scholarly journals Behavioral Interactions between Bacterivorous Nematodes and Predatory Bacteria in a Synthetic Community

2021 ◽  
Vol 9 (7) ◽  
pp. 1362
Author(s):  
Nicola Mayrhofer ◽  
Gregory J. Velicer ◽  
Kaitlin A. Schaal ◽  
Marie Vasse
Keyword(s):  
Empirical Studies ◽  
Predatory Behavior ◽  
Trophic Levels ◽  
Apex Predators ◽  
Behavioral Interactions ◽  
E Coli ◽  
C Elegans ◽  
Predatory Bacteria ◽  
Ecological Importance ◽  
Microbial Food Chain

Theory and empirical studies in metazoans predict that apex predators should shape the behavior and ecology of mesopredators and prey at lower trophic levels. Despite the ecological importance of microbial communities, few studies of predatory microbes examine such behavioral res-ponses and the multiplicity of trophic interactions. Here, we sought to assemble a three-level microbial food chain and to test for behavioral interactions between the predatory nematode Caenorhabditis elegans and the predatory social bacterium Myxococcus xanthus when cultured together with two basal prey bacteria that both predators can eat—Escherichia coli and Flavobacterium johnsoniae. We found that >90% of C. elegans worms failed to interact with M. xanthus even when it was the only potential prey species available, whereas most worms were attracted to pure patches of E. coli and F. johnsoniae. In addition, M. xanthus altered nematode predatory behavior on basal prey, repelling C. elegans from two-species patches that would be attractive without M. xanthus, an effect similar to that of C. elegans pathogens. The nematode also influenced the behavior of the bacterial predator: M. xanthus increased its predatory swarming rate in response to C. elegans in a manner dependent both on basal-prey identity and on worm density. Our results suggest that M. xanthus is an unattractive prey for some soil nematodes and is actively avoided when other prey are available. Most broadly, we found that nematode and bacterial predators mutually influence one another’s predatory behavior, with likely consequences for coevolution within complex microbial food webs.

scholarly journals Behavioral interactions between bacterivorous nematodes and predatory bacteria in a synthetic community

2021 ◽  
Author(s):  
Nicola Mayrhofer ◽  
Gregory J. Velicer ◽  
Kaitlin A. Schaal ◽  
Marie Vasse
Keyword(s):  
Empirical Studies ◽  
Predatory Behavior ◽  
Trophic Levels ◽  
Apex Predators ◽  
Behavioral Interactions ◽  
E Coli ◽  
C Elegans ◽  
Predatory Bacteria ◽  
Ecological Importance ◽  
Microbial Food Chain

AbstractTheory and empirical studies in metazoans predict that apex predators should shape the behavior and ecology of mesopredators and prey at lower trophic levels. Despite the ecological importance of microbial communities, few studies of predatory microbes examine such behavioral responses and the multiplicity of trophic interactions. Here, we sought to assemble a three-level microbial food chain and to test for behavioral interactions between the predatory nematode Caenorhabditis elegans and the predatory social bacterium Myxococcus xanthus when cultured together with two basal prey bacteria that both predators can eat - Escherichia coli and Flavobacterium johnsoniae. We find that >90% of C. elegans worms failed to interact with M. xanthus even when it was the only potential prey species available, whereas most worms were attracted to pure patches of E. coli and F. johnsoniae. In addition, M. xanthus altered nematode predatory behavior on basal prey, repelling C. elegans from two-species patches that would be attractive without M. xanthus, an effect similar to that of C. elegans pathogens. The nematode also influenced the behavior of the bacterial predator: M. xanthus increased its predatory swarming rate in response to C. elegans in a manner dependent both on basal-prey identity and on worm density. Our results suggest that M. xanthus is an unattractive prey for some soil nematodes and is actively avoided when more lucrative prey are available. Most broadly, we find that nematode and bacterial predators mutually influence one another’s predatory behavior, with likely consequences for coevolution within complex microbial food webs.

scholarly journals A Novel Determination of the Relationship Between Exposure to Industrial Toxicant HFPO-DA and pqm-1-related Aging in C. elegans

2021 ◽  
Author(s):  
Vishruth Nagam
Keyword(s):  
Protein Interactions ◽  
Rna Extraction ◽  
Trophic Levels ◽  
Toxicant Exposure ◽  
E Coli ◽  
C Elegans ◽  
Dimer Acid ◽  
Treated Sample ◽  
Free Living Nematode ◽  
Hexafluoropropylene Oxide

Abstract Hexafluoropropylene oxide dimer acid (HFPO-DA, ammonium salt with trade name “GenX”) is an industrial toxicant that has recently been detected in the environment [1]. However, HFPO-DA’s potential aging-related effects on organisms of higher trophic levels, including worms and humans, have not been extensively explored. The purpose of this study is to quantify influences on C. elegans (free-living nematode) lifespan by HFPO-DA exposure, specifically via ingestion of food to simulate the mechanisms of toxicant exposure, through lower trophic-level organisms, commonly found in nature. C. elegans N2 (wild-type) samples were prepared with a uracil-based medium and E. coli OP50 (food source) at room temperature; C. elegans in the experimental, treated sample was fed E. coli OP50 incubated with 280 ng/L HFPO-DA. The target gene pqm-1 was selected due to its role in an evolutionarily conserved insulin signaling pathway and in promoting development. Molecular biology laboratory techniques (RNA extraction, qRT-PCR, fluorescence tagging, etc.) were used to quantify pqm-1 expression to yield four technical replicates for each sample. The data was analyzed through null hypothesis t-tests, heatmaps, protein interactions, and gene homology tools. HFPO-DA exposure through E. coli caused a statistically insignificant (0.811-fold) change in pqm-1-related aging in C. elegans. Future work includes investigating the effects of different levels of HFPO-DA exposure on C. elegans aging.

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 Iron Acquisition of Urinary Tract Infection Escherichia coli Involves Pathogenicity in Caenorhabditis elegans

2021 ◽  
Vol 9 (2) ◽  
pp. 310
Author(s):  
Masayuki Hashimoto ◽  
Yi-Fen Ma ◽  
Sin-Tian Wang ◽  
Chang-Shi Chen ◽  
Ching-Hao Teng
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Caenorhabditis Elegans ◽  
Large Scale ◽  
Iron Acquisition ◽  
Infection Model ◽  
High Throughput Analysis ◽  
E Coli ◽  
C Elegans ◽  
Tract Infections

Uropathogenic Escherichia coli (UPEC) is a major bacterial pathogen that causes urinary tract infections (UTIs). The mouse is an available UTI model for studying the pathogenicity; however, Caenorhabditis elegans represents as an alternative surrogate host with the capacity for high-throughput analysis. Then, we established a simple assay for a UPEC infection model with C. elegans for large-scale screening. A total of 133 clinically isolated E. coli strains, which included UTI-associated and fecal isolates, were applied to demonstrate the simple pathogenicity assay. From the screening, several virulence factors (VFs) involved with iron acquisition (chuA, fyuA, and irp2) were significantly associated with high pathogenicity. We then evaluated whether the VFs in UPEC were involved in the pathogenicity. Mutants of E. coli UTI89 with defective iron acquisition systems were applied to a solid killing assay with C. elegans. As a result, the survival rate of C. elegans fed with the mutants significantly increased compared to when fed with the parent strain. The results demonstrated, the simple assay with C. elegans was useful as a UPEC infectious model. To our knowledge, this is the first report of the involvement of iron acquisition in the pathogenicity of UPEC in a C. elegans model.

scholarly journals A Pathoadaptive Deletion in an Enteroaggregative Escherichia coli Outbreak Strain Enhances Virulence in a Caenorhabditis elegans Model

2010 ◽  
Vol 78 (9) ◽  
pp. 4068-4076 ◽  
Author(s):  
Jennifer Hwang ◽  
Lisa M. Mattei ◽  
Laura G. VanArendonk ◽  
Philip M. Meneely ◽  
Iruka N. Okeke
Keyword(s):  
Escherichia Coli ◽  
Caenorhabditis Elegans ◽  
Epithelial Cells ◽  
Genetic Material ◽  
Decarboxylase Activity ◽  
Multicopy Plasmid ◽  
Lysine Decarboxylase ◽  
Outbreak Strain ◽  
E Coli ◽  
C Elegans

ABSTRACT Enteroaggregative Escherichia coli (EAEC) strains are important diarrheal pathogens. EAEC strains are defined by their characteristic stacked-brick pattern of adherence to epithelial cells but show heterogeneous virulence and have different combinations of adhesin and toxin genes. Pathoadaptive deletions in the lysine decarboxylase (cad) genes have been noted among hypervirulent E. coli subtypes of Shigella and enterohemorrhagic E. coli. To test the hypothesis that cad deletions might account for heterogeneity in EAEC virulence, we developed a Caenorhabditis elegans pathogenesis model. Well-characterized EAEC strains were shown to colonize and kill C. elegans, and differences in virulence could be measured quantitatively. Of 49 EAEC strains screened for lysine decarboxylase activity, 3 tested negative. Most notable is isolate 101-1, which was recovered in Japan, from the largest documented EAEC outbreak. EAEC strain 101-1 was unable to decarboxylate lysine in vitro due to deletions in cadA and cadC, which, respectively, encode lysine decarboxylase and a transcriptional activator of the cadAB genes. Strain 101-1 was significantly more lethal to C. elegans than control strain OP50. Lethality was attenuated when the lysine decarboxylase defect was complemented from a multicopy plasmid and in single copy. In addition, restoring lysine decarboxylase function produced derivatives of 101-1 deficient in aggregative adherence to cultured human epithelial cells. Lysine decarboxylase inactivation is pathoadapative in an important EAEC outbreak strain, and deletion of cad genes could produce hypervirulent EAEC lineages in the future. These results suggest that loss, as well as gain, of genetic material can account for heterogeneous virulence among EAEC strains.

scholarly journals E. coli OxyS non-coding RNA does not trigger RNAi in C. elegans

2014 ◽  
Author(s):  
Alper Akay ◽  
Peter Sarkies ◽  
Eric Alexander Miska
Keyword(s):  
Small Rnas ◽  
Biological Function ◽  
Rapid Development ◽  
Rnai Pathway ◽  
Regulate Gene Expression ◽  
Double Stranded Rna ◽  
E Coli ◽  
C Elegans ◽  
Non Coding Rna ◽  
Rnai Response

The discovery of RNA interference (RNAi) in C. elegans has had a major impact on scientific research, led to the rapid development of RNAi tools and has inspired RNA-based therapeutics. Astonishingly, nematodes, planaria and many insects take up double-stranded RNA (dsRNA) from their environment to elicit RNAi; the biological function of this mechanism is unclear. Recently, the E. coli OxyS non-coding RNA was shown to regulate gene expression in C. elegans when E. coli is offered as food. This was surprising given that C. elegans is unlikely to encounter E. coli in nature. To directly test the hypothesis that the E. coli OxyS non-coding RNA triggers the C. elegans RNAi pathway, we sequenced small RNAs from C. elegans after feeding with bacteria. We clearly demonstrate that the OxyS non-coding RNA does not trigger an RNAi response in C. elegans. We conclude that the biology of environmental RNAi remains to be discovered.

scholarly journals Individual Variation in Predatory Behavior, Scavenging and Seasonal Prey Availability as Potential Drivers of Coexistence between Wolves and Bears

Diversity ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 356
Author(s):  
Andrés Ordiz ◽  
Cyril Milleret ◽  
Antonio Uzal ◽  
Barbara Zimmermann ◽  
Petter Wabakken ◽  
...  
Keyword(s):  
Prey Availability ◽  
Interspecific Interactions ◽  
Brown Bear ◽  
Predatory Behavior ◽  
Early Summer ◽  
Gray Wolf ◽  
Apex Predators ◽  
Main Prey ◽  
Large Carnivore ◽  
Age Class

Several large carnivore populations are recovering former ranges, and it is important to understand interspecific interactions between overlapping species. In Scandinavia, recent research has reported that brown bear presence influences gray wolf habitat selection and kill rates. Here, we characterized the temporal use of a common prey resource by sympatric wolves and bears and described individual and seasonal variation in their direct and/or indirect interactions. Most bear–wolf interactions were indirect, via bear scavenging of wolf kills. Bears used >50% of wolf kills, whereas we did not record any wolf visit at bear kills. Adult and subadult bears visited wolf kills, but female bears with cubs of the year, the most vulnerable age class to conspecifics and other predators, did not. Wolf and bear kill rates peaked in early summer, when both targeted neonate moose calves, which coincided with a reduction in bear scavenging rate. Some bears were highly predatory and some did not kill any calf. Individual and age-class variation (in bear predation and scavenging patterns) and seasonality (in bear scavenging patterns and main prey availability of both wolves and bears) could mediate coexistence of these apex predators. Similar processes likely occur in other ecosystems with varying carnivore assemblages.

scholarly journals Conditioning Protects C. elegans from Lethal Effects of Enteropathogenic E. coli by Activating Genes that Regulate Lifespan and Innate Immunity

2009 ◽  
Vol 5 (5) ◽  
pp. 450-462 ◽  
Author(s):  
Akwasi Anyanful ◽  
Kirk A. Easley ◽  
Guy M. Benian ◽  
Daniel Kalman
Keyword(s):  
Innate Immunity ◽  
Lethal Effects ◽  
E Coli ◽  
C Elegans

scholarly journals Giardia duodenalis-induced alterations of commensal bacteria killCaenorhabditis elegans: a new model to study microbial-microbial interactions in the gut

2015 ◽  
Vol 308 (6) ◽  
pp. G550-G561 ◽  
Author(s):  
Teklu K. Gerbaba ◽  
Pratyush Gupta ◽  
Kevin Rioux ◽  
Dave Hansen ◽  
Andre G. Buret
Keyword(s):  
Bacterial Colonization ◽  
Giardia Duodenalis ◽  
Microbial Interactions ◽  
Commensal Bacteria ◽  
In Vivo Model ◽  
Functional Changes ◽  
E Coli ◽  
C Elegans ◽  
Human Microbiota

Giardia duodenalis is the most common cause of parasitic diarrhea worldwide and a well-established risk factor for postinfectious irritable bowel syndrome. We hypothesized that Giardia-induced disruptions in host-microbiota interactions may play a role in the pathogenesis of giardiasis and in postgiardiasis disease. Functional changes induced by Giardia in commensal bacteria and the resulting effects on Caenorhabditis elegans were determined. Although Giardia or bacteria alone did not affect worm viability, combining commensal Escherichia coli bacteria with Giardia became lethal to C. elegans. Giardia also induced killing of C. elegans with attenuated Citrobacter rodentium espF and map mutant strains, human microbiota from a healthy donor, and microbiota from inflamed colonic sites of ulcerative colitis patient. In contrast, combinations of Giardia with microbiota from noninflamed sites of the same patient allowed for worm survival. The synergistic lethal effects of Giardia and E. coli required the presence of live bacteria and were associated with the facilitation of bacterial colonization in the C. elegans intestine. Exposure to C. elegans and/or Giardia altered the expression of 172 genes in E. coli. The genes affected by Giardia included hydrogen sulfide biosynthesis (HSB) genes, and deletion of a positive regulator of HSB genes, cysB, was sufficient to kill C. elegans even in the absence of Giardia. Our findings indicate that Giardia induces functional changes in commensal bacteria, possibly making them opportunistic pathogens, and alters host-microbe homeostatic interactions. This report describes the use of a novel in vivo model to assess the toxicity of human microbiota.

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