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Bacterial survival necessitates endurance of many types of antimicrobial compound. Many Gram-negative envelope stress responses, which must contend with an outer membrane and a dense periplasm containing the cell wall, have been associated with the status of protein folding, membrane homeostasis, and physiological functions such as efflux and the proton motive force (PMF). In this review, we discuss evidence that indicates an emerging role for Gram-negative envelope stress responses in enduring exposure to diverse antimicrobial substances, focusing on recent studies of the γ-proteobacterial Cpx envelope stress response., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Gram-negative bacteria use N-acyl homoserine lactones (acyl-HSLs) for communication, predominantly mediated by LuxR-type receptors. Recent studies uncovered aryl-HSLs, α-pyrones and dialkylresorcinols as further chemical languages of Gram-negative bacteria. These findings extend the number of bacterial signaling molecules and suggest that cell-cell communication goes far beyond acyl-HSL signaling in nature., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Quorum sensing is a form of intercellular communication used by many species of bacteria that facilitates concerted interactions between the cells comprising a population. The phenotypes regulated by quorum sensing are extremely diverse, with many having a significant impact upon healthcare, agriculture, and the environment. Consequently there has been significant interest in developing methods to manipulate this signalling process and recent years have witnessed significant theoretical and practical developments. A wide range of small molecule modulators of quorum sensing systems has been discovered, providing an expansive chemical toolbox for the study and modulation of this signalling mechanism. In this review, a selection of recent case studies which illustrate the value of both activators and inhibitors of quorum sensing in Gram-negative bacteria are discussed., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Bacteria encounter a myriad of potentially growth-compromising conditions in nature and in hosts of pathogenic bacteria. These 'stresses' typically elicit protective and/or adaptive responses that serve to enhance bacterial survivability. Because they impact upon many of the same cellular components and processes that are targeted by antimicrobials, adaptive stress responses can influence antimicrobial susceptibility. In targeting and interfering with key cellular processes, antimicrobials themselves are 'stressors' to which protective stress responses have also evolved. Cellular responses to nutrient limitation (nutrient stress), oxidative and nitrosative stress, cell envelope damage (envelope stress), antimicrobial exposure and other growth-compromising stresses, have all been linked to the development of antimicrobial resistance in Gram-negative bacteria - resulting from the stimulation of protective changes to cell physiology, activation of resistance mechanisms, promotion of resistant lifestyles (biofilms), and induction of resistance mutations., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Bacterial pili have long been recognized as mediators of initial host-pathogen interactions important for the progression of Gram-negative bacterial diseases. An appreciation of the role of pili on virulence in Gram-positive bacteria and the unique properties of their biogenesis is a rapidly emerging area of research. In this review, we focus on recent advances in one of the longest-studied Gram-negative pilus systems, the chaperone/usher assembled pili, along with the newcomer to the field, the sortase-assembled pili of Gram-positive bacteria. In both systems, a wealth of new structural and molecular details has emerged recently. In light of this, we explore similarities between chaperone/usher and sortase-assembled pilus biogenesis and highlight paradigms unique to each, with the goal of using knowledge of each system to raise new questions and inform future studies of the other., (Copyright 2010 Elsevier Ltd. All rights reserved.)

Biofilms might result in healthcare-associated infections and substantially impact healthcare delivery. Bacteriophage (phage) has been used to treat infectious diseases in humans and there is interest in phage to control biofilms. Phages propagate in their bacterial host and many phages produce depolymerases that hydrolyze biofilm extracellular polymers. Drawbacks of phage to consider include narrow host range, bacterial resistance to phage and phage-encoded virulence genes that can incorporate into the host bacterial genome. The immune system might inactivate phage, and impure phage preparations could contain endotoxin. Phage mixtures or engineered phages could provide effective strategies to overcome these obstacles. Lytic bacteriophages could become a new class of anti-biofilm agents.

Swarming is the fastest known bacterial mode of surface translocation and enables the rapid colonization of a nutrient-rich environment and host tissues. This complex multicellular behavior requires the integration of chemical and physical signals, which leads to the physiological and morphological differentiation of the bacteria into swarmer cells. Here, we provide a review of recent advances in the study of the regulatory pathways that lead to swarming behavior of different model bacteria. It has now become clear that many of these pathways also affect the formation of biofilms, surface-attached bacterial colonies. Decision-making between rapidly colonizing a surface and biofilm formation is central to bacterial survival among competitors. In the second part of this article, we review recent developments in the understanding of the transition between motile and sessile lifestyles of bacteria.

Trimeric autotransporter adhesins (TAAs) are important virulence factors in gram-negative pathogens. Despite the variety of hosts ranging from plants to mammals and the specialized regulation of TAAs, their molecular organization follows surprisingly simple rules: they form trimeric surface structures with a head-stalk-anchor architecture. The head and stalk are composed of a small set of domains, building blocks that are frequently arranged repetitively. We propose that this repetitive arrangement facilitates recombination of domains to modulate the specificity of the common function: adhesion to the host.

The term 'type III secretion' has seen widespread use. However, problems persist in nomenclature. We propose that the standard abbreviation for this kind of secretion should be 'T3S' and that 'type III secretion system' should be abbreviated to 'T3SS'. There is also a need for a new terminology to distinguish flagellar and non-flagellar type III secretion systems that reflects their common evolutionary ancestry but does not obscure their distinctive features. Finally, the use of the term 'type III secretion' to cover cytolysin-mediated translocation is to be deprecated because an authentic type III secretion system has already been described in gram-positive bacteria, namely the flagellar protein export apparatus.

Bacterial type III secretion systems are thought to translocate virulence proteins directly from the bacterial cytoplasm into host cells through a continuous molecular channel. Little is known about how the apparatus itself interacts with membranes and whether insertion of this structure into the host membrane has consequences for the bacteria apart from its beneficial role in delivering virulence proteins. New evidence suggests that membrane insertion of the bacterial type III apparatus might turn on a calcium-dependent signaling pathway resulting in phagolysosomal fusion.

Bacteria use type IV secretion systems (T4SS) to translocate macromolecular substrates destined for bacterial, plant or human target cells. The T4SS are medically important, contributing to virulence-gene spread, genome plasticity and the alteration of host cellular processes during infection. The T4SS are ancestrally related to bacterial conjugation machines, but present-day functions include (i) conjugal transfer of DNA by cell-to-cell contact, (ii) translocation of effector molecules to eukaryotic target cells, and (iii) DNA uptake from or release to the extracellular milieu. Rapid progress has been made toward identification of type IV secretion substrates and the requirements for substrate recognition.

DNA-packaging and the control of gene expression constitute a major challenge for bacteria to survive and adapt to environmental changes. The use of multiple strategies to solve these problems could explain the presence of various nucleoid-associated proteins in bacteria. H-NS, one of these proteins, has been extensively studied in Escherichia coli, and a variety of phenotypes have been associated with a mutation in its structural gene. However, the role of H-NS in bacterial physiology and its mechanism of action are still a matter of debate. The expanding number of H-NS-related proteins identified in Gram-negative bacteria reveals interesting clues about their structure-function-evolution relationship.

Many Gram-negative bacteria use type III secretion systems to secrete virulence factors as well as the structural components of the flagellum. Some bacterial secretion systems use a secretion signal contained in the amino acid sequence of the secreted substrate. However, substrates of type III systems lack a single, defined secretion signal. There is evidence for the existence of three independent secretion signals - the 5' region of the mRNA, the amino terminus of the substrate and the ability of a secretion chaperone to bind the substrate before secretion - that direct substrates for secretion through the type III pathways. One or more of these signals might be used for a given substrate. A recent study of flagellar assembly presented evidence for a role of translation in the type III secretion mechanism. We present a unifying model for type III secretion that can be applied to flagellar assembly, needle assembly and the secretion of virulence factors. The potential role of translation in regulating the timing of substrate secretion is also discussed.

N2-fixing bacteria such as Azoarcus spp., Herbaspirillum spp, and Acetobacter diazotrophicus can infect the interior of gramineous plants without causing symptoms of plant disease but do not survive in soil. Like phytopathogens, they can penetrate into central tissues and spread systemically. There is no evidence for an endosymbiosis in living plant cells; however, the bacteria are physiologically active in the plant apoplast.

The outer membranes of Gram-negative bacteria constitute a semi-permeable barrier, as indicated by the corresponding alterations in outer membrane permeability and in antibiotic susceptibility resulting from mutation or polycation action. Restricted outer membrane permeability works in synergy with co-determinant resistance mechanisms, such as the periplasmic enzyme beta-lactamase or active efflux mechanisms, bringing about antibiotic resistance.

Lipo-oligosaccharides (LOS) and lipopolysaccharides (LPS) are major constituents of the outer membrane, and major antigenic and toxic components of Gram-negative bacteria. Although many diverse biological activities have been associated with LPS/LOS, their role in adherence to host cells has been recognized only recently.

The ability of bacterial cells to use small signalling molecules to monitor population growth may help them to react rapidly to environmental change. Regulatory systems made up of a small sensor molecule, an N-acyl homoserine lactone and a protein effector have been identified recently in a wide range of Gram-negative bacteria. These mediate signal cascades that amplify and coordinate the induction of single or multiple regulons.