RESUMO
Infections of the lung cause observable sickness thought to be secondary to inflammation. Signs of sickness are crucial to alert others via behavioral-immune responses to limit contact with contagious individuals. Gram-negative bacteria produce exopolysaccharide (EPS) that provides microbial protection; however, the impact of EPS on sickness remains uncertain. Using genome-engineered Pseudomonas aeruginosa (P. aeruginosa) strains, we compared EPS-producers versus non-producers and a virulent Escherichia coli (E. coli) lung infection model in male and female mice. EPS-negative P. aeruginosa and virulent E. coli infection caused severe sickness, behavioral alterations, inflammation, and hypothermia mediated by TLR4 detection of the exposed lipopolysaccharide (LPS) in lung TRPV1+ sensory neurons. However, inflammation did not account for sickness. Stimulation of lung nociceptors induced acute stress responses in the paraventricular hypothalamic nuclei by activating corticotropin-releasing hormone neurons responsible for sickness behavior and hypothermia. Thus, EPS-producing biofilm pathogens evade initiating a lung-brain sensory neuronal response that results in sickness.
Assuntos
Infecções por Escherichia coli , Escherichia coli , Pulmão , Polissacarídeos Bacterianos , Infecções por Pseudomonas , Pseudomonas aeruginosa , Animais , Feminino , Masculino , Camundongos , Biofilmes , Escherichia coli/fisiologia , Hipotermia/metabolismo , Hipotermia/patologia , Inflamação/metabolismo , Inflamação/patologia , Pulmão/microbiologia , Pulmão/patologia , Pneumonia/microbiologia , Pneumonia/patologia , Pseudomonas aeruginosa/fisiologia , Células Receptoras Sensoriais , Polissacarídeos Bacterianos/metabolismo , Infecções por Escherichia coli/metabolismo , Infecções por Escherichia coli/microbiologia , Infecções por Escherichia coli/patologia , Infecções por Pseudomonas/metabolismo , Infecções por Pseudomonas/microbiologia , Infecções por Pseudomonas/patologia , Nociceptores/metabolismoRESUMO
Biofilm formation is generally recognized as a bacterial defense mechanism against environmental threats, including antibiotics, bacteriophages, and leukocytes of the human immune system. Here, we show that for the human pathogen Vibrio cholerae, biofilm formation is not only a protective trait but also an aggressive trait to collectively predate different immune cells. We find that V. cholerae forms biofilms on the eukaryotic cell surface using an extracellular matrix comprising primarily mannose-sensitive hemagglutinin pili, toxin-coregulated pili, and the secreted colonization factor TcpF, which differs from the matrix composition of biofilms on other surfaces. These biofilms encase immune cells and establish a high local concentration of a secreted hemolysin to kill the immune cells before the biofilms disperse in a c-di-GMP-dependent manner. Together, these results uncover how bacteria employ biofilm formation as a multicellular strategy to invert the typical relationship between human immune cells as the hunters and bacteria as the hunted.
Assuntos
Vibrio cholerae , Animais , Humanos , Vibrio cholerae/metabolismo , Comportamento Predatório , Biofilmes , Fímbrias Bacterianas , Proteínas de Bactérias/metabolismo , Regulação Bacteriana da Expressão GênicaRESUMO
Mycobacterium tuberculosis (Mtb) cultured axenically without detergent forms biofilm-like cords, a clinical identifier of virulence. In lung-on-chip (LoC) and mouse models, cords in alveolar cells contribute to suppression of innate immune signaling via nuclear compression. Thereafter, extracellular cords cause contact-dependent phagocyte death but grow intercellularly between epithelial cells. The absence of these mechanopathological mechanisms explains the greater proportion of alveolar lesions with increased immune infiltration and dissemination defects in cording-deficient Mtb infections. Compression of Mtb lipid monolayers induces a phase transition that enables mechanical energy storage. Agent-based simulations demonstrate that the increased energy storage capacity is sufficient for the formation of cords that maintain structural integrity despite mechanical perturbation. Bacteria in cords remain translationally active despite antibiotic exposure and regrow rapidly upon cessation of treatment. This study provides a conceptual framework for the biophysics and function in tuberculosis infection and therapy of cord architectures independent of mechanisms ascribed to single bacteria.
Assuntos
Mycobacterium tuberculosis , Tuberculose , Animais , Camundongos , Biofilmes , Pulmão/microbiologia , Pulmão/patologia , Mycobacterium tuberculosis/fisiologia , Tuberculose/microbiologia , Tuberculose/patologia , Virulência , Fenômenos BiomecânicosRESUMO
Contrary to multicellular organisms that display segmentation during development, communities of unicellular organisms are believed to be devoid of such sophisticated patterning. Unexpectedly, we find that the gene expression underlying the nitrogen stress response of a developing Bacillus subtilis biofilm becomes organized into a ring-like pattern. Mathematical modeling and genetic probing of the underlying circuit indicate that this patterning is generated by a clock and wavefront mechanism, similar to that driving vertebrate somitogenesis. We experimentally validated this hypothesis by showing that predicted nutrient conditions can even lead to multiple concentric rings, resembling segments. We additionally confirmed that this patterning mechanism is driven by cell-autonomous oscillations. Importantly, we show that the clock and wavefront process also spatially patterns sporulation within the biofilm. Together, these findings reveal a biofilm segmentation clock that organizes cellular differentiation in space and time, thereby challenging the paradigm that such patterning mechanisms are exclusive to plant and animal development.
Assuntos
Bacillus subtilis/crescimento & desenvolvimento , Bacillus subtilis/genética , Biofilmes/crescimento & desenvolvimento , Padronização Corporal/genética , Bacillus subtilis/metabolismo , Expressão Gênica , Regulação da Expressão Gênica no Desenvolvimento , Cinética , Modelos Biológicos , Nitrogênio/metabolismo , Transdução de Sinais/genética , Somitos/crescimento & desenvolvimento , Esporos Bacterianos/crescimento & desenvolvimento , Estresse Fisiológico/genética , Fatores de TempoRESUMO
Biofilms are community architectures adopted by bacteria inclusive of a self-formed extracellular matrix that protects resident bacteria from diverse environmental stresses and, in many species, incorporates extracellular DNA (eDNA) and DNABII proteins for structural integrity throughout biofilm development. Here, we present evidence that this eDNA-based architecture relies on the rare Z-form. Z-form DNA accumulates as biofilms mature and, through stabilization by the DNABII proteins, confers structural integrity to the biofilm matrix. Indeed, substances known to drive B-DNA into Z-DNA promoted biofilm formation whereas those that drive Z-DNA into B-DNA disrupted extant biofilms. Importantly, we demonstrated that the universal bacterial DNABII family of proteins stabilizes both bacterial- and host-eDNA in the Z-form in situ. A model is proposed that incorporates the role of Z-DNA in biofilm pathogenesis, innate immune response, and immune evasion.
Assuntos
Bactérias/genética , Biofilmes , DNA Bacteriano/química , Matriz Extracelular/metabolismo , Espaço Extracelular/química , Animais , Especificidade de Anticorpos , Proteínas de Bactérias/metabolismo , Linhagem Celular , Chinchila , DNA Cruciforme , Desoxirribonucleases/metabolismo , Armadilhas Extracelulares/metabolismo , Humanos , Acetato de Tetradecanoilforbol/farmacologiaRESUMO
Redox cycling of extracellular electron shuttles can enable the metabolic activity of subpopulations within multicellular bacterial biofilms that lack direct access to electron acceptors or donors. How these shuttles catalyze extracellular electron transfer (EET) within biofilms without being lost to the environment has been a long-standing question. Here, we show that phenazines mediate efficient EET through interactions with extracellular DNA (eDNA) in Pseudomonas aeruginosa biofilms. Retention of pyocyanin (PYO) and phenazine carboxamide in the biofilm matrix is facilitated by eDNA binding. In vitro, different phenazines can exchange electrons in the presence or absence of DNA and can participate directly in redox reactions through DNA. In vivo, biofilm eDNA can also support rapid electron transfer between redox active intercalators. Together, these results establish that PYO:eDNA interactions support an efficient redox cycle with rapid EET that is faster than the rate of PYO loss from the biofilm.
Assuntos
Biofilmes/crescimento & desenvolvimento , DNA/química , Pseudomonas aeruginosa/fisiologia , Piocianina/química , DNA/metabolismo , Técnicas Eletroquímicas , Eletrodos , Transporte de Elétrons/efeitos dos fármacos , Corantes Fluorescentes/química , Concentração de Íons de Hidrogênio , Oxirredução , Fenazinas/química , Fenazinas/metabolismo , Fenazinas/farmacologia , Piocianina/metabolismoRESUMO
Long-range (>10 µm) transport of electrons along networks of Geobacter sulfurreducens protein filaments, known as microbial nanowires, has been invoked to explain a wide range of globally important redox phenomena. These nanowires were previously thought to be type IV pili composed of PilA protein. Here, we report a 3.7 Å resolution cryoelectron microscopy structure, which surprisingly reveals that, rather than PilA, G. sulfurreducens nanowires are assembled by micrometer-long polymerization of the hexaheme cytochrome OmcS, with hemes packed within â¼3.5-6 Å of each other. The inter-subunit interfaces show unique structural elements such as inter-subunit parallel-stacked hemes and axial coordination of heme by histidines from neighboring subunits. Wild-type OmcS filaments show 100-fold greater conductivity than other filaments from a ΔomcS strain, highlighting the importance of OmcS to conductivity in these nanowires. This structure explains the remarkable capacity of soil bacteria to transport electrons to remote electron acceptors for respiration and energy sharing.
Assuntos
Transporte de Elétrons/fisiologia , Geobacter/metabolismo , Heme/metabolismo , Biofilmes , Condutividade Elétrica , Elétrons , Proteínas de Fímbrias/química , Fímbrias Bacterianas/química , Nanofios , OxirreduçãoRESUMO
Vibrio cholerae uses a quorum-sensing (QS) system composed of the autoinducer 3,5-dimethylpyrazin-2-ol (DPO) and receptor VqmA (VqmAVc), which together repress genes for virulence and biofilm formation. vqmA genes exist in Vibrio and in one vibriophage, VP882. Phage-encoded VqmA (VqmAPhage) binds to host-produced DPO, launching the phage lysis program via an antirepressor that inactivates the phage repressor by sequestration. The antirepressor interferes with repressors from related phages. Like phage VP882, these phages encode DNA-binding proteins and partner antirepressors, suggesting that they, too, integrate host-derived information into their lysis-lysogeny decisions. VqmAPhage activates the host VqmAVc regulon, whereas VqmAVc cannot induce phage-mediated lysis, suggesting an asymmetry whereby the phage influences host QS while enacting its own lytic-lysogeny program without interference. We reprogram phages to activate lysis in response to user-defined cues. Our work shows that a phage, causing bacterial infections, and V. cholerae, causing human infections, rely on the same signal molecule for pathogenesis.
Assuntos
Lisogenia/fisiologia , Pirazóis/metabolismo , Percepção de Quorum/fisiologia , Bacteriófagos/metabolismo , Biofilmes , Proteínas de Ligação a DNA/metabolismo , Regulação Bacteriana da Expressão Gênica/genética , Percepção de Quorum/genética , Vibrio/metabolismo , Vibrio cholerae/metabolismo , Vibrio cholerae/fisiologia , Virulência , Latência ViralRESUMO
Antibiotic tolerance, the capacity of genetically susceptible bacteria to survive the lethal effects of antibiotic treatment, plays a critical and underappreciated role in the disease burden of bacterial infections. Here, we take a pathogen-by-pathogen approach to illustrate the clinical significance of antibiotic tolerance and discuss how the physiology of specific pathogens in their infection environments impacts the mechanistic underpinnings of tolerance. We describe how these insights are leading to the development of species-specific therapeutic strategies for targeting antibiotic tolerance and highlight experimental platforms that are enabling us to better understand the complexities of drug-tolerant pathogens in in vivo settings.
Assuntos
Antibacterianos/farmacologia , Bactérias/efeitos dos fármacos , Infecções Bacterianas/tratamento farmacológico , Tolerância a Medicamentos , Animais , Bactérias/classificação , Infecções Bacterianas/microbiologia , Fenômenos Fisiológicos Bacterianos/efeitos dos fármacos , Biofilmes/efeitos dos fármacos , Biofilmes/crescimento & desenvolvimento , Interações Hospedeiro-Patógeno/efeitos dos fármacos , Humanos , Especificidade da EspécieRESUMO
Many community- and hospital-acquired bacterial infections are caused by antibiotic-resistant pathogens. Methicillin-resistant Staphylococcus aureus (MRSA) predisposes humans to invasive infections that are difficult to eradicate. We designed a closed-loop gene network programming mammalian cells to autonomously detect and eliminate bacterial infections. The genetic circuit contains human Toll-like receptors as the bacterial sensor and a synthetic promoter driving reversible and adjustable expression of lysostaphin, a bacteriolytic enzyme highly lethal to S. aureus. Immunomimetic designer cells harboring this genetic circuit exhibited fast and robust sense-and-destroy kinetics against live staphylococci. When tested in a foreign-body infection model in mice, microencapsulated cell implants prevented planktonic MRSA infection and reduced MRSA biofilm formation by 91%. Notably, this system achieved a 100% cure rate of acute MRSA infections, whereas conventional vancomycin treatment failed. These results suggest that immunomimetic designer cells could offer a therapeutic approach for early detection, prevention, and cure of pathogenic infections in the post-antibiotic era.
Assuntos
Biomimética/métodos , Staphylococcus aureus Resistente à Meticilina/fisiologia , Infecções Estafilocócicas/prevenção & controle , Fosfatase Alcalina/sangue , Fosfatase Alcalina/genética , Fosfatase Alcalina/metabolismo , Animais , Antibacterianos/farmacologia , Biofilmes/efeitos dos fármacos , Testes de Sensibilidade a Antimicrobianos por Disco-Difusão , Feminino , Células HEK293 , Humanos , Receptores de Lipopolissacarídeos/genética , Lisostafina/metabolismo , Lisostafina/farmacologia , Staphylococcus aureus Resistente à Meticilina/efeitos dos fármacos , Camundongos , Camundongos Endogâmicos C57BL , Plasmídeos/genética , Plasmídeos/metabolismo , Infecções Estafilocócicas/microbiologia , Infecções Estafilocócicas/veterinária , Receptor 1 Toll-Like/genética , Receptor 2 Toll-Like/genética , Receptor 6 Toll-Like/genética , Fator de Transcrição AP-1/metabolismoRESUMO
Microorganisms often live in habitats characterized by fluid flow, from lakes and oceans to soil and the human body. Bacteria and plankton experience a broad range of flows, from the chaotic motion characteristic of turbulence to smooth flows at boundaries and in confined environments. Flow creates forces and torques that affect the movement, behavior, and spatial distribution of microorganisms and shapes the chemical landscape on which they rely for nutrient acquisition and communication. Methodological advances and closer interactions between physicists and biologists have begun to reveal the importance of flow-microorganism interactions and the adaptations of microorganisms to flow. Here we review selected examples of such interactions from bacteria, phytoplankton, larvae, and zooplankton. We hope that this article will serve as a blueprint for a more in-depth consideration of the effects of flow in the biology of microorganisms and that this discussion will stimulate further multidisciplinary effort in understanding this important component of microorganism habitats.
Assuntos
Fenômenos Fisiológicos Bacterianos , Fenômenos Biomecânicos , Plâncton/fisiologia , Microbiologia da Água , Animais , Biofilmes , Invertebrados/crescimento & desenvolvimento , Invertebrados/fisiologia , Percepção de QuorumRESUMO
Severe changes in the environmental redox potential, and resulting alterations in the oxidation states of intracellular metabolites and enzymes, have historically been considered negative stressors, requiring responses that are strictly defensive. However, recent work in diverse organisms has revealed that more subtle changes in the intracellular redox state can act as signals, eliciting responses with benefits beyond defense and detoxification. Changes in redox state have been shown to influence or trigger chromosome segregation, sporulation, aerotaxis, and social behaviors, including luminescence as well as biofilm establishment and dispersal. Connections between redox state and complex behavior allow bacteria to link developmental choices with metabolic state and coordinate appropriate responses. Promising future directions for this area of study include metabolomic analysis of species- and condition-dependent changes in metabolite oxidation states and elucidation of the mechanisms whereby the redox state influences circadian regulation.
Assuntos
Biofilmes/crescimento & desenvolvimento , Proteínas de Escherichia coli/metabolismo , Regulação Bacteriana da Expressão Gênica , Proteínas de Membrana/metabolismo , Proteínas Quinases/metabolismo , Proteínas Serina-Treonina Quinases/metabolismo , Esporos Bacterianos/metabolismo , Aliivibrio fischeri/genética , Aliivibrio fischeri/crescimento & desenvolvimento , Aliivibrio fischeri/metabolismo , Bacillus subtilis/genética , Bacillus subtilis/crescimento & desenvolvimento , Bacillus subtilis/metabolismo , Caulobacter crescentus/genética , Caulobacter crescentus/crescimento & desenvolvimento , Caulobacter crescentus/metabolismo , Escherichia coli/genética , Escherichia coli/crescimento & desenvolvimento , Escherichia coli/metabolismo , Proteínas de Escherichia coli/genética , Glutationa/metabolismo , Proteínas de Membrana/genética , Oxirredução , Proteínas Quinases/genética , Proteínas Serina-Treonina Quinases/genética , Pseudomonas aeruginosa/genética , Pseudomonas aeruginosa/crescimento & desenvolvimento , Pseudomonas aeruginosa/metabolismo , Transdução de Sinais , Esporos Bacterianos/genética , Esporos Bacterianos/crescimento & desenvolvimento , Streptomyces/genética , Streptomyces/crescimento & desenvolvimento , Streptomyces/metabolismoRESUMO
While chemical forms of cell-to-cell communication are well recognized to coordinate bacterial populations, electrical signaling has been relatively ignored. Humphries et al. show that Bacillus subtilis biofilms utilize potassium production to attract far away, motile cells of even phylogenetically distant species by altering their membrane potential.
Assuntos
Bacillus subtilis , BiofilmesRESUMO
Bacteria residing within biofilm communities can coordinate their behavior through cell-to-cell signaling. However, it remains unclear if these signals can also influence the behavior of distant cells that are not part of the community. Using a microfluidic approach, we find that potassium ion channel-mediated electrical signaling generated by a Bacillus subtilis biofilm can attract distant cells. Integration of experiments and mathematical modeling indicates that extracellular potassium emitted from the biofilm alters the membrane potential of distant cells, thereby directing their motility. This electrically mediated attraction appears to be a generic mechanism that enables cross-species interactions, as Pseudomonas aeruginosa cells also become attracted to the electrical signal released by the B. subtilis biofilm. Cells within a biofilm community can thus not only coordinate their own behavior but also influence the behavior of diverse bacteria at a distance through long-range electrical signaling. PAPERCLIP.
Assuntos
Bacillus subtilis/fisiologia , Biofilmes , Fenômenos Eletrofisiológicos , Pseudomonas aeruginosa/fisiologia , Biofilmes/classificação , Potenciais da Membrana , Técnicas Analíticas Microfluídicas , Modelos Biológicos , Potássio/metabolismoRESUMO
The role of electricity in biological systems was first appreciated through electrical stimulation experiments performed by Luigi Galvani in the 18th century. These pioneering experiments demonstrated that the behavior of living tissues is governed by the flow of electrochemical species-an insight that gave rise to the modern field of electrophysiology. Since then, electrophysiology has largely remained a bastion of neuroscience. However, exciting recent developments have demonstrated that even simple bacteria residing in communities use electrochemical communication to coordinate population-level behaviors. These recent works are defining the emerging field of bacterial biofilm electrophysiology. To view this SnapShot, open or download the PDF.
Assuntos
Biofilmes , Bactérias/classificação , Bactérias/metabolismo , Fenômenos Fisiológicos Bacterianos , Fenômenos EletrofisiológicosRESUMO
In the wild, bacteria are predominantly associated with surfaces as opposed to existing as free-swimming, isolated organisms. They are thus subject to surface-specific mechanics, including hydrodynamic forces, adhesive forces, the rheology of their surroundings, and transport rules that define their encounters with nutrients and signaling molecules. Here, we highlight the effects of mechanics on bacterial behaviors on surfaces at multiple length scales, from single bacteria to the development of multicellular bacterial communities such as biofilms.
Assuntos
Escherichia coli/fisiologia , Pseudomonas aeruginosa/fisiologia , Aderência Bacteriana , Biofilmes , Transporte Biológico , Fenômenos Biomecânicos , Escherichia coli/citologia , Locomoção , Pseudomonas aeruginosa/citologiaRESUMO
When transcription regulatory networks are compared among distantly related eukaryotes, a number of striking similarities are observed: a larger-than-expected number of genes, extensive overlapping connections, and an apparently high degree of functional redundancy. It is often assumed that the complexity of these networks represents optimized solutions, precisely sculpted by natural selection; their common features are often asserted to be adaptive. Here, we discuss support for an alternative hypothesis: the common structural features of transcription networks arise from evolutionary trajectories of "least resistance"--that is, the relative ease with which certain types of network structures are formed during their evolution.
Assuntos
Evolução Biológica , Redes Reguladoras de Genes , Animais , Biofilmes , Células-Tronco Embrionárias , Fungos/classificação , Fungos/genética , Fungos/metabolismo , Regulação da Expressão Gênica , Plantas/classificação , Plantas/genética , Plantas/metabolismoRESUMO
Changes in the gut microbiome have pivotal roles in the pathogenesis of acute graft-versus-host disease (aGVHD) after allogenic haematopoietic cell transplantation (allo-HCT)1-6. However, effective methods for safely resolving gut dysbiosis have not yet been established. An expansion of the pathogen Enterococcus faecalis in the intestine, associated with dysbiosis, has been shown to be a risk factor for aGVHD7-10. Here we analyse the intestinal microbiome of patients with allo-HCT, and find that E. faecalis escapes elimination and proliferates in the intestine by forming biofilms, rather than by acquiring drug-resistance genes. We isolated cytolysin-positive highly pathogenic E. faecalis from faecal samples and identified an anti-E. faecalis enzyme derived from E. faecalis-specific bacteriophages by analysing bacterial whole-genome sequencing data. The antibacterial enzyme had lytic activity against the biofilm of E. faecalis in vitro and in vivo. Furthermore, in aGVHD-induced gnotobiotic mice that were colonized with E. faecalis or with patient faecal samples characterized by the domination of Enterococcus, levels of intestinal cytolysin-positive E. faecalis were decreased and survival was significantly increased in the group that was treated with the E. faecalis-specific enzyme, compared with controls. Thus, administration of a phage-derived antibacterial enzyme that is specific to biofilm-forming pathogenic E. faecalis-which is difficult to eliminate with existing antibiotics-might provide an approach to protect against aGVHD.
Assuntos
Bacteriófagos , Enterococcus faecalis , Microbioma Gastrointestinal , Doença Enxerto-Hospedeiro , Adulto , Idoso , Animais , Feminino , Humanos , Masculino , Camundongos , Pessoa de Meia-Idade , Adulto Jovem , Bacteriófagos/enzimologia , Bacteriófagos/genética , Biofilmes/efeitos dos fármacos , Biofilmes/crescimento & desenvolvimento , Disbiose/complicações , Disbiose/microbiologia , Enterococcus faecalis/efeitos dos fármacos , Enterococcus faecalis/genética , Enterococcus faecalis/crescimento & desenvolvimento , Enterococcus faecalis/metabolismo , Enterococcus faecalis/virologia , Fezes/microbiologia , Vida Livre de Germes , Doença Enxerto-Hospedeiro/complicações , Doença Enxerto-Hospedeiro/microbiologia , Doença Enxerto-Hospedeiro/prevenção & controle , Doença Enxerto-Hospedeiro/terapia , Transplante de Células-Tronco Hematopoéticas/efeitos adversos , Técnicas In Vitro , Intestinos/efeitos dos fármacos , Intestinos/microbiologia , Perforina/metabolismo , Fatores de Risco , Transplante Homólogo/efeitos adversos , Sequenciamento Completo do Genoma , Farmacorresistência Bacteriana/efeitos dos fármacos , Antibacterianos/farmacologiaRESUMO
Formation of Bacillus subtilis biofilms, consisting of cells encapsulated within an extracellular matrix of exopolysaccharide and protein, requires the polyamine spermidine. A recent study reported that (1) related polyamine norspermidine is synthesized by B. subtilis using the equivalent of the Vibrio cholerae biosynthetic pathway, (2) exogenous norspermidine at 25 µM prevents B. subtilis biofilm formation, (3) endogenous norspermidine is present in biofilms at 50-80 µM, and (4) norspermidine prevents biofilm formation by condensing biofilm exopolysaccharide. In contrast, we find that, at concentrations up to 200 µM, exogenous norspermidine promotes biofilm formation. We find that norspermidine is absent in wild-type B. subtilis biofilms at all stages, and higher concentrations of exogenous norspermidine eventually inhibit planktonic growth and biofilm formation in an exopolysaccharide-independent manner. Moreover, orthologs of the V. cholerae norspermidine biosynthetic pathway are absent from B. subtilis, confirming that norspermidine is not physiologically relevant to biofilm function in this species.
Assuntos
Bacillus subtilis/fisiologia , Biofilmes/crescimento & desenvolvimento , Espermidina/análogos & derivados , Sequência de Aminoácidos , Bacillus subtilis/crescimento & desenvolvimento , Dados de Sequência Molecular , Plâncton/crescimento & desenvolvimento , Alinhamento de Sequência , Espermidina/biossíntese , Espermidina/metabolismo , Espermidina/fisiologia , Vibrio cholerae/fisiologia , Ácido gama-Aminobutírico/metabolismoRESUMO
Tractable microbial communities are needed to bridge the gap between observations of patterns of microbial diversity and mechanisms that can explain these patterns. We developed cheese rinds as model microbial communities by characterizing in situ patterns of diversity and by developing an in vitro system for community reconstruction. Sequencing of 137 different rind communities across 10 countries revealed 24 widely distributed and culturable genera of bacteria and fungi as dominant community members. Reproducible community types formed independent of geographic location of production. Intensive temporal sampling demonstrated that assembly of these communities is highly reproducible. Patterns of community composition and succession observed in situ can be recapitulated in a simple in vitro system. Widespread positive and negative interactions were identified between bacterial and fungal community members. Cheese rind microbial communities represent an experimentally tractable system for defining mechanisms that influence microbial community assembly and function.