scholarly journals Inositol 1,4,5-Trisphosphate Signaling Regulates Mating Behavior in Caenorhabditis elegans Males

2005 ◽  
Vol 16 (9) ◽  
pp. 3978-3986 ◽  
Author(s):  
Nicholas J. D. Gower ◽  
Denise S. Walker ◽  
Howard A. Baylis
Keyword(s):  
Caenorhabditis Elegans ◽  
Male Fertility ◽  
Mating Disruption ◽  
Sperm Transfer ◽  
Male Mating ◽  
Turning Behavior ◽  
C Elegans ◽  
Inositol 1,4,5 Trisphosphate ◽  
Genes Encoding ◽  
Physiological Outcomes

Complex behavior requires the coordinated action of the nervous system and nonneuronal targets. Male mating in Caenorhabditis elegans consists of a series of defined behavioral steps that lead to the physiological outcomes required for successful impregnation. We demonstrate that signaling mediated by inositol 1,4,5-trisphosphate (IP3) is required at several points during mating. Disruption of IP3 receptor (itr-1) function results in dramatic loss of male fertility, due to defects in turning behavior (during vulva location), spicule insertion and sperm transfer. To elucidate the signaling pathways responsible, we knocked down the six C. elegans genes encoding phospholipase C (PLC) family members. egl-8, which encodes PLC-β, functions in spicule insertion and sperm transfer. itr-1 and egl-8 are widely expressed in the male reproductive system. An itr-1 gain-of-function mutation rescues infertility caused by egl-8 RNA interference, indicating that egl-8 and itr-1 function together as central components of the signaling events controlling sperm transfer.

Characterization of the xenobiotic response of Caenorhabditis elegans to the anthelmintic drug albendazole and the identification of novel drug glucoside metabolites

2010 ◽  
Vol 432 (3) ◽  
pp. 505-516 ◽  
Author(s):  
Steven T. Laing ◽  
Al Ivens ◽  
Roz Laing ◽  
Sai Ravikumar ◽  
Victoria Butler ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Stress Responses ◽  
Transcriptional Response ◽  
Metabolizing Enzymes ◽  
C Elegans ◽  
Genes Encoding ◽  
Minimal Importance ◽  
Xenobiotic Response ◽  
Novel Drug ◽  
Anthelmintic Drugs

Knowledge of how anthelmintics are metabolized and excreted in nematodes is an integral part of understanding the factors that determine their potency, spectrum of activity and for investigating mechanisms of resistance. Although there is remarkably little information on these processes in nematodes, it is often suggested that they are of minimal importance for the major anthelmintic drugs. Consequently, we have investigated how the model nematode Caenorhabditis elegans responds to and metabolizes albendazole, one of the most important anthelmintic drugs for human and animal use. Using a mutant strain lacking the β-tubulin drug target to minimize generalized stress responses, we show that the transcriptional response is dominated by genes encoding XMEs (xenobiotic-metabolizing enzymes), particularly cytochrome P450s and UGTs (UDP-glucuronosyl transferases). The most highly induced genes are predominantly expressed in the worm intestine, supporting their role in drug metabolism. HPLC-MS/MS revealed the production of two novel glucoside metabolites in C. elegans identifying a major difference in the biotransformation of this drug between nematodes and mammals. This is the first demonstration of metabolism of a therapeutic anthelmintic in C. elegans and provides a framework for its use to functionally investigate nematode anthelmintic metabolism.

A cilia-mediated environmental input induces solitary behaviour in Caenorhabditis elegans and Pristionchus pacificus nematodes

Nematology ◽  
2018 ◽  
Vol 20 (3) ◽  
pp. 201-209 ◽  
Author(s):  
Eduardo Moreno ◽  
Ralf J. Sommer
Keyword(s):  
Caenorhabditis Elegans ◽  
Social Behaviour ◽  
Intraflagellar Transport ◽  
Large Protein ◽  
Pristionchus Pacificus ◽  
C Elegans ◽  
The Social ◽  
Genes Encoding ◽  
Social Behaviours ◽  
Ciliated Neurons

Nematodes respond to a multitude of environmental cues. For example, the social behaviours clumping and bordering were described as a mechanism of hyperoxia avoidance in Caenorhabditis elegans and Pristionchus pacificus. A recent study in P. pacificus revealed a novel regulatory pathway that inhibits social behaviour in a response to an as yet unknown environmental cue. This environmental signal is recognised by ciliated neurons, as mutants defective in intraflagellar transport (IFT) proteins display social behaviours. The IFT machinery represents a large protein complex and many mutants in genes encoding IFT proteins are available in C. elegans. However, social phenotypes in C. elegans IFT mutants have never been reported. Here, we examined 15 previously isolated C. elegans IFT mutants and found that most of them showed strong social behaviour. These findings indicate conservation in the inhibitory mechanism of social behaviour between P. pacificus and C. elegans.

scholarly journals Mitochondrial Dysfunction Confers Resistance to Multiple Drugs in Caenorhabditis elegans

2010 ◽  
Vol 21 (6) ◽  
pp. 956-969 ◽  
Author(s):  
Iryna O. Zubovych ◽  
Sarah Straud ◽  
Michael G. Roth
Keyword(s):  
Drug Resistance ◽  
Caenorhabditis Elegans ◽  
Mitochondrial Protein ◽  
Drug Resistant ◽  
Wild Type ◽  
C Elegans ◽  
Mitochondrial Inhibitors ◽  
Mitochondrial Superoxide ◽  
Genes Encoding ◽  
Multiple Drugs

In a previous genetic screen for Caenorhabditis elegans mutants that survive in the presence of an antimitotic drug, hemiasterlin, we identified eight strong mutants. Two of these were found to be resistant to multiple toxins, and in one of these we identified a missense mutation in phb-2, which encodes the mitochondrial protein prohibitin 2. Here we identify two additional mutations that confer drug resistance, spg-7 and har-1, also in genes encoding mitochondrial proteins. Other mitochondrial mutants, isp-1, eat-3, and clk-1, were also found to be drug-resistant. Respiratory complex inhibitors, FCCP and oligomycin, and a producer of reactive oxygen species (ROS), paraquat, all rescued wild-type worms from hemiasterlin toxicity. Worms lacking mitochondrial superoxide dismutase (MnSOD) were modestly drug-resistant, and elimination of MnSOD in the phb-2, har-1, and spg-7 mutants enhanced resistance. The antioxidant N-acetyl-l-cysteine prevented mitochondrial inhibitors from rescuing wild-type worms from hemiasterlin and sensitized mutants to the toxin, suggesting that a mechanism sensitive to ROS is necessary to trigger drug resistance in C. elegans. Using genetics, we show that this drug resistance requires pkc-1, the C. elegans ortholog of human PKCε.

scholarly journals Fabrication of sharp silicon arrays to wound Caenorhabditis elegans

2019 ◽  
Author(s):  
Jérôme Belougne ◽  
Igor Ozerov ◽  
Céline Caillard ◽  
Frédéric Bedu ◽  
Jonathan J. Ewbank
Keyword(s):  
Gene Expression ◽  
Caenorhabditis Elegans ◽  
Optical Lithography ◽  
Wet Etching ◽  
C Elegans ◽  
Genes Encoding ◽  
Nematode Cuticle ◽  
Peptide Gene ◽  
Silicon Arrays ◽  
Regular Arrays

ABSTRACTUnderstanding how animals respond to injury and how wounds heal remains a challenge. These questions can be addressed using genetically tractable animals, including the nematode Caenorhabditis elegans. Given its small size, the current methods for inflicting wounds in a controlled manner are demanding. To facilitate and accelerate the procedure, we fabricated regular arrays of pyramidal features (“pins”) sharp enough to pierce the tough nematode cuticle. The pyramids were made from monocrystalline silicon wafers that were micro-structured using optical lithography and alkaline wet etching. The fabrication protocol and the geometry of the pins, determined by electron microscopy, are described in detail. Upon wounding, C. elegans expresses genes encoding antimicrobial peptides. A comparison of the induction of antimicrobial peptide gene expression using traditional needles and the pin arrays demonstrates the utility of this new method.

Analysis of the VPE sequences in the Caenorhabditis elegans vit-2 promoter with extrachromosomal tandem array-containing transgenic strains

1994 ◽  
Vol 14 (1) ◽  
pp. 484-491
Author(s):  
M MacMorris ◽  
J Spieth ◽  
C Madej ◽  
K Lea ◽  
T Blumenthal
Keyword(s):  
Caenorhabditis Elegans ◽  
Fusion Gene ◽  
Caenorhabditis Briggsae ◽  
Unique Role ◽  
Promoter Function ◽  
C Elegans ◽  
Low Copy Number ◽  
Genes Encoding ◽  
Transgenic Lines ◽  
Adult Hermaphrodite

The Caenorhabditis elegans vit genes, encoding vitellogenins, are abundantly expressed in the adult hermaphrodite intestine. Two repeated elements, vit promoter element 1 (VPE1 [TGTCAAT]) and VPE2 (CTGATAA), have been identified in the 5' flanking DNA of each of the vit genes of C. elegans and Caenorhabditis briggsae. These elements have previously been shown to be needed for correctly regulated expression of a vit-2/vit-6 fusion gene in low-copy-number, integrated transgenes. Here we extend the analysis of the function of VPE1 and VPE2 by using transgenic lines carrying large, extrachromosomal arrays of the test genes. The results validate the use of such arrays for transgenic analysis of gene regulation in C. elegans, by confirming previous findings showing that the VPE1 at -45 and both VPE2s are sites of activation. Additional experiments now indicate that when the -45 VPE1 is inverted or replaced by a VPE2, nearly total loss of promoter function results, suggesting that the highly conserved -45 VPE1 plays a unique role in vit-2 promoter function. In contrast, single mutations eliminating the three upstream VPE1s are without effect. However, in combination in double and triple mutants, these upstream VPE1 mutations cause drastic reductions in expression levels. The -150 VPE2 can be replaced by a XhoI site (CTCGAG), and the -90 VPE2 can be eliminated, as long as the overlapping VPE1 is left intact, but when these two replacements are combined, activity is lost. Thus, the promoter must have at least one VPE2 and it must have at least two VPE1s, one at -45 and one additional upstream element.

abf-1 and abf-2, ASABF-type antimicrobial peptide genes in Caenorhabditis elegans

2002 ◽  
Vol 361 (2) ◽  
pp. 221-230 ◽  
Author(s):  
Yusuke KATO ◽  
Tomoyasu AIZAWA ◽  
Hirokazu HOSHINO ◽  
Keiichi KAWANO ◽  
Katsutoshi NITTA ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Antimicrobial Peptide ◽  
Fluorescent Protein ◽  
Fusion Gene ◽  
C Elegans ◽  
Specific Distribution ◽  
Genes Encoding ◽  
Precursor Rna ◽  
Factor Type ◽  
Green Fluorescent

Two genes encoding the ASABF (Ascarissuumantibacterial factor)-type antimicrobial peptide, abf-1 and abf-2, were identified in Caenorhabditis elegans. Recombinant ABF-2 exhibited potent microbicidal activity against Gram-positive and Gram-negative bacteria, and yeasts. The tissue-specific distribution estimated by immunofluorescence staining and transgenic analysis of a gfp fusion gene (where GFP corresponds to green fluorescent protein) suggested that ABF-2 contributes to surface defence in the pharynx. abf-1 contains a single intron at a conserved position, suggesting that asabf and abf originated from a common ancestor. Both transcripts for abf-1 and abf-2 were detected as two distinct forms, i.e. spliced leader (SL)1-trans-spliced with a long 5′-untranslated region (UTR) and SL-less with a short 5′-UTR. A polycistronic precursor RNA encoding ABF-1 and ABF-2 was detected, suggesting that these genes form an operon. An ‘opportunistic operon’ model for regulation of abf genes, including the generation of short SL-less transcripts, is proposed. In conclusion, C. elegans should have an immune defence system due to the antimicrobial peptides. C. elegans can be a novel model for innate immunity. Furthermore, the combination of biochemical identification in Ascaris suum and homologue hunting in C. elegans should be a powerful method of finding rapidly evolved proteins, such as some immune-related molecules in C. elegans.

Molecular characterization of the metabotropic glutamate receptor family in Caenorhabditis elegans

2006 ◽  
Vol 34 (5) ◽  
pp. 942-948 ◽  
Author(s):  
J. Dillon ◽  
N.A. Hopper ◽  
L. Holden-Dye ◽  
V. O'Connor
Keyword(s):  
Caenorhabditis Elegans ◽  
Molecular Characterization ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate Receptor ◽  
Model Organism ◽  
Metabotropic Glutamate ◽  
C Elegans ◽  
Genes Encoding ◽  
G Protein Coupled

mGluRs (metabotropic glutamate receptors) are G-protein-coupled receptors that play an important neuromodulatory role in the brain. Glutamatergic transmission itself plays a fundamental role in the simple nervous system of the model organism Caenorhabditis elegans, but little is known about the contribution made by mGluR signalling. The sequenced genome of C. elegans predicts three distinct genes, mgl-1, mgl-2 and mgl-3 (designated Y4C6A.2). We have used in silico and cDNA analyses to investigate the genes encoding mgls. Our results indicate that mgl genes constitute a gene family made up of three distinct subclasses of receptor. Our transcript analysis highlights potential for complex gene regulation with respect to both expression and splicing. Further, we identify that the predicted proteins encoded by mgls harbour structural motifs that are likely to regulate function. Taken together, this molecular characterization provides a platform to further investigate mGluR function in the model organism C. elegans.

scholarly journals Caenorhabditis elegans Teneurin, ten-1, Is Required for Gonadal and Pharyngeal Basement Membrane Integrity and Acts Redundantly with Integrin ina-1 and Dystroglycan dgn-1

2008 ◽  
Vol 19 (9) ◽  
pp. 3898-3908 ◽  
Author(s):  
Agnieszka Trzebiatowska ◽  
Ulrike Topf ◽  
Ursula Sauder ◽  
Krzysztof Drabikowski ◽  
Ruth Chiquet-Ehrismann
Keyword(s):  
Caenorhabditis Elegans ◽  
Basement Membrane ◽  
Membrane Integrity ◽  
Precursor Cells ◽  
Basement Membranes ◽  
Synthetic Lethal ◽  
C Elegans ◽  
Somatic Gonad ◽  
Genes Encoding ◽  
Membrane Components

The Caenorhabditis elegans teneurin ortholog, ten-1, plays an important role in gonad and pharynx development. We found that lack of TEN-1 does not affect germline proliferation but leads to local basement membrane deficiency and early gonad disruption. Teneurin is expressed in the somatic precursor cells of the gonad that appear to be crucial for gonad epithelialization and basement membrane integrity. Ten-1 null mutants also arrest as L1 larvae with malformed pharynges and disorganized pharyngeal basement membranes. The pleiotropic phenotype of ten-1 mutant worms is similar to defects found in basement membrane receptor mutants ina-1 and dgn-1 as well as in the mutants of the extracellular matrix component laminin, epi-1. We show that the ten-1 mutation is synthetic lethal with mutations of genes encoding basement membrane components and receptors due to pharyngeal or hypodermal defects. This indicates that TEN-1 could act redundantly with integrin INA-1, dystroglycan DGN-1, and laminin EPI-1 in C. elegans development. Moreover, ten-1 deletion sensitizes worms to loss of nidogen nid-1 causing a pharynx unattached phenotype in ten-1;nid-1 double mutants. We conclude that TEN-1 is important for basement membrane maintenance and/or adhesion in particular organs and affects the function of somatic gonad precursor cells.

scholarly journals Inositol 1,4,5-Trisphosphate Signaling Regulates Rhythmic Contractile Activity of Myoepithelial Sheath Cells in Caenorhabditis elegans

2004 ◽  
Vol 15 (8) ◽  
pp. 3938-3949 ◽  
Author(s):  
Xiaoyan Yin ◽  
Nicholas J.D. Gower ◽  
Howard A. Baylis ◽  
Kevin Strange
Keyword(s):  
Caenorhabditis Elegans ◽  
Contractile Activity ◽  
Receptor Gene ◽  
Tyrosine Kinase Receptor ◽  
Sheath Cell ◽  
Cell Contraction ◽  
C Elegans ◽  
Inositol 1,4,5 Trisphosphate ◽  
Intracellular Ca ◽  
Sheath Cells

Intercellular communication between germ cells and neighboring somatic cells is essential for reproduction. Caenorhabditis elegans oocytes are surrounded by and coupled via gap junctions to smooth muscle-like myoepithelial sheath cells. Rhythmic sheath cell contraction drives ovulation and is triggered by a factor secreted from oocytes undergoing meiotic maturation. We demonstrate for the first time that signaling through the epidermal growth factor-like ligand LIN-3 and the LET-23 tyrosine kinase receptor induces ovulatory contractions of sheath cells. Reduction-of-function mutations in the inositol 1,4,5-trisphosphate (IP3) receptor gene itr-1 and knockdown of itr-1 expression by RNA interference inhibit sheath contractile activity. itr-1 gain-of-function mutations increase the rate and force of basal contractions and induce tonic sheath contraction during ovulation. Sheath contractile activity is disrupted by RNAi of plc-3, one of six phospholipase C-encoding genes in the C. elegans genome. PLC-3 is a PLC-γ homolog and is expressed in contractile sheath cells of the proximal gonad. Maintenance of sheath contractile activity requires plasma membrane Ca2+ entry. We conclude that IP3 generated by LET-23 mediated activation of PLC-γ induces repetitive intracellular Ca2+ release that drives rhythmic sheath cell contraction. Calcium entry may function to trigger Ca2+ release via IP3 receptors and/or refill intracellular Ca2+ stores.

scholarly journals Analysis of the VPE sequences in the Caenorhabditis elegans vit-2 promoter with extrachromosomal tandem array-containing transgenic strains.

1994 ◽  
Vol 14 (1) ◽  
pp. 484-491 ◽  
Author(s):  
M MacMorris ◽  
J Spieth ◽  
C Madej ◽  
K Lea ◽  
T Blumenthal
Keyword(s):  
Caenorhabditis Elegans ◽  
Fusion Gene ◽  
Caenorhabditis Briggsae ◽  
Unique Role ◽  
Promoter Function ◽  
C Elegans ◽  
Low Copy Number ◽  
Genes Encoding ◽  
Transgenic Lines ◽  
Adult Hermaphrodite

The Caenorhabditis elegans vit genes, encoding vitellogenins, are abundantly expressed in the adult hermaphrodite intestine. Two repeated elements, vit promoter element 1 (VPE1 [TGTCAAT]) and VPE2 (CTGATAA), have been identified in the 5' flanking DNA of each of the vit genes of C. elegans and Caenorhabditis briggsae. These elements have previously been shown to be needed for correctly regulated expression of a vit-2/vit-6 fusion gene in low-copy-number, integrated transgenes. Here we extend the analysis of the function of VPE1 and VPE2 by using transgenic lines carrying large, extrachromosomal arrays of the test genes. The results validate the use of such arrays for transgenic analysis of gene regulation in C. elegans, by confirming previous findings showing that the VPE1 at -45 and both VPE2s are sites of activation. Additional experiments now indicate that when the -45 VPE1 is inverted or replaced by a VPE2, nearly total loss of promoter function results, suggesting that the highly conserved -45 VPE1 plays a unique role in vit-2 promoter function. In contrast, single mutations eliminating the three upstream VPE1s are without effect. However, in combination in double and triple mutants, these upstream VPE1 mutations cause drastic reductions in expression levels. The -150 VPE2 can be replaced by a XhoI site (CTCGAG), and the -90 VPE2 can be eliminated, as long as the overlapping VPE1 is left intact, but when these two replacements are combined, activity is lost. Thus, the promoter must have at least one VPE2 and it must have at least two VPE1s, one at -45 and one additional upstream element.

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