scholarly journals Genome-Wide Evaluation of the Interplay between Caenorhabditis elegans and Yersinia pseudotuberculosis duringIn VivoBiofilm Formation

2014 ◽  
Vol 83 (1) ◽  
pp. 17-27 ◽  
Author(s):  
George W. P. Joshua ◽  
Steve Atkinson ◽  
Robert J. Goldstone ◽  
Hannah L. Patrick ◽  
Richard A. Stabler ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Biofilm Formation ◽  
Yersinia Pseudotuberculosis ◽  
Regulatory Gene ◽  
Transcriptomic Analysis ◽  
Wild Type ◽  
Content Type ◽  
C Elegans ◽  
Regulatory Cascade ◽  
Genome Wide

The formation of an incapacitating biofilm onCaenorhabditis elegansbyYersinia pseudotuberculosisrepresents a tractable model for investigating the genetic basis for host-pathogen interplay during the biofilm-mediated infection of a living surface. Previously we established a role for quorum sensing (QS) and the master motility regulator, FlhDC, in biofilm formation byY. pseudotuberculosisonC. elegans. To obtain further genome-wide insights, we used transcriptomic analysis to obtain comparative information onC. elegansin the presence and absence of biofilm and on wild-typeY. pseudotuberculosisandY. pseudotuberculosisQS mutants. Infection ofC. eleganswith the wild-typeY. pseudotuberculosisresulted in the differential regulation of numerous genes, including a distinct subset of nematode C-lectin (clec) and fatty acid desaturase (fat) genes. Evaluation of the correspondingC. elegansclec-49andfat-3deletion mutants showed delayed biofilm formation and abolished biofilm formation, respectively. Transcriptomic analysis ofY. pseudotuberculosisrevealed that genes located in both of the histidine utilization (hut) operons were upregulated in both QS andflhDCmutants. In addition, mutation of the regulatory genehutCresulted in the loss of biofilm, increased expression offlhDC, and enhanced swimming motility. These data are consistent with the existence of a regulatory cascade in which the Hut pathway links QS andflhDC. This work also indicates that biofilm formation byY. pseudotuberculosisonC. elegansis an interactive process during which the initial attachment/recognition ofYersiniato/byC. elegansis followed by bacterial growth and biofilm formation.

scholarly journals Temporal Transcriptomics of Gut Escherichia coli in Caenorhabditis elegans Models of Aging

2021 ◽  
Author(s):  
Joshua D. Brycki ◽  
Jeremy R. Chen See ◽  
Gillian R. Letson ◽  
Cade S. Emlet ◽  
Lavinia V. Unverdorben ◽  
...  
Keyword(s):  
Gene Expression ◽  
Escherichia Coli ◽  
Caenorhabditis Elegans ◽  
Life Span ◽  
Wild Type ◽  
Health Span ◽  
Content Type ◽  
C Elegans ◽  
Evolutionarily Conserved

Previous research has reported effects of the microbiome on health span and life span of Caenorhabditis elegans , including interactions with evolutionarily conserved pathways in humans. We build on this literature by reporting the gene expression of Escherichia coli OP50 in wild-type (N2) and three long-lived mutants of C. elegans .

scholarly journals Identification of gmhA, a Yersinia pestis Gene Required for Flea Blockage, by Using a Caenorhabditis elegans Biofilm System

2005 ◽  
Vol 73 (11) ◽  
pp. 7236-7242 ◽  
Author(s):  
Creg Darby ◽  
Sandya L. Ananth ◽  
Li Tan ◽  
B. Joseph Hinnebusch
Keyword(s):  
Caenorhabditis Elegans ◽  
Yersinia Pestis ◽  
Biofilm Formation ◽  
Yersinia Pseudotuberculosis ◽  
C Elegans ◽  
Transposon Insertion ◽  
Insertion Mutants ◽  
Random Screening

ABSTRACT Yersinia pestis, the cause of bubonic plague, blocks feeding by its vector, the flea. Recent evidence indicates that blockage is mediated by an in vivo biofilm. Y. pestis and the closely related Yersinia pseudotuberculosis also make biofilms on the cuticle of the nematode Caenorhabditis elegans, which block this laboratory animal's feeding. Random screening of Y. pseudotuberculosis transposon insertion mutants with a C. elegans biofilm assay identified gmhA as a gene required for normal biofilms. gmhA encodes phosphoheptose isomerase, an enzyme required for synthesis of heptose, a conserved component of lipopolysaccharide and lipooligosaccharide. A Y. pestis gmhA mutant was constructed and was severely defective for C. elegans biofilm formation and for flea blockage but only moderately defective in an in vitro biofilm assay. These results validate use of the C. elegans biofilm system to identify genes and pathways involved in Y. pestis flea blockage.

scholarly journals Pseudomonas brassicacearum Strain DF41 Kills Caenorhabditis elegans through Biofilm-Dependent and Biofilm-Independent Mechanisms

2016 ◽  
Vol 82 (23) ◽  
pp. 6889-6898 ◽  
Author(s):  
Munmun Nandi ◽  
Chrystal Berry ◽  
Ann Karen C. Brassinga ◽  
Mark F. Belmonte ◽  
W. G. Dilantha Fernando ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Biofilm Formation ◽  
Fungal Pathogens ◽  
Biocontrol Agent ◽  
Regulatory System ◽  
Xenorhabdus Nematophila ◽  
Content Type ◽  
C Elegans ◽  
Pathogen Control ◽  
Pseudomonas Brassicacearum

ABSTRACTPseudomonas brassicacearumDF41 is a biocontrol agent that suppresses disease caused by the fungal pathogenSclerotinia sclerotiorum. A number of exometabolites are produced by DF41, including the lipopeptide sclerosin, hydrogen cyanide (HCN), and degradative enzymes. The production of these compounds is controlled at both the transcriptional and posttranscriptional levels by quorum sensing (QS) and the Gac two-component regulatory system. In order to be successful, a biocontrol agent must persist in the environment at levels sufficient for pathogen control. Bacterivorous predators, including nematodes, represent a challenge to the establishment of introduced microorganisms. In the current study, DF41 was investigated for its ability to resist predation byCaenorhabditis elegans. We discovered that this bacterium is capable of killingC. elegansthrough two different mechanisms: the first involves exposure to toxic metabolites, and the second entails biofilm formation on the nematode head blocking the buccal cavity. Biofilm formation on nematodes, which has been reported only forYersiniaspp. andXenorhabdus nematophila, is dependent upon the Gac system. Biofilms were not observed when bacteria were grown on NaCl-containing medium or onC. elegansbiofilm-resistant mutants. Coculturing with nematodes led to the increased expression of thepdfRI-rfiAQS genes andhcnA, which is under QS control. HCN was the most nematicidal of the exometabolites, suggesting that this bacterium can respond to predator cues and upregulate expression of toxins accordingly. In summary, DF41 is able to respond to the presence ofC. elegans, and through two distinct mechanisms, it can escape predation.IMPORTANCEPseudomonas brassicacearumDF41 can suppress fungal pathogens through a process known as biocontrol. To be successful, a biocontrol agent must be able to persist in the environment at levels sufficient for pathogen control. Predators, including the nematodeCaenorhabditis elegans, represent a threat to persistence. The aim of the current study was to investigate the DF41-C. elegansinteraction. We discovered that DF41 is able to escape predation through two distinct mechanisms. The first involves exposure to toxic bacterial metabolites, and the second entails the formation of a sticky coating on the nematode head, called a biofilm, which blocks feeding and causes starvation. We report here a pseudomonad forming biofilms on theC. eleganssurface. When grown withC. elegans, DF41 exhibits altered gene expression and metabolite production, indicating that this bacterium can sense the presence of these predators and adjust its physiology accordingly.

scholarly journals Competition and Resilience between Founder and Introduced Bacteria in the Caenorhabditis elegans Gut

2011 ◽  
Vol 80 (3) ◽  
pp. 1288-1299 ◽  
Author(s):  
Cynthia Portal-Celhay ◽  
Martin J. Blaser
Keyword(s):  
Caenorhabditis Elegans ◽  
Wild Type ◽  
Content Type ◽  
E Coli ◽  
C Elegans ◽  
Serovar Typhimurium ◽  
Colonization Factors

The microbial communities that reside within the intestinal tract in vertebrates are complex and dynamic. In this report, we establish the utility ofCaenorhabditis elegansas a model system for identifying the factors that contribute to bacterial persistence and for host control of gut luminal populations. We found that for N2 worms grown on mixed lawns of bacteria,Salmonella entericaserovar Typhimurium substantially outcompetedEscherichia coli, even whenE. coliwas initially present at 100-fold-higher concentrations. To address whether innate immunity affects the competition, thedaf-2anddaf-16mutants were studied; their total gut bacterial levels reflect overall capacity for colonization, butSalmonellaoutcompetedE. colito an extent similar to wild-type worms. To address the role of virulence properties,SalmonellaΔspi-1Δspi-2was used to compete withE. coli. The net differential was significantly less than that for wild-typeSalmonella; thus,spi-1 spi-2encodesC. eleganscolonization factors. AnE. colistrain with repeatedin vivopassage had an enhanced ability to compete against anin vitro-passedE. colistrain and againstSalmonella. Our data provide evidence of active competition for colonization niches in theC. elegansgut, as determined by bacterial factors and subject toin vivoselection.

scholarly journals Biofilm Formation Protects Escherichia coli against Killing by Caenorhabditis elegans and Myxococcus xanthus

2014 ◽  
Vol 80 (22) ◽  
pp. 7079-7087 ◽  
Author(s):  
William H. DePas ◽  
Adnan K. Syed ◽  
Margarita Sifuentes ◽  
John S. Lee ◽  
David Warshaw ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Caenorhabditis Elegans ◽  
Biofilm Formation ◽  
Myxococcus Xanthus ◽  
Enteric Bacteria ◽  
Content Type ◽  
E Coli ◽  
C Elegans ◽  
The Matrix ◽  
Nutritional Environment

ABSTRACTEnteric bacteria, such asEscherichia coli, are exposed to a variety of stresses in the nonhost environment. The development of biofilms providesE. coliwith resistance to environmental insults, such as desiccation and bleach. We found that biofilm formation, specifically production of the matrix components curli and cellulose, protectedE. coliagainst killing by the soil-dwelling nematodeCaenorhabditis elegansand the predatory bacteriumMyxococcus xanthus. Additionally, matrix-encased bacteria at the air-biofilm interface exhibited ∼40-fold-increased survival afterC. elegansandM. xanthuskilling compared to the non-matrix-encased cells that populate the interior of the biofilm. To determine if nonhostEnterobacteriaceaereservoirs supported biofilm formation, we grewE. colion media composed of pig dung or commonly contaminated foods, such as beef, chicken, and spinach. Each of these medium types provided a nutritional environment that supported matrix production and biofilm formation. Altogether, we showed that common, nonhost reservoirs ofE. colisupported the formation of biofilms that subsequently protectedE. coliagainst predation.

A Caenorhabditis elegans model of Yersinia infection: biofilm formation on a biotic surface

Microbiology ◽  
2003 ◽  
Vol 149 (11) ◽  
pp. 3221-3229 ◽  
Author(s):  
G. W. P. Joshua ◽  
A. V. Karlyshev ◽  
M. P. Smith ◽  
K. E. Isherwood ◽  
R. W. Titball ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Biofilm Formation ◽  
Yersinia Pseudotuberculosis ◽  
Model Organism ◽  
Severe Infection ◽  
Evolutionary Divergence ◽  
Control Mechanisms ◽  
C Elegans ◽  
Pathway Gene ◽  
Genes Encoding

To investigate Yersinia pathogenicity and the evolutionary divergence of the genus, the effect of pathogenic yersiniae on the model organism Caenorhabditis elegans was studied. Three strains of Yersinia pestis, including a strain lacking pMT1, caused blockage and death of C. elegans; one strain, lacking the haemin storage (hms) locus, caused no effect. Similarly, 15 strains of Yersinia enterocolitica caused no effect. Strains of Yersinia pseudotuberculosis showed different levels of pathogenicity. The majority of strains (76 %) caused no discernible effect; 5 % caused a weak infection, 9·5 % an intermediate infection, and 9·5 % a severe infection. There was no consistent relationship between serotype and severity of infection; nor was there any relationship between strains causing infection of C. elegans and those able to form a biofilm on an abiotic surface. Electron microscope and cytochemical examination of infected worms indicated that the infection phenotype is a result of biofilm formation on the head of the worm. Seven transposon mutants of Y. pseudotuberculosis strain YPIII pIB1 were completely or partially attenuated; mutated genes included genes encoding proteins involved in haemin storage and lipopolysaccharide biosynthesis. A screen of 15 defined C. elegans mutants identified four where mutation caused (complete) resistance to infection by Y. pseudotuberculosis YPIII pIB1. These mutants, srf-2, srf-3, srf-5 and the dauer pathway gene daf-1, also exhibit altered binding of lectins to the nematode surface. This suggests that biofilm formation on a biotic surface is an interactive process involving both bacterial and invertebrate control mechanisms.

The Effect of Mianserin on Lifespan of Caenorhabditis elegans is Abolished by Glucose

2021 ◽  
Vol 13 ◽  
Author(s):  
Abdullah Almotayri ◽  
Jency Thomas ◽  
Mihiri Munasinghe ◽  
Markandeya Jois
Keyword(s):  
Caenorhabditis Elegans ◽  
Scaffolding Protein ◽  
Lifespan Extension ◽  
Wild Type ◽  
E Coli ◽  
C Elegans ◽  
Risk Of Death ◽  
Increased Risk ◽  
Antidepressant Use ◽  
Extension Effect

Background: The antidepressant mianserin has been shown to extend the lifespan of Caenorhabditis elegans (C. elegans), a well-established model organism used in aging research. The extension of lifespan in C. elegans was shown to be dependent on increased expression of the scaffolding protein (ANK3/unc-44). In contrast, antidepressant use in humans is associated with an increased risk of death. The C. elegans in the laboratory are fed Escherichia coli (E. coli), a diet high in protein and low in carbohydrate, whereas a typical human diet is high in carbohydrates. We hypothesized that dietary carbohydrates might mitigate the lifespan-extension effect of mianserin. Objective: To investigate the effect of glucose added to the diet of C. elegans on the lifespan-extension effect of mianserin. Methods: Wild-type Bristol N2 and ANK3/unc-44 inactivating mutants were cultured on agar plates containing nematode growth medium and fed E. coli. Treatment groups included (C) control, (M50) 50 μM mianserin, (G) 73 mM glucose, and (M50G) 50 μM mianserin and 73 mM glucose. Lifespan was determined by monitoring the worms until they died. Statistical analysis was performed using the Kaplan-Meier version of the log-rank test. Results: Mianserin treatment resulted in a 12% increase in lifespan (P<0.05) of wild-type Bristol N2 worms but reduced lifespan by 6% in ANK3/unc-44 mutants, consistent with previous research. The addition of glucose to the diet reduced the lifespan of both strains of worms and abolished the lifespan-extension by mianserin. Conclusion: The addition of glucose to the diet of C. elegans abolishes the lifespan-extension effects of mianserin.

scholarly journals Sperm Competition in the Absence of Fertilization in Caenorhabditis elegans

Genetics ◽  
1999 ◽  
Vol 152 (1) ◽  
pp. 201-208 ◽  
Author(s):  
Andrew Singson ◽  
Katherine L Hill ◽  
Steven W L’Hernault
Keyword(s):  
Caenorhabditis Elegans ◽  
Sperm Competition ◽  
Sperm Function ◽  
Sperm Precedence ◽  
Wild Type ◽  
Nematode Caenorhabditis Elegans ◽  
C Elegans ◽  
Normal Sperm ◽  
Self Fertilization ◽  
Competition Assays

Abstract Hermaphrodite self-fertilization is the primary mode of reproduction in the nematode Caenorhabditis elegans. However, when a hermaphrodite is crossed with a male, nearly all of the oocytes are fertilized by male-derived sperm. This sperm precedence during reproduction is due to the competitive superiority of male-derived sperm and results in a functional suppression of hermaphrodite self-fertility. In this study, mutant males that inseminate fertilization-defective sperm were used to reveal that sperm competition within a hermaphrodite does not require successful fertilization. However, sperm competition does require normal sperm motility. Additionally, sperm competition is not an absolute process because oocytes not fertilized by male-derived sperm can sometimes be fertilized by hermaphrodite-derived sperm. These results indicate that outcrossed progeny result from a wild-type cross because male-derived sperm are competitively superior and hermaphrodite-derived sperm become unavailable to oocytes. The sperm competition assays described in this study will be useful in further classifying the large number of currently identified mutations that alter sperm function and development in C. elegans.

Streblus asper Lour. exerts MAPK and SKN-1 mediated anti-aging, anti-photoaging activities and imparts neuroprotection by ameliorating Aβ in Caenorhabditis elegans

2021 ◽  
pp. 1-17
Author(s):  
Mani Iyer Prasanth ◽  
James Michael Brimson ◽  
Dicson Sheeja Malar ◽  
Anchalee Prasansuklab ◽  
Tewin Tencomnao
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Stress Resistance ◽  
Vital Role ◽  
Transgenic Strain ◽  
Wild Type ◽  
Neuroprotective Effects ◽  
C Elegans ◽  
Streblus Asper

BACKGROUND: Streblus asper Lour., has been reported to have anti-aging and neuroprotective efficacies in vitro. OBJECTIVE: To analyze the anti-aging, anti-photoaging and neuroprotective efficacies of S. asper in Caenorhabditis elegans. METHODS: C. elegans (wild type and gene specific mutants) were treated with S. asper extract and analyzed for lifespan and other health benefits through physiological assays, fluorescence microscopy, qPCR and Western blot. RESULTS: The plant extract was found to increase the lifespan, reduce the accumulation of lipofuscin and modulate the expression of candidate genes. It could extend the lifespan of both daf-16 and daf-2 mutants whereas the pmk-1 mutant showed no effect. The activation of skn-1 was observed in skn-1::GFP transgenic strain and in qPCR expression. Further, the extract can extend the lifespan of UV-A exposed nematodes along with reducing ROS levels. Additionally, the extract also extends lifespan and reduces paralysis in Aβ transgenic strain, apart from reducing Aβ expression. CONCLUSIONS: S. asper was able to extend the lifespan and healthspan of C. elegans which was independent of DAF-16 pathway but dependent on SKN-1 and MAPK which could play a vital role in eliciting the anti-aging, anti-photoaging and neuroprotective effects, as the extract could impart oxidative stress resistance and neuroprotection.

scholarly journals Genetic, Behavioral and Environmental Determinants of Male Longevity in Caenorhabditis elegans

Genetics ◽  
2000 ◽  
Vol 154 (4) ◽  
pp. 1597-1610 ◽  
Author(s):  
David Gems ◽  
Donald L Riddle
Keyword(s):  
Caenorhabditis Elegans ◽  
Life Span ◽  
Wild Type ◽  
Neuronal Function ◽  
Nematode Caenorhabditis Elegans ◽  
Wild Isolate ◽  
Young Males ◽  
C Elegans ◽  
Single Sex ◽  
Solitary Males

Abstract Males of the nematode Caenorhabditis elegans are shorter lived than hermaphrodites when maintained in single-sex groups. We observed that groups of young males form clumps and that solitary males live longer, indicating that male-male interactions reduce life span. By contrast, grouped or isolated hermaphrodites exhibited the same longevity. In one wild isolate of C. elegans, AB2, there was evidence of copulation between males. Nine uncoordinated (unc) mutations were used to block clumping behavior. These mutations had little effect on hermaphrodite life span in most cases, yet many increased male longevity even beyond that of solitary wild-type males. In one case, the neuronal function mutant unc-64(e246), hermaphrodite life span was also increased by up to 60%. The longevity of unc-4(e120), unc-13(e51), and unc-32(e189) males exceeded that of hermaphrodites by 70–120%. This difference appears to reflect a difference in sex-specific life span potential revealed in the absence of male behavior that is detrimental to survival. The greater longevity of males appears not to be affected by daf-2, but is influenced by daf-16. In the absence of male-male interactions, median (but not maximum) male life span was variable. This variability was reduced when dead bacteria were used as food. Maintenance on dead bacteria extended both male and hermaphrodite longevity.

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