Operon and non-operon gene clusters in the C. elegans genome

A Genomic Virulence Reference Map of Enterococcus faecalis Reveals an Important Contribution of Phage03-Like Elements in Nosocomial Genetic Lineages to Pathogenicity in a Caenorhabditis elegans Infection Model

Infection and Immunity ◽

10.1128/iai.02801-14 ◽

2015 ◽

Vol 83 (5) ◽

pp. 2156-2167 ◽

Cited By ~ 7

Author(s):

Sabina Leanti La Rosa ◽

Lars-Gustav Snipen ◽

Barbara E. Murray ◽

Rob J. L. Willems ◽

Michael S. Gilmore ◽

...

Keyword(s):

Caenorhabditis Elegans ◽

Enterococcus Faecalis ◽

Principal Component ◽

Gene Clusters ◽

Clinical Strain ◽

Comparative Genomic ◽

Infection Model ◽

Content Type ◽

C Elegans ◽

Virulence Traits

In the present study, the commensal and pathogenic host-microbe interaction ofEnterococcus faecaliswas explored using aCaenorhabditis elegansmodel system. The virulence of 28E. faecalisisolates representing 24 multilocus sequence types (MLSTs), including human commensal and clinical isolates as well as isolates from animals and of insect origin, was investigated usingC. elegansstrainglp-4(bn2ts);sek-1(km4). This revealed that 6E. faecalisisolates behaved in a commensal manner with no nematocidal effect, while the remaining strains showed a time to 50% lethality ranging from 47 to 120 h. Principal component analysis showed that the difference in nematocidal activity explained 94% of the variance in the data. Assessment of known virulence traits revealed that gelatinase and cytolysin production accounted for 40.8% and 36.5% of the observed pathogenicity, respectively. However, coproduction of gelatinase and cytolysin did not increase virulence additively, accounting for 50.6% of the pathogenicity and therefore indicating a significant (26.7%) saturation effect. We employed a comparative genomic analysis approach using the 28 isolates comprising a collection of 82,356 annotated coding sequences (CDS) to identify 2,325 patterns of presence or absence among the investigated strains. Univariate statistical analysis of variance (ANOVA) established that individual patterns positively correlated (n= 61) with virulence. The patterns were investigated to identify potential new virulence traits, among which we found five patterns consisting of the phage03-like gene clusters. Strains harboring phage03 showed, on average, 17% higher killing ofC. elegans(P= 4.4e−6). The phage03 gene cluster was also present in gelatinase-and-cytolysin-negative strainE. faecalisJH2-2. Deletion of this phage element from the JH2-2 clinical strain rendered the mutant apathogenic inC. elegans, and a similar mutant of the nosocomial V583 isolate showed significantly attenuated virulence. Bioinformatics investigation indicated that, unlike otherE. faecalisvirulence traits, phage03-like elements were found at a higher frequency among nosocomial isolates. In conclusion, our report provides a valuable virulence map that explains enhancement inE. faecalisvirulence and contributes to a deeper comprehension of the genetic mechanism leading to the transition from commensalism to a pathogenic lifestyle.

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A Functional Phenylacetic Acid Catabolic Pathway Is Required for Full Pathogenicity of Burkholderia cenocepacia in the Caenorhabditis elegans Host Model

Journal of Bacteriology ◽

10.1128/jb.00481-08 ◽

2008 ◽

Vol 190 (21) ◽

pp. 7209-7218 ◽

Cited By ~ 48

Author(s):

Robyn J. Law ◽

Jason N. R. Hamlin ◽

Aida Sivro ◽

Stuart J. McCorrister ◽

Georgina A. Cardama ◽

...

Keyword(s):

Caenorhabditis Elegans ◽

Phenylacetic Acid ◽

Gene Clusters ◽

Degradation Pathway ◽

Burkholderia Cenocepacia ◽

Insertion Mutagenesis ◽

Infection Model ◽

Catabolic Pathway ◽

C Elegans ◽

Ring Hydroxylation

ABSTRACT Burkholderia cenocepacia is a member of the Burkholderia cepacia complex, a group of metabolically versatile bacteria that have emerged as opportunistic pathogens in cystic fibrosis and immunocompromised patients. Previously a screen of transposon mutants in a rat pulmonary infection model identified an attenuated mutant with an insertion in paaE, a gene related to the phenylacetic acid (PA) catabolic pathway. In this study, we characterized gene clusters involved in the PA degradation pathway of B. cenocepacia K56-2 in relation to its pathogenicity in the Caenorhabditis elegans model of infection. We demonstrated that targeted-insertion mutagenesis of paaA and paaE, which encode part of the putative PA-coenzyme A (CoA) ring hydroxylation system, paaZ, coding for a putative ring opening enzyme, and paaF, encoding part of the putative beta-oxidation system, severely reduces growth on PA as a sole carbon source. paaA and paaE insertional mutants were attenuated for virulence, and expression of paaE in trans restored pathogenicity of the paaE mutant to wild-type levels. Interruption of paaZ and paaF slightly increased virulence. Using gene interference by ingested double-stranded RNA, we showed that the attenuated phenotype of the paaA and paaE mutants is dependent on a functional p38 mitogen-activated protein kinase pathway in C. elegans. Taken together, our results demonstrate that B. cenocepacia possesses a functional PA degradation pathway and that the putative PA-CoA ring hydroxylation system is required for full pathogenicity in C. elegans.

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Deep evolutionary origin of nematode SL2 trans-splicing revealed by genome-wide analysis of the Trichinella spiralis transcriptome

10.1101/642082 ◽

2019 ◽

Author(s):

Marius Wenzel ◽

Christopher Johnston ◽

Berndt Müller ◽

Jonathan Pettitt ◽

Bernadette Connolly

Keyword(s):

Trichinella Spiralis ◽

Nematode Species ◽

Limited Data ◽

Stem Loop ◽

Spliced Leader ◽

C Elegans ◽

Genome Wide ◽

Recent Innovation ◽

Operon Gene ◽

Polycistronic Rna

ABSTRACTSpliced leader trans-splicing is intimately associated with the presence of eukaryotic operons, allowing the processing of polycistronic RNAs into individual mRNAs. Most of our understanding of spliced leader trans-splicing as it relates to operon gene expression comes from studies in C. elegans. In this organism, two distinct spliced leader trans-splicing events are recognised: SL1, which is used to replace the 5’ ends of pre-mRNAs that have a nascent monomethyl guanosine cap; and SL2, which provides the 5’ end to uncapped pre-mRNAs derived from polycistronic RNAs. Limited data on operons and spliced leader trans-splicing in other nematodes suggested that SL2-type trans-splicing is a relatively recent innovation, associated with increased efficiency of polycistronic processing, and confined to only one of the five major nematode clades, Clade V. We have conducted the first transcriptome-wide analysis of spliced leader trans-splicing in a nematode species, Trichinella spiralis, which belongs to a clade distantly related to Clade V. Our work identifies a set of T. spiralis SL2-type spliced leaders that are specifically used to process polycistronic RNAs, the first examples of specialised spliced leaders that have been found outside of Clade V. These T. spiralis spliced leader RNAs possess a perfectly conserved stem-loop motif previously shown to be essential for polycistronic RNA processing in C. elegans. We show that this motif is found in specific sets of spliced leader RNAs broadly distributed across the nematode phylum. This work substantially revises our understanding of the evolution of nematode spliced leader trans-splicing, showing that the machinery for SL2 trans-splicing evolved much earlier during nematode evolution than was previously appreciated, and has been conserved throughout the radiation of the nematode phylum.

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Difference and variation of the sef14 operon gene clusters in S. pullorum

Journal of Basic Microbiology ◽

10.1002/jobm.200900262 ◽

2010 ◽

Vol 50 (S1) ◽

pp. S120-S123 ◽

Cited By ~ 2

Author(s):

C. H. Zhu ◽

J. Wu ◽

W. W. Chen ◽

H. Musa Hassan ◽

G. Q. Zhu

Keyword(s):

Gene Clusters ◽

Operon Gene

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Genetic analysis of a major segment [LGV(left)] of the genome of Caenorhabditis elegans.

Genetics ◽

10.1093/genetics/129.3.735 ◽

1991 ◽

Vol 129 (3) ◽

pp. 735-752 ◽

Cited By ~ 2

Author(s):

R C Johnsen ◽

D L Baillie

Keyword(s):

Caenorhabditis Elegans ◽

Essential Gene ◽

Genome Structure ◽

Gene Clusters ◽

Essential Genes ◽

C Elegans ◽

New Genes ◽

Induced Mutagenesis ◽

Relationship Of ◽

The Relationship

Abstract From 10,900 F1 progeny of ethyl methanesulfonate (EMS)-mutagenized Caenorhabditis elegans nematodes, we isolated 194 lethal mutations on the left arm of LGV, a region balanced by the reciprocal translocation of eT1. The analysis of 166 of those mutations resulted in the identification of one deficiency and alleles of 78 genes including 38 new genes, thus increasing the number of identified essential genes to 101. We estimate that there are a minimum of 120 essential genes in this region, which comprises approximately 7% of the recombinational distance, although only about 4.2% of the genes, in C. elegans. We calculate that there are a minimum of 2850 essential genes in the genome. The left arm of LGV has two recombinational gene clusters separated by a high-recombination and/or essential gene-sparse region. One gene in this region, let-330, is the largest EMS target on the left arm of LGV, with twice as many alleles (16) as the next most EMS-mutable genes, let-332 and rol-3. Another gene in the sparse region, lin-40, and the region near lin-40 are major targets for Tc1 mobilization-induced mutagenesis. The analysis of essential genes in large regions should help to define C. elegans in terms of all its genes and aid in the understanding of the relationship of genome structure to genome function.

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The glycomes of Caenorhabditis elegans and other model organisms

Biochemical Society Symposium ◽

10.1042/bss0690117 ◽

2002 ◽

Vol 69 ◽

pp. 117-134 ◽

Cited By ~ 47

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.

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How do histone modifications contribute to transgenerational epigenetic inheritance in C. elegans?

Biochemical Society Transactions ◽

10.1042/bst20190944 ◽

2020 ◽

Vol 48 (3) ◽

pp. 1019-1034 ◽

Cited By ~ 1

Author(s):

Rachel M. Woodhouse ◽

Alyson Ashe

Keyword(s):

Histone Modifications ◽

Molecular Mechanisms ◽

Epigenetic Inheritance ◽

Nematode Caenorhabditis Elegans ◽

Histone Methyltransferases ◽

Transgenerational Epigenetic Inheritance ◽

C Elegans ◽

Recent Developments ◽

Gene Regulatory

Gene regulatory information can be inherited between generations in a phenomenon termed transgenerational epigenetic inheritance (TEI). While examples of TEI in many animals accumulate, the nematode Caenorhabditis elegans has proven particularly useful in investigating the underlying molecular mechanisms of this phenomenon. In C. elegans and other animals, the modification of histone proteins has emerged as a potential carrier and effector of transgenerational epigenetic information. In this review, we explore the contribution of histone modifications to TEI in C. elegans. We describe the role of repressive histone marks, histone methyltransferases, and associated chromatin factors in heritable gene silencing, and discuss recent developments and unanswered questions in how these factors integrate with other known TEI mechanisms. We also review the transgenerational effects of the manipulation of histone modifications on germline health and longevity.

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Centrosome Aurora A gradient ensures single polarity axis in C. elegans embryos

Biochemical Society Transactions ◽

10.1042/bst20200298 ◽

2020 ◽

Vol 48 (3) ◽

pp. 1243-1253 ◽

Cited By ~ 1

Author(s):

Sukriti Kapoor ◽

Sachin Kotak

Keyword(s):

Symmetry Breaking ◽

Cell Fate ◽

Cell Cortex ◽

Axis Formation ◽

Aurora A Kinase ◽

Aurora A ◽

C Elegans ◽

Cell Embryo ◽

Polarity Establishment

Cellular asymmetries are vital for generating cell fate diversity during development and in stem cells. In the newly fertilized Caenorhabditis elegans embryo, centrosomes are responsible for polarity establishment, i.e. anterior–posterior body axis formation. The signal for polarity originates from the centrosomes and is transmitted to the cell cortex, where it disassembles the actomyosin network. This event leads to symmetry breaking and the establishment of distinct domains of evolutionarily conserved PAR proteins. However, the identity of an essential component that localizes to the centrosomes and promotes symmetry breaking was unknown. Recent work has uncovered that the loss of Aurora A kinase (AIR-1 in C. elegans and hereafter referred to as Aurora A) in the one-cell embryo disrupts stereotypical actomyosin-based cortical flows that occur at the time of polarity establishment. This misregulation of actomyosin flow dynamics results in the occurrence of two polarity axes. Notably, the role of Aurora A in ensuring a single polarity axis is independent of its well-established function in centrosome maturation. The mechanism by which Aurora A directs symmetry breaking is likely through direct regulation of Rho-dependent contractility. In this mini-review, we will discuss the unconventional role of Aurora A kinase in polarity establishment in C. elegans embryos and propose a refined model of centrosome-dependent symmetry breaking.

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