals and pathogens multiple times (e.g., mosaic penA and mtr alleles). Here, we underscore the importance of commensal Neisseria as a bubbling cauldron of adaptive solutions for pathogenic Neisseria, review the mechanisms of resistance harbored by commensals and transferred to the gonococcus, and discuss the impact of contemporary selective pressures on the future evolutionary trajectory of the genus. Ultimately, we believe that predicting the future efficacy of antimicrobials for the treatment of gonorrhea will only be successful if the commensal Neisseria are also considered.

In the environment, bacteria often encounter a mixture of different carbon sources (C-sources) that can potentially be used. However, their uptake and utilization are selective and controlled in a hierarchical order by a complex regulatory pathway named carbon catabolite repression (CCR). Currently, two major types of CCR mechanisms have been described: (a) In Escherichia coli, Bacillota (formerly Firmicutes) and Vibrio, CCR depends on the phosphorylation state of the components of the phosphoenolpyruvate-sugar phosphotransferase system (PTS) and their subsequent regulatory activity, and (b) in pseudomonads, transcripts under CCR control are repressed by the posttranscriptional regulators Hfq and Crc. The repressive effect is antagonized by Hfq- and Crc-titrating RNAs (e.g., CrcZ, CrcY, and CrcX) that are expressed in response to the preference for C-sources. In addition, the importance of CCR as a sensor linking carbon availability with the regulation of virulence, chemotaxis, quorum sensing, and antibiotic susceptibility is addressed in this article.

Cytochrome c (cyt c) is ubiquitous in nature, having evolved billions of years ago to function in respiration and photosynthesis. All c-type cytochromes require covalently attached heme, typically at a CXXCH motif. We highlight new studies from the past five years that address the structural and mechanistic bases for the three cyt c biogenesis pathways (Systems I-III). The solved structures of most of the proteins that comprise these systems provide insights into heme transport, the binding of heme, and the mechanism of apocytochrome c (apocyt c) interaction with the synthases. Detailed analyses of the active sites of each cyt c synthase have elucidated chemical mechanisms underlying cyt c biogenesis and their potential as novel antimicrobial targets. This potential is suggested from an evolutionary perspective, as bacteria use two pathways (Systems I and II) that are structurally and mechanistically distinct from the mitochondrial System III. Genomic analyses of bacteria's respiratory capacity, including their use of c-type cytochromes, reveal how the inhibition of cyt c biogenesis could attenuate growth.

The assembly of marine benthic communities has become a focal point in marine ecology. We address how the bottom layers of benthic communities (i.e., the microbes inhabiting the basal biofilm) influence the complex accumulation of eukaryotes that grow on top of them. Specifically, we discuss (a) what organisms make up benthic biofilms, what brings about their attachment to surfaces, and how they vary in space and time; (b) what eukaryotic organisms are in marine benthic communities, how they vary in space and time, and the nature of microbial cues that bring about their recruitment to particular benthic sites; (c) the roles of bacterial-animal symbiosis in the composition of benthic communities; (d) what is happening to biofilms and their roles as habitat engineers in the rapidly changing world; and (e) how the geological history of bacteria and microbial mats on the ocean floor powerfully influenced the evolution of larval-bacterial interactions.

Human infectious diseases are unique in that the discovery of their environmental trigger, the microbe, was sufficient to drive the development of extraordinarily effective principles and tools for their prevention or cure. This unique medical prowess has outpaced, and perhaps even hindered, the development of scientific progress of equal magnitude in the biological understanding of infectious diseases. Indeed, the hope kindled by the germ theory of disease was rapidly subdued by the infection enigma, in need of a host solution, when it was realized that most individuals infected with most infectious agents continue to do well. The root causes of disease and death in the unhappy few remained unclear. While canonical approaches in vitro (cellular microbiology), in vivo (animal models), and in natura (clinical studies) analyzed the consequences of infection with a microbe, considered to be the cause of disease, in cells, tissues, or organisms seen as a uniform host, alternative approaches searched for preexisting causes of disease, particularly human genetic and immunological determinants in populations of diverse individuals infected with a trigger microbe.

Pore-forming toxins (PFTs) are released by one cell to directly inflict damage on another cell. Hosts use PFTs, including members of the membrane attack complex/perforin protein family, to fight infections and cancer, while bacteria and parasites deploy PFTs to promote infection. Apicomplexan parasites secrete perforin-like proteins as PFTs to egress from infected cells and traverse tissue barriers. Other protozoa, along with helminth parasites, utilize saposin-like PFTs prospectively for nutrient acquisition during infection. This review discusses seminal and more recent advances in understanding how parasite PFTs promote infection and describes how they are regulated and fulfill their roles without causing parasite self-harm. Although exciting progress has been made in defining mechanisms of pore formation by PFTs, many open questions remain to be addressed to gain additional key insights into these remarkable determinants of parasitic infections.

The major human spirochetal pathogens (Leptospira, Borrelia, and Treponema) are difficult to diagnose and lack vaccines to prevent infections. Infection by these spirochetes does not generate general protective immunity, allowing reinfection by different strains to occur. These stealth pathogens have uncommon physiology, pathogenesis, and clinical presentations and possess unique immune evasion mechanisms to facilitate their host adaptation and persistence. Collectively, host-spirochete interactions orchestrate systemic infections in a manner distinct from organ- and tissue-specific diseases caused by many bacterial pathogens. Difficulties in growing and genetic manipulation of infectious spirochetes have hindered the full understanding of their virulence factors despite decades to centuries of research. This article highlights the current understanding of the intricacies of spirochetal pathogenesis and diseases. Our comprehensive review of the progress versus gaps in knowledge lays a foundation for researchers to direct their studies toward the development of effective diagnostics and vaccines to protect patients from serious, chronic spirochetal diseases.

Staphylococcus aureus is a commensal of the skin and nares of humans as well as the causative agent of infections associated with significant mortality. The acquisition of antibiotic resistance traits complicates the treatment of such infections and has prompted the development of monoclonal antibodies. The selection of protective antigens is typically guided by studying the natural antibody responses to a pathogen. What happens when the pathogen masks these antigens and subverts adaptive responses, or when the pathogen inhibits or alters the effector functions of antibodies? S. aureus is constantly exposed to its human host and has evolved all these strategies. Here, we review how anti-S. aureus targets have been selected and how antibodies have been engineered to overcome the formidable immune evasive activities of this pathogen. We discuss the prospects of antibody-based therapeutics in the context of disease severity, immune competence, and history of past infections.