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Author (up) Baylis, H.A.; Furuichi, T.; Yoshikawa, F.; Mikoshiba, K.; Sattelle, D.B. file  url
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  Title Inositol 1,4,5-trisphosphate receptors are strongly expressed in the nervous system, pharynx, intestine, gonad and excretory cell of Caenorhabditis elegans and are encoded by a single gene (itr-1) Type Journal Article
  Year 1999 Publication Journal of Molecular Biology Abbreviated Journal J Mol Biol  
  Volume 294 Issue 2 Pages 467-476  
  Keywords Amino Acid Sequence; Animals; Animals, Genetically Modified; Binding Sites; Caenorhabditis elegans/*genetics; Calcium Channels/*genetics/*metabolism; Cell Membrane/genetics/metabolism; Conserved Sequence; Gene Expression Profiling; Gonads/metabolism; Helminth Proteins/*genetics/*metabolism; Inositol 1,4,5-Trisphosphate Receptors; Intestines/metabolism; Molecular Sequence Data; Nervous System/metabolism; Pharynx/metabolism; RNA, Messenger; Receptors, Cytoplasmic and Nuclear/*genetics/*metabolism; Rectum/cytology/metabolism  
  Abstract Inositol 1,4,5-trisphosphate (InsP3) activates receptors (InsP3Rs) that mediate intracellular Ca(2+ )release, thereby modulating intracellular calcium signals and regulating important aspects of cellular physiology and gene expression. To further our understanding of InsP3Rs we have characterised InsP3Rs and the InsP3R gene, itr-1, from the model organism Caenorhabditis elegans. cDNAs encoding InsP3Rs were cloned enabling us to: (a) identify three putative transcription start sites that result in alternative mRNA 5' ends: (b) detect alternative splicing at three sites and: (c) determine the full genomic organisation of the itr-1 gene. The InsP3R protein (ITR-1) is approximately 42 % identical with known InsP3Rs and possesses conserved structural features. When the putative InsP3 binding domain was expressed in Escherichia coli, specific binding of InsP3 was detected. Using antibodies against ITR-1 we detected a protein of 220 kDa in C. elegans membranes. These antibodies and itr-1::GFP (green fluorescent protein) reporter constructs were used to determine the expression pattern of itr-1 in C. elegans. Strong expression was observed in the intestine, pharynx, nerve ring, excretory cell and gonad. These results demonstrate the high degree of structural and functional conservation of InsP3Rs from nematodes to mammals and the utility of C. elegans as a system for studies on InsP3R mediated signalling.  
  Call Number Serial 309  
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Author (up) Sterken, M.G.; Snoek, L.B.; Kammenga, J.E.; Andersen, E.C. file  url
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  Title The laboratory domestication of Caenorhabditis elegans Type Journal Article
  Year 2015 Publication Trends in Genetics : TIG Abbreviated Journal Trends Genet  
  Volume 31 Issue 5 Pages 224-231  
  Keywords Adaptation, Biological/genetics; Alleles; Animals; Caenorhabditis elegans/*genetics; Gene-Environment Interaction; Genetic Variation; *Models, Animal; Caenorhabditis elegans; aerotaxis; laboratory derived; npr-1; selection  
  Abstract Model organisms are of great importance to our understanding of basic biology and to making advances in biomedical research. However, the influence of laboratory cultivation on these organisms is underappreciated, and especially how that environment can affect research outcomes. Recent experiments led to insights into how the widely used laboratory reference strain of the nematode Caenorhabditis elegans compares with natural strains. Here we describe potential selective pressures that led to the fixation of laboratory-derived alleles for the genes npr-1, glb-5, and nath-10. These alleles influence a large number of traits, resulting in behaviors that affect experimental interpretations. Furthermore, strong phenotypic effects caused by these laboratory-derived alleles hinder the discovery of natural alleles. We highlight strategies to reduce the influence of laboratory-derived alleles and to harness the full power of C. elegans.  
  Call Number Serial 1669  
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Author (up) Ventura, N.; Rea, S.L. file  url
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  Title Caenorhabditis elegans mitochondrial mutants as an investigative tool to study human neurodegenerative diseases associated with mitochondrial dysfunction Type Journal Article
  Year 2007 Publication Biotechnology Journal Abbreviated Journal Biotechnol J  
  Volume 2 Issue 5 Pages 584-595  
  Keywords Aging/*genetics; Animals; Caenorhabditis elegans/*genetics; Caenorhabditis elegans Proteins/*genetics; *Disease Models, Animal; Genetic Predisposition to Disease/genetics; Humans; Mitochondrial Diseases/*genetics; Mitochondrial Proteins/*genetics; Mutation; Neurodegenerative Diseases/*genetics  
  Abstract In humans, well over one hundred diseases have been linked to mitochondrial dysfunction and many of these are associated with neurodegeneration. At the root of most of these diseases lay ineffectual energy production, caused either by direct or indirect disruption to components of the mitochondrial electron transport chain. It is surprising then to learn that, in the nematode Caenorhabditis elegans, a collection of mutants which share disruptions in some of the same genes that cause mitochondrial pathogenesis in humans are in fact long-lived. Recently, we resolved this paradox by showing that the C. elegans “Mit mutants” only exhibit life extension in a defined window of mitochondrial dysfunction. Similar to humans, when mitochondrial dysfunction becomes too severe these mutants also exhibit pathogenic life reduction. We have proposed that life extension in the Mit mutants occurs as a by-product of compensatory processes specifically activated to maintain mitochondrial function. We have also proposed that similar kinds of processes may act to delay the symptomatic appearance in many human mitochondrial-associated disorders. In the present report, we describe our progress in using the Mit mutants as an investigative tool to study some of the processes potentially employed by human cells to offset pathological mitochondrial dysfunction.  
  Call Number Serial 462  
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