scholarly journals Stenotrophomonas strain CPCC 101271, an intestinal lifespan-prolonging bacterium for Caenorhabditis elegans that assists in host resistance to “Bacillus nematocida” colonization

2021 ◽  
Author(s):  
Rui Han ◽  
Yu Wang ◽  
Yang Deng ◽  
Yuqin Zhang ◽  
Lin Zhang ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Host Resistance ◽  
Intestinal Bacteria ◽  
Pathogenic Bacterium ◽  
Agricultural Pests ◽  
Natural Habitats ◽  
Metagenomic Sequence ◽  
C Elegans ◽  
Resistance To Infection ◽  
Opportunistic Pathogenic

AbstractThe soil-dwelling, opportunistic pathogenic bacterium "Bacillus nematocida" B16 exhibits strong killing activities against a variety of pathogenic nematodes via a “Trojan horse” mechanism that can kill worm species like Caenorhabditis elegans. The bacterial strain CPCC 101271 was previously isolated from the intestines of C. elegans that were recovered from natural habitats and can serve as a probiotic for C. elegans, while also assisting in resistance to infection by the pathogenic strain B16. In this study, the lifespan of C. elegans fed with strain CPCC 101271 cells was extended by approximately 40% compared with that of worms fed with Escherichia coli OP50 cells. In addition, the colonization of C. elegans by the pathogenic bacterium "B. nematocida" B16 was inhibited when pre-fed with strain CPCC 101271. Metagenomic sequence analysis of intestinal microbiota of C. elegans fed with strain CPCC 101271 and infected with B16 revealed that pre-feeding worms with CPCC 101271 improved the diversity of the intestinal bacteria. Moreover, community structure significantly varied in coordination with Stenotrophomonas spp. and Bacillus spp. abundances when competition between strains CPCC 101271 and B16 was evaluated. In conclusion, the nematode microbiota strain CPCC 101271 assisted in its host resistance to colonization by the pathogen "Bacillus nematocida" and can also promote life span-prolongation in C. elegans. These results underscore that understanding the interactions between C. elegans microbiota and pathogens can provide new insights into achieving effective biological control of agricultural pests.

scholarly journals Stenotrophomonas Nematodicola Sp. Nov., a Novel Intestinal Lifespan-Prolonging Bacterium for Caenorhabditis Elegans That Assists in Host Resistance to Bacillus Nematocida Colonization

2021 ◽  
Author(s):  
Rui Han ◽  
Yu Wang ◽  
Yang Deng ◽  
Yuqin Zhang ◽  
Lin Zhang ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Host Resistance ◽  
Type Strain ◽  
Novel Species ◽  
Bacterial Species ◽  
Intestinal Bacteria ◽  
Phenotypic Characteristics ◽  
Natural Habitats ◽  
Metagenomic Sequence ◽  
C Elegans

Abstract The soil-dwelling opportunistic bacterium Bacillus nematocida B16 shows comparatively strong killing activities against a variety of pathogenic nematodes. A bacterial strain CPCC 101271T, isolated from intestines of C. elegans in natural habitats, was found not only to be probiotics for C. elegans but also assist in resisting pathogen B16 infection. The lifespan of Caenorhabditis elegans fed on strain CPCC 101271T was extended by approximately 40% compared with that of worms fed on Escherichia coli OP50. In addition, the colonization of C. elegans by the pathogenic bacterium B. nematocida B16 was inhibited when it was pre-fed with strain CPCC 101271T. Based on a polyphasic taxonomy study including genotypic, chemotaxonomic and phenotypic characteristics, we propose that strain CPCC 101271T represents a novel bacterial species with the name Stenotrophomonas nematodicola sp. nov. and CPCC 101271T as the type strain. Metagenomic sequence analysis of the intestinal microbiota of C. elegans fed with strain CPCC 101271T and then infected with B16 revealed that pre-feeding with CPCC 101271T improved the diversity of intestinal bacteria, while the community structure varied significantly together with the fluctuation of Stenotrophomonas spp. and Bacillus spp. abundance during competition between strain CPCC 101271T and B16. In conclusion, the nematode microbiota strain CPCC 101271T, a novel species of the genus Stenotrophomonas, assisted in its host resistance to the pathogen Bacillus nematocida colonization, so as to act as an intestinal life span-prolonging for C. elegans.

scholarly journals Stenotrophomonas nematodicola sp. nov., a novel intestinal lifespan-prolonging bacterium for Caenorhabditis elegans that assists in host resistance to Bacillus nematocida colonization

2021 ◽  
Author(s):  
Lin Zhang ◽  
Yang Deng ◽  
Xuyang Wei ◽  
Yuqin Zhang ◽  
Qiuhong Niu
Keyword(s):  
Caenorhabditis Elegans ◽  
Host Resistance ◽  
Bacterial Species ◽  
Intestinal Flora ◽  
Intestinal Bacteria ◽  
Agricultural Pests ◽  
Phenotypic Properties ◽  
Metagenomic Sequence ◽  
C Elegans ◽  
Bacillus Spp

Abstract Background: The gut microbiota of Caenorhabditis elegans, a tiny worm that feeds on bacteria, is significantly dominated by the bacteria upon which it feeds. These bacteria may not only interfere with the intestinal flora of C. elegans but also assist in resisting pathogen infection. Understanding the interactions between the microbiota of C. elegans and pathogens will shed light on how to achieve biological control of agricultural pests. Results: The lifespan of Caenorhabditis elegans fed on strain CPCC 101271T was extended by approximately 40% compared with that of worms fed on Escherichia coli OP50. In addition, the colonization of C. elegans by the pathogenic bacterium Bacillus nematocida B16 was inhibited when it was pre-fed with strain CPCC 101271T. Based on a polyphasic taxonomy study including genotypic, chemotaxonomic and phenotypic characteristics, we propose that strain CPCC 101271T represents a novel bacterial species with the name Stenotrophomonas nematodicola sp. nov. and CPCC 101271T as the type strain. Metagenomic sequence analysis of the intestinal microbiota of C. elegans fed with strain CPCC 101271T and then infected with B16 revealed that pre-feeding with CPCC 101271T improved the diversity of intestinal bacteria, while the community structure varied significantly together with the fluctuation of Stenotrophomonas spp. and Bacillus spp. abundance during competition between strain CPCC 101271T and B16. Conclusions: The nematode microbiota strain CPCC 101271T assisted in its host resistance to the pathogen Bacillus nematocida colonization, so as to act as an intestinal life span-prolonging bacterium for C. elegans. The genotypic and phenotypic properties of strain CPCC 101271T supported to the proposal of strain CPCC 101271T as a novel species of the genus Stenotrophomonas.

scholarly journals Caenorhabditis elegans responses to bacteria from its natural habitats

2016 ◽  
Vol 113 (27) ◽  
pp. E3941-E3949 ◽  
Author(s):  
Buck S. Samuel ◽  
Holli Rowedder ◽  
Christian Braendle ◽  
Marie-Anne Félix ◽  
Gary Ruvkun
Keyword(s):  
Escherichia Coli ◽  
Caenorhabditis Elegans ◽  
Physiological Responses ◽  
Bacterial Community Composition ◽  
Beneficial Bacteria ◽  
Natural Habitats ◽  
C Elegans ◽  
16S Ribosomal Dna ◽  
Microbial Environment ◽  
Alpha Proteobacteria

Most Caenorhabditis elegans studies have used laboratory Escherichia coli as diet and microbial environment. Here we characterize bacteria of C. elegans' natural habitats of rotting fruits and vegetation to provide greater context for its physiological responses. By the use of 16S ribosomal DNA (rDNA)-based sequencing, we identified a large variety of bacteria in C. elegans habitats, with phyla Proteobacteria, Bacteroidetes, Firmicutes, and Actinobacteria being most abundant. From laboratory assays using isolated natural bacteria, C. elegans is able to forage on most bacteria (robust growth on ∼80% of >550 isolates), although ∼20% also impaired growth and arrested and/or stressed animals. Bacterial community composition can predict wild C. elegans population states in both rotting apples and reconstructed microbiomes: alpha-Proteobacteria-rich communities promote proliferation, whereas Bacteroidetes or pathogens correlate with nonproliferating dauers. Combinatorial mixtures of detrimental and beneficial bacteria indicate that bacterial influence is not simply nutritional. Together, these studies provide a foundation for interrogating how bacteria naturally influence C. elegans physiology.

scholarly journals C. elegans heritably adapts to P. vranovensis infection via a mechanism that requires the cysteine synthases cysl-1 and cysl-2

2019 ◽  
Author(s):  
Nicholas O. Burton ◽  
Cristian Riccio ◽  
Alexandra Dallaire ◽  
Jon Price ◽  
Benjamin Jenkins ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Soil Bacteria ◽  
Hypoxia Inducible Factor ◽  
Offspring Survival ◽  
Pathogen Infection ◽  
C Elegans ◽  
Parental Exposure ◽  
Resistance To Infection ◽  
Dependent Mechanism

AbstractParental exposure to pathogens can prime offspring immunity in diverse organisms. The mechanisms by which this heritable priming occurs are largely unknown. Here we report that the soil bacteria Pseudomonas vranovensis is a natural pathogen of the nematode Caenorhabditis elegans and that parental exposure of animals to P. vranovensis promotes offspring resistance to infection. Furthermore, we demonstrate a transgenerational enhancement of progeny survival when three consecutive generations of animals are exposed to P. vranovensis. By investigating the mechanisms by which animals heritably adapt to P. vranovensis infection, we found that parental infection by P. vranovensis results in increased expression of the cysteine synthases CYSL-1 and CYSL-2 and the regulator of hypoxia inducible factor RHY-1 in progeny and that these three genes are required for adaptation to P. vranovensis. To our knowledge, these observations represent the largest heritable increase in offspring survival in response to a pathogen infection reported in any organism to date and establish a new CYSL-1, CYSL-2, and RHY-1 dependent mechanism by which animals adapt to infection.

The glycomes of Caenorhabditis elegans and other model organisms

2002 ◽  
Vol 69 ◽  
pp. 117-134 ◽  
Author(s):  
Stuart M. Haslam ◽  
David Gems ◽  
Howard R. Morris ◽  
Anne Dell
Keyword(s):  
Caenorhabditis Elegans ◽  
Current Knowledge ◽  
Structural Data ◽  
Model Organisms ◽  
Entire Genome ◽  
C Elegans ◽  
The Face ◽  
Area Of Concern ◽  
Nematode Worm

There is no doubt that the immense amount of information that is being generated by the initial sequencing and secondary interrogation of various genomes will change the face of glycobiological research. However, a major area of concern is that detailed structural knowledge of the ultimate products of genes that are identified as being involved in glycoconjugate biosynthesis is still limited. This is illustrated clearly by the nematode worm Caenorhabditis elegans, which was the first multicellular organism to have its entire genome sequenced. To date, only limited structural data on the glycosylated molecules of this organism have been reported. Our laboratory is addressing this problem by performing detailed MS structural characterization of the N-linked glycans of C. elegans; high-mannose structures dominate, with only minor amounts of complex-type structures. Novel, highly fucosylated truncated structures are also present which are difucosylated on the proximal N-acetylglucosamine of the chitobiose core as well as containing unusual Fucα1–2Gal1–2Man as peripheral structures. The implications of these results in terms of the identification of ligands for genomically predicted lectins and potential glycosyltransferases are discussed in this chapter. Current knowledge on the glycomes of other model organisms such as Dictyostelium discoideum, Saccharomyces cerevisiae and Drosophila melanogaster is also discussed briefly.

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 Functional Redundancy of the B9 Proteins and Nephrocystins in Caenorhabditis elegans Ciliogenesis

2008 ◽  
Vol 19 (5) ◽  
pp. 2154-2168 ◽  
Author(s):  
Corey L. Williams ◽  
Marlene E. Winkelbauer ◽  
Jenny C. Schafer ◽  
Edward J. Michaud ◽  
Bradley K. Yoder
Keyword(s):  
Caenorhabditis Elegans ◽  
Joubert Syndrome ◽  
Cystic Kidney ◽  
Basal Bodies ◽  
The Novel ◽  
C Elegans ◽  
Human Genes ◽  
Cilia Formation ◽  
Strong Candidate ◽  
Candidate Loci

Meckel-Gruber syndrome (MKS), nephronophthisis (NPHP), and Joubert syndrome (JBTS) are a group of heterogeneous cystic kidney disorders with partially overlapping loci. Many of the proteins associated with these diseases interact and localize to cilia and/or basal bodies. One of these proteins is MKS1, which is disrupted in some MKS patients and contains a B9 motif of unknown function that is found in two other mammalian proteins, B9D2 and B9D1. Caenorhabditis elegans also has three B9 proteins: XBX-7 (MKS1), TZA-1 (B9D2), and TZA-2 (B9D1). Herein, we report that the C. elegans B9 proteins form a complex that localizes to the base of cilia. Mutations in the B9 genes do not overtly affect cilia formation unless they are in combination with a mutation in nph-1 or nph-4, the homologues of human genes (NPHP1 and NPHP4, respectively) that are mutated in some NPHP patients. Our data indicate that the B9 proteins function redundantly with the nephrocystins to regulate the formation and/or maintenance of cilia and dendrites in the amphid and phasmid ciliated sensory neurons. Together, these data suggest that the human homologues of the novel B9 genes B9D2 and B9D1 will be strong candidate loci for pathologies in human MKS, NPHP, and JBTS.

scholarly journals Characterization of Caenorhabditis elegans Homologs of the Down Syndrome Candidate Gene DYRK1A

Genetics ◽  
2003 ◽  
Vol 163 (2) ◽  
pp. 571-580 ◽  
Author(s):  
William B Raich ◽  
Celine Moorman ◽  
Clay O Lacefield ◽  
Jonah Lehrer ◽  
Dusan Bartsch ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Caenorhabditis Elegans ◽  
Trisomy 21 ◽  
Gene Dosage ◽  
Inducible Promoters ◽  
C Elegans ◽  
Dual Specificity ◽  
Specificity Protein

Abstract The pathology of trisomy 21/Down syndrome includes cognitive and memory deficits. Increased expression of the dual-specificity protein kinase DYRK1A kinase (DYRK1A) appears to play a significant role in the neuropathology of Down syndrome. To shed light on the cellular role of DYRK1A and related genes we identified three DYRK/minibrain-like genes in the genome sequence of Caenorhabditis elegans, termed mbk-1, mbk-2, and hpk-1. We found these genes to be widely expressed and to localize to distinct subcellular compartments. We isolated deletion alleles in all three genes and show that loss of mbk-1, the gene most closely related to DYRK1A, causes no obvious defects, while another gene, mbk-2, is essential for viability. The overexpression of DYRK1A in Down syndrome led us to examine the effects of overexpression of its C. elegans ortholog mbk-1. We found that animals containing additional copies of the mbk-1 gene display behavioral defects in chemotaxis toward volatile chemoattractants and that the extent of these defects correlates with mbk-1 gene dosage. Using tissue-specific and inducible promoters, we show that additional copies of mbk-1 can impair olfaction cell-autonomously in mature, fully differentiated neurons and that this impairment is reversible. Our results suggest that increased gene dosage of human DYRK1A in trisomy 21 may disrupt the function of fully differentiated neurons and that this disruption is reversible.

Maternal-effect lethal mutations on linkage group II of Caenorhabditis elegans.

Genetics ◽  
1988 ◽  
Vol 120 (4) ◽  
pp. 977-986
Author(s):  
K J Kemphues ◽  
M Kusch ◽  
N Wolf
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
Maternal Effect ◽  
Essential Genes ◽  
The Other ◽  
C Elegans ◽  
Lethal Mutations ◽  
Embryonic Lethal ◽  
Embryonic Lethal Mutations ◽  
F1 Progeny

Abstract We have analyzed a set of linkage group (LG) II maternal-effect lethal mutations in Caenorhabditis elegans isolated by a new screening procedure. Screens of 12,455 F1 progeny from mutagenized adults resulted in the recovery of 54 maternal-effect lethal mutations identifying 29 genes. Of the 54 mutations, 39 are strict maternal-effect mutations defining 17 genes. These 17 genes fall into two classes distinguished by frequency of mutation to strict maternal-effect lethality. The smaller class, comprised of four genes, mutated to strict maternal-effect lethality at a frequency close to 5 X 10(-4), a rate typical of essential genes in C. elegans. Two of these genes are expressed during oogenesis and required exclusively for embryogenesis (pure maternal genes), one appears to be required specifically for meiosis, and the fourth has a more complex pattern of expression. The other 13 genes were represented by only one or two strict maternal alleles each. Two of these are identical genes previously identified by nonmaternal embryonic lethal mutations. We interpret our results to mean that although many C. elegans genes can mutate to strict maternal-effect lethality, most genes mutate to that phenotype rarely. Pure maternal genes, however, are among a smaller class of genes that mutate to maternal-effect lethality at typical rates. If our interpretation is correct, we are near saturation for pure maternal genes in the region of LG II balanced by mnC1. We conclude that the number of pure maternal genes in C. elegans is small, being probably not much higher than 12.

scholarly journals Improving skeleton algorithm for helping Caenorhabditis elegans trackers

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Pablo E. Layana Castro ◽  
Joan Carles Puchalt ◽  
Antonio-José Sánchez-Salmerón
Keyword(s):  
Computer Vision ◽  
Caenorhabditis Elegans ◽  
Transformation Function ◽  
Simple Solution ◽  
New Method ◽  
Vision Systems ◽  
Distance Transformation ◽  
Automatic Computer ◽  
C Elegans ◽  
Computer Vision Systems

AbstractOne of the main problems when monitoring Caenorhabditis elegans nematodes (C. elegans) is tracking their poses by automatic computer vision systems. This is a challenge given the marked flexibility that their bodies present and the different poses that can be performed during their behaviour individually, which become even more complicated when worms aggregate with others while moving. This work proposes a simple solution by combining some computer vision techniques to help to determine certain worm poses and to identify each one during aggregation or in coiled shapes. This new method is based on the distance transformation function to obtain better worm skeletons. Experiments were performed with 205 plates, each with 10, 15, 30, 60 or 100 worms, which totals 100,000 worm poses approximately. A comparison of the proposed method was made to a classic skeletonisation method to find that 2196 problematic poses had improved by between 22% and 1% on average in the pose predictions of each worm.

Sign in / Sign up

Export Citation Format

Share Document