scholarly journals Biofilms Comprise a Component of the Annual Cycle ofVibrio choleraein the Bay of Bengal Estuary

mBio ◽  
2018 ◽  
Vol 9 (2) ◽  
pp. e00483-18 ◽  
Author(s):  
Marzia Sultana ◽  
Suraia Nusrin ◽  
Nur A. Hasan ◽  
Abdus Sadique ◽  
Kabir U. Ahmed ◽  
...  
Keyword(s):  
Life Cycle ◽  
Vibrio Cholerae ◽  
Causative Agent ◽  
Aquatic Environment ◽  
Morphological Changes ◽  
Living Cells ◽  
Estuarine Environment ◽  
Annual Life Cycle ◽  
Free Living ◽  
Content Type

ABSTRACTVibrio cholerae, an estuarine bacterium, is the causative agent of cholera, a severe diarrheal disease that demonstrates seasonal incidence in Bangladesh. In an extensive study ofV. choleraeoccurrence in a natural aquatic environment, water and plankton samples were collected biweekly between December 2005 and November 2006 from Mathbaria, an estuarine village of Bangladesh near the mangrove forests of the Sundarbans. ToxigenicV. choleraeexhibited two seasonal growth peaks, one in spring (March to May) and another in autumn (September to November), corresponding to the two annual seasonal outbreaks of cholera in this region. The total numbers of bacteria determined by heterotrophic plate count (HPC), representing culturable bacteria, accounted for 1% to 2.7% of the total numbers obtained using acridine orange direct counting (AODC). The highest bacterial culture counts, including toxigenicV. cholerae, were recorded in the spring. The direct fluorescent antibody (DFA) assay was used to detectV. choleraeO1 cells throughout the year, as free-living cells, within clusters, or in association with plankton.V. choleraeO1 varied significantly in morphology, appearing as distinctly rod-shaped cells in the spring months, while small coccoid cells within thick clusters of biofilm were observed during interepidemic periods of the year, notably during the winter months. ToxigenicV. choleraeO1 was culturable in natural water during the spring when the temperature rose sharply. The results of this study confirmed biofilms to be a means of persistence for bacteria and an integral component of the annual life cycle of toxigenicV. choleraein the estuarine environment of Bangladesh.IMPORTANCEVibrio cholerae, the causative agent of cholera, is autochthonous in the estuarine aquatic environment. This study describes morphological changes in naturally occurringV. choleraeO1 in the estuarine environment of Mathbaria, where the bacterium is culturable when the water temperature rises and is observable predominantly as distinct rods and dividing cells. In the spring and fall, these morphological changes coincide with the two seasonal peaks of endemic cholera in Bangladesh.V. choleraeO1 cells are predominantly coccoid within biofilms but are rod shaped as free-living cells and when attached to plankton or to particulate matter in interepidemic periods of the year. It is concluded that biofilms represent a stage of the annual life cycle ofV. choleraeO1, the causative agent of cholera in Bangladesh.

scholarly journals Identification of Fis1 Interactors in Toxoplasma gondii Reveals a Novel Protein Required for Peripheral Distribution of the Mitochondrion

mBio ◽  
2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Kylie Jacobs ◽  
Robert Charvat ◽  
Gustavo Arrizabalaga
Keyword(s):  
Life Cycle ◽  
Toxoplasma Gondii ◽  
Morphological Changes ◽  
Dominant Negative Effect ◽  
Mitochondrial Outer Membrane ◽  
Mitochondrial Morphology ◽  
Content Type ◽  
Membrane Contact Sites ◽  
Intracellular Parasites ◽  
Single Mitochondrion

ABSTRACT Toxoplasma gondii’s single mitochondrion is very dynamic and undergoes morphological changes throughout the parasite’s life cycle. During parasite division, the mitochondrion elongates, enters the daughter cells just prior to cytokinesis, and undergoes fission. Extensive morphological changes also occur as the parasite transitions from the intracellular environment to the extracellular environment. We show that treatment with the ionophore monensin causes reversible constriction of the mitochondrial outer membrane and that this effect depends on the function of the fission-related protein Fis1. We also observed that mislocalization of the endogenous Fis1 causes a dominant-negative effect that affects the morphology of the mitochondrion. As this suggests that Fis1 interacts with proteins critical for maintenance of mitochondrial structure, we performed various protein interaction trap screens. In this manner, we identified a novel outer mitochondrial membrane protein, LMF1, which is essential for positioning of the mitochondrion in intracellular parasites. Normally, while inside a host cell, the parasite mitochondrion is maintained in a lasso shape that stretches around the parasite periphery where it has regions of coupling with the parasite pellicle, suggesting the presence of membrane contact sites. In intracellular parasites lacking LMF1, the mitochondrion is retracted away from the pellicle and instead is collapsed, as normally seen only in extracellular parasites. We show that this phenotype is associated with defects in parasite fitness and mitochondrial segregation. Thus, LMF1 is necessary for mitochondrial association with the parasite pellicle during intracellular growth, and proper mitochondrial morphology is a prerequisite for mitochondrial division. IMPORTANCE Toxoplasma gondii is an opportunistic pathogen that can cause devastating tissue damage in the immunocompromised and congenitally infected. Current therapies are not effective against all life stages of the parasite, and many cause toxic effects. The single mitochondrion of this parasite is a validated drug target, and it changes its shape throughout its life cycle. When the parasite is inside a cell, the mitochondrion adopts a lasso shape that lies in close proximity to the pellicle. The functional significance of this morphology is not understood and the proteins involved are currently not known. We have identified a protein that is required for proper mitochondrial positioning at the periphery and that likely plays a role in tethering this organelle. Loss of this protein results in dramatic changes to the mitochondrial morphology and significant parasite division and propagation defects. Our results give important insight into the molecular mechanisms regulating mitochondrial morphology.

scholarly journals Dynamics of Chromosome Replication and Its Relationship to Predatory Attack Lifestyles inBdellovibrio bacteriovorus

2019 ◽  
Vol 85 (14) ◽  
Author(s):  
Łukasz Makowski ◽  
Damian Trojanowski ◽  
Rob Till ◽  
Carey Lambert ◽  
Rebecca Lowry ◽  
...  
Keyword(s):  
Life Cycle ◽  
Subcellular Localization ◽  
Bacterial Infections ◽  
Chromosome Replication ◽  
Free Living ◽  
Gram Negative ◽  
Content Type ◽  
Reproductive Phase ◽  
Attack Phase ◽  
Two Phases

ABSTRACTBdellovibrio bacteriovorusis a small Gram-negative, obligate predatory bacterium that is largely found in wet, aerobic environments (e.g., soil). This bacterium attacks and invades other Gram-negative bacteria, including animal and plant pathogens. The intriguing life cycle ofB. bacteriovorusconsists of two phases: a free-living nonreplicative attack phase, in which the predatory bacterium searches for its prey, and a reproductive phase, in whichB. bacteriovorusdegrades a host’s macromolecules and reuses them for its own growth and chromosome replication. Although the cell biology of this predatory bacterium has gained considerable interest in recent years, we know almost nothing about the dynamics of its chromosome replication. Here, we performed a real-time investigation into the subcellular localization of the replisome(s) in single cells ofB. bacteriovorus. Our results show that inB. bacteriovorus, chromosome replication takes place only during the reproductive phase and exhibits a novel spatiotemporal arrangement of replisomes. The replication process starts at the invasive pole of the predatory bacterium inside the prey cell and proceeds until several copies of the chromosome have been completely synthesized. Chromosome replication is not coincident with the predator cell division, and it terminates shortly before synchronous predator filament septation occurs. In addition, we demonstrate that if thisB. bacteriovoruslife cycle fails in some cells ofEscherichia coli, they can instead use second prey cells to complete their life cycle.IMPORTANCENew strategies are needed to combat multidrug-resistant bacterial infections. Application of the predatory bacteriumBdellovibrio bacteriovorus, which kills other bacteria, including pathogens, is considered promising for combating bacterial infections. TheB. bacteriovoruslife cycle consists of two phases, a free-living, invasive attack phase and an intracellular reproductive phase, in which this predatory bacterium degrades the host’s macromolecules and reuses them for its own growth. To understand the use ofB. bacteriovorusas a “living antibiotic,” it is first necessary to dissect its life cycle, including chromosome replication. Here, we present a real-time investigation into subcellular localization of chromosome replication in a single cell ofB. bacteriovorus. This process initiates at the invasion pole ofB. bacteriovorusand proceeds until several copies of the chromosome have been completely synthesized. Interestingly, we demonstrate that some cells ofB. bacteriovorusrequire two prey cells sequentially to complete their life cycle.

scholarly journals Phobalysin, a Small β-Pore-Forming Toxin of Photobacterium damselae subsp. damselae

2015 ◽  
Vol 83 (11) ◽  
pp. 4335-4348 ◽  
Author(s):  
Amable J. Rivas ◽  
Gisela von Hoven ◽  
Claudia Neukirch ◽  
Martina Meyenburg ◽  
Qianqian Qin ◽  
...  
Keyword(s):  
Lactate Dehydrogenase ◽  
Epithelial Cells ◽  
Necrotizing Fasciitis ◽  
Vibrio Cholerae ◽  
Gene Product ◽  
Morphological Changes ◽  
Marine Animals ◽  
Content Type ◽  
Membrane Pores ◽  
Photobacterium Damselae

ABSTRACTPhotobacterium damselaesubsp.damselae, an important pathogen of marine animals, may also cause septicemia or hyperaggressive necrotizing fasciitis in humans. We previously showed that hemolysin genes are critical for virulence of this organism in mice and fish. In the present study, we characterized thehlyAgene product, a putative small β-pore-forming toxin, and termed it phobalysin P (PhlyP), for “photobacterial lysin encoded on a plasmid.” PhlyP formed stable oligomers and small membrane pores, causing efflux of K+, with no significant leakage of lactate dehydrogenase but entry of vital dyes. The latter feature distinguished PhlyP from the relatedVibrio choleraecytolysin. Attack by PhlyP provoked a loss of cellular ATP, attenuated translation, and caused profound morphological changes in epithelial cells. In coculture experiments with epithelial cells,Photobacterium damselaesubsp.damselaeled to rapid hemolysin-dependent membrane permeabilization. Unexpectedly, hemolysins also promoted the association ofP. damselaesubsp.damselaewith epithelial cells. The collective observations of this study suggest that membrane-damaging toxins commonly enhance bacterial adherence.

scholarly journals Vibriophages Differentially Influence Biofilm Formation by Vibrio anguillarum Strains

2015 ◽  
Vol 81 (13) ◽  
pp. 4489-4497 ◽  
Author(s):  
Demeng Tan ◽  
Amalie Dahl ◽  
Mathias Middelboe
Keyword(s):  
Biofilm Formation ◽  
Vibrio Anguillarum ◽  
Living Cells ◽  
Phage Infection ◽  
Host Cells ◽  
Free Living ◽  
Marine Aquaculture ◽  
Content Type ◽  
Host Interactions ◽  
Biofilm Development

ABSTRACTVibrio anguillarumis an important pathogen in marine aquaculture, responsible for vibriosis. Bacteriophages can potentially be used to control bacterial pathogens; however, successful application of phages requires a detailed understanding of phage-host interactions under both free-living and surface-associated growth conditions. In this study, we exploredin vitrophage-host interactions in two different strains ofV. anguillarum(BA35 and PF430-3) during growth in microcolonies, biofilms, and free-living cells. Two vibriophages, ΦH20 (Siphoviridae) and KVP40 (Myoviridae), had completely different effects on the biofilm development. Addition of phage ΦH20 to strain BA35 showed efficient control of biofilm formation and density of free-living cells. The interactions between BA35 and ΦH20 were thus characterized by a strong phage control of the phage-sensitive population and subsequent selection for phage-resistant mutants. Addition of phage KVP40 to strain PF430-3 resulted in increased biofilm development, especially during the early stage. Subsequent experiments in liquid cultures showed that addition of phage KVP40 stimulated the aggregation of host cells, which protected the cells against phage infection. By the formation of biofilms, strain PF430-3 created spatial refuges that protected the host from phage infection and allowed coexistence between phage-sensitive cells and lytic phage KVP40. Together, the results demonstrate highly variable phage protection mechanisms in two closely relatedV. anguillarumstrains, thus emphasizing the challenges of using phages to control vibriosis in aquaculture and adding to the complex roles of phages as drivers of prokaryotic diversity and population dynamics.

scholarly journals Genes Activated byVibrio choleraeupon Exposure toCaenorhabditis elegansReveal the Mannose-Sensitive Hemagglutinin To Be Essential for Colonization

mSphere ◽  
2018 ◽  
Vol 3 (3) ◽  
Author(s):  
Cornelia List ◽  
Andreas Grutsch ◽  
Claudia Radler ◽  
Fatih Cakar ◽  
Franz G. Zingl ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Vibrio Cholerae ◽  
Developmental Delay ◽  
Growth Retardation ◽  
Aquatic Environment ◽  
Diarrheal Disease ◽  
Phenotypic Characterization ◽  
Human Pathogen ◽  
Content Type ◽  
Human Host

ABSTRACTDuring its life cycle, the facultative human pathogenVibrio cholerae, which is the causative agent of the diarrheal disease cholera, needs to adapt to a variety of different conditions, such as the human host or the aquatic environment. Importantly, cholera infections originate from the aquatic reservoir whereV. choleraepersists between the outbreaks. In the aquatic environment, bacteria are constantly threatened by predatory protozoa and nematodes, but our knowledge of the response pathways and adaptation strategies ofV. choleraeto such stressors is limited. Using a temporally controlled reporter system of transcription, we identified more than 100 genes ofV. choleraeinduced upon exposure to the nematodeCaenorhabditis elegans, which emerged recently as a valuable model for environmental predation during the aquatic lifestyle ofV. cholerae. Besides others, we identified and validated the genes encoding the mannose-sensitive hemagglutinin (MSHA) type IV pilus to be significantly induced upon exposure to the nematode. Subsequent analyses demonstrated that the mannose-sensitive hemagglutinin is crucial for attachment ofV. choleraein the pharynx of the worm and initiation of colonization, which results in growth retardation and developmental delay ofC. elegans. Thus, the surface adhesion factor MSHA could be linked to a fitness advantage ofV. choleraeupon contact with bacterium-grazing nematodes.IMPORTANCEThe waterborne diarrheal disease cholera is caused by the bacteriumVibrio cholerae. The facultative human pathogen persists as a natural inhabitant in the aquatic ecosystem between outbreaks. In contrast to the human host,V. choleraerequires a different set of genes to survive in this hostile environment. For example, predatory micrograzers are commonly found in the aquatic environment and use bacteria as a nutrient source, but knowledge of the interaction between bacterivorous grazers andV. choleraeis limited. In this study, we successfully adapted a genetic reporter technology and identified more than 100 genes activated byV. choleraeupon exposure to the bacterium-grazing nematodeCaenorhabditis elegans. This screen provides a first glimpse into responses and adaptational strategies of the bacterial pathogen against such natural predators. Subsequent phenotypic characterization revealed the mannose-sensitive hemagglutinin to be crucial for colonization of the worm, which causes developmental delay and growth retardation.

scholarly journals NtrC Adds a New Node to the Complex Regulatory Network of Biofilm Formation andvpsExpression inVibrio cholerae

2018 ◽  
Vol 200 (15) ◽  
Author(s):  
Andrew T. Cheng ◽  
David Zamorano-Sánchez ◽  
Jennifer K. Teschler ◽  
Daniel Wu ◽  
Fitnat H. Yildiz
Keyword(s):  
Life Cycle ◽  
Vibrio Cholerae ◽  
Biofilm Formation ◽  
Nitrogen Availability ◽  
Nitrogen Sources ◽  
Growth Mode ◽  
Biofilm Growth ◽  
Content Type ◽  
Regulatory Systems

ABSTRACTThe biofilm growth mode is important in both the intestinal and environmental phases of theVibrio choleraelife cycle. Regulation of biofilm formation involves several transcriptional regulators and alternative sigma factors. One such factor is the alternative sigma factor RpoN, which positively regulates biofilm formation. RpoN requires bacterial enhancer-binding proteins (bEBPs) to initiate transcription. TheV. choleraegenome encodes seven bEBPs (LuxO, VC1522, VC1926 [DctD-1], FlrC, NtrC, VCA0142 [DctD-2], and PgtA) that belong to the NtrC family of response regulators (RRs) of two-component regulatory systems. The contribution of these regulators to biofilm formation is not well understood. In this study, we analyzed biofilm formation and the regulation ofvpsLexpression by RpoN activators. Mutants lacking NtrC had increased biofilm formation andvpsLexpression. NtrC negatively regulates the expression of core regulators of biofilm formation (vpsR,vpsT, andhapR). NtrC fromV. choleraesupported growth and activatedglnAexpression when nitrogen availability was limited. However, the repressive activity of NtrC towardvpsLexpression was not affected by the nitrogen sources present. This study unveils the role of NtrC as a regulator ofvpsexpression and biofilm formation inV. cholerae.IMPORTANCEBiofilms play an important role in theVibrio choleraelife cycle, contributing to both environmental survival and transmission to a human host. Identifying key regulators ofV. choleraebiofilm formation is necessary to fully understand how this important growth mode is modulated in response to various signals encountered in the environment and the host. In this study, we characterized the role of RRs that function as coactivators of RpoN in regulating biofilm formation and identified new components in theV. choleraebiofilm regulatory circuitry.

scholarly journals Identification of Small Molecule Inhibitors of the Pathogen Box against Vibrio cholerae

2021 ◽  
Vol 9 (3) ◽  
Author(s):  
Haeun Kim ◽  
Brianne J. Burkinshaw ◽  
Linh G. Lam ◽  
Kevin Manera ◽  
Tao G. Dong
Keyword(s):  
Public Health ◽  
Infectious Disease ◽  
Antibiotic Resistance ◽  
Vibrio Cholerae ◽  
Small Molecule ◽  
Causative Agent ◽  
Treatment Strategies ◽  
Current Treatment ◽  
Content Type ◽  
Tropical Regions

Cholera is a serious infectious disease in tropical regions causing millions of infections annually. Vibrio cholerae , the causative agent of cholera, has gained multi-antibiotic resistance over the years, posing greater threat to public health and current treatment strategies. Here we report two compounds that effectively target the growth of V. cholerae and have the potential to control cholera infection.

scholarly journals The Histone-Like Nucleoid Structuring Protein (H-NS) Is a Repressor of Vibrio cholerae Exopolysaccharide Biosynthesis (vps) Genes

2012 ◽  
Vol 78 (7) ◽  
pp. 2482-2488 ◽  
Author(s):  
Hongxia Wang ◽  
Julio C. Ayala ◽  
Anisia J. Silva ◽  
Jorge A. Benitez
Keyword(s):  
Vibrio Cholerae ◽  
Disease Transmission ◽  
Aquatic Environment ◽  
Biofilm Formation ◽  
Content Type ◽  
Exopolysaccharide Biosynthesis

ABSTRACTThe capacity ofVibrio choleraeto form biofilms has been shown to enhance its survival in the aquatic environment and play important roles in pathogenesis and disease transmission. In this study, we demonstrated that the histone-like nucleoid structuring protein is a repressor of exopolysaccharide (vps) biosynthesis genes and biofilm formation.

scholarly journals Response of Vibrio cholerae to Low-Temperature Shifts: CspV Regulation of Type VI Secretion, Biofilm Formation, and Association with Zooplankton

2016 ◽  
Vol 82 (14) ◽  
pp. 4441-4452 ◽  
Author(s):  
Loni Townsley ◽  
Marilou P. Sison Mangus ◽  
Sanjin Mehic ◽  
Fitnat H. Yildiz
Keyword(s):  
Low Temperature ◽  
Vibrio Cholerae ◽  
Causative Agent ◽  
Biofilm Formation ◽  
Cold Shock ◽  
Diarrheal Disease ◽  
Dependent Manner ◽  
Natural Habitats ◽  
Content Type ◽  
Type Vi Secretion

ABSTRACTThe ability to sense and adapt to temperature fluctuation is critical to the aquatic survival, transmission, and infectivity ofVibrio cholerae, the causative agent of the disease cholera. Little information is available on the physiological changes that occur whenV. choleraeexperiences temperature shifts. The genome-wide transcriptional profile ofV. choleraeupon a shift in human body temperature (37°C) to lower temperatures, 15°C and 25°C, which mimic those found in the aquatic environment, was determined. Differentially expressed genes included those involved in the cold shock response, biofilm formation, type VI secretion, and virulence. Analysis of a mutant lacking the cold shock genecspV, which was upregulated >50-fold upon a low-temperature shift, revealed that it regulates genes involved in biofilm formation and type VI secretion. CspV controls biofilm formation through modulation of the second messenger cyclic diguanylate and regulates type VI-mediated interspecies killing in a temperature-dependent manner. Furthermore, a strain lackingcspVhad significant defects for attachment and type VI-mediated killing on the surface of the aquatic crustaceanDaphnia magna. Collectively, these studies reveal thatcspVis a major regulator of the temperature downshift response and plays an important role in controlling cellular processes crucial to the infectious cycle ofV. cholerae.IMPORTANCELittle is known about how human pathogens respond and adapt to ever-changing parameters of natural habitats outside the human host and how environmental adaptation alters dissemination.Vibrio cholerae, the causative agent of the severe diarrheal disease cholera, experiences fluctuations in temperature in its natural aquatic habitats and during the infection process. Furthermore, temperature is a critical environmental signal governing the occurrence ofV. choleraeand cholera outbreaks. In this study, we showed thatV. choleraereprograms its transcriptome in response to fluctuations in temperature, which results in changes to biofilm formation and type VI secretion system activation. These processes in turn impact environmental survival and the virulence potential of this pathogen.

Modulation effects of hexamethylene bisacetamide on growth and differentiation of cultured human malignant glioma cells

1996 ◽  
Vol 84 (5) ◽  
pp. 831-838 ◽  
Author(s):  
Xiao-Nan Li ◽  
Zi-Wei Du ◽  
Qiang Huang
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Malignant Glioma ◽  
Culture Media ◽  
Morphological Changes ◽  
Control Group ◽  
Cell Cycle Distribution ◽  
Content Type ◽  
Hexamethylene Bisacetamide ◽  
Human Malignant Glioma

✓ The modulation effects of hexamethylene bisacetamide (HMBA), a differentiation-inducing agent, on growth and differentiation of cells from human malignant glioma cell line SHG-44 were studied. At cytostatic doses (2.5 mM, 5 mM, 7.5 mM, and 10 mM for 15 days), HMBA exerted a marked inhibitory effect on cell proliferation. Exposure to HMBA (5 mM and 10 mM for 12 days) also resulted in an accumulation of cells in G0/G1 phase and a decrease of cells in S phase as analyzed by flow cytometry. The reversible effects of 7.5 mM HMBA and 10 mM HMBA on cell proliferation and 10 mM HMBA on disruption of cell cycle distribution were observed when HMBA was removed from culture media on Day 6 and replaced with HMBA-free media. Colony-forming efficiency (CFE) in soft agar was remarkably decreased by HMBA (2.5 mM, 5 mM, 7.5 mM, and 10 mM for 14 days), and in 7.5 mM HMBA— and 10 mM HMBA—treated cells, the CFEs were reduced to 25% and 12.5%, respectively, of that in untreated cells. Cells treated with HMBA (5 mM and 10 mM for 15 days) remained tumorigenic in athymic nude mice, but the growth rates of the xenografts were much slower than those in the control group. The effects of HMBA on cell proliferation, cell cycle distribution, CFE, and growth of xenografts were dose dependent. A more mature phenotype was confirmed by the morphological changes from spindle shape to large polygonal stellate shape and remarkably elevated expression of glial fibrillary acidic protein in cells exposed to HMBA (5 mM, 10 mM for 15 days). Our results showed that a more differentiated phenotype with marked growth arrest was induced in SHG-44 cells by HMBA.

Sign in / Sign up

Export Citation Format

Share Document