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Author (up) Ardiel, E.L.; Rankin, C.H. file  url
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  Title C. elegans: social interactions in a “nonsocial” animal Type Journal Article
  Year 2009 Publication Advances in Genetics Abbreviated Journal Adv Genet  
  Volume 68 Issue Pages 1-22  
  Keywords Animals; Behavior, Animal; Caenorhabditis elegans/genetics/*physiology; Caenorhabditis elegans Proteins/genetics; Ecosystem; Female; Genetics, Behavioral; Male; Pheromones/physiology; Social Behavior  
  Abstract As self-fertilizing nematodes, Caenorhabditis elegans do not normally come to mind when one thinks of social animals. However, their reproductive mode is optimized for rapid population growth, and although they do not form structured societies, conspecifics are an important source of sensory input. A pheromone signal underlies multiple complex behaviors, including diapause, male-mating, and aggregation. The use of C. elegans in sociogenetics research allows for the analysis of social interactions at the level of genes, circuits, and behaviors. This chapter describes natural polymorphisms in mab-23, plg-1, npr-1, and glb-5 as they relate to two C. elegans social behaviors: male-mating and aggregation.  
  Call Number Serial 1074  
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Author (up) Biron, D.; Shibuya, M.; Gabel, C.; Wasserman, S.M.; Clark, D.A.; Brown, A.; Sengupta, P.; Samuel, A.D.T. file  url
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  Title A diacylglycerol kinase modulates long-term thermotactic behavioral plasticity in C. elegans Type Journal Article
  Year 2006 Publication Nature Neuroscience Abbreviated Journal Nat Neurosci  
  Volume 9 Issue 12 Pages 1499-1505  
  Keywords Animals; Association Learning/physiology; Behavior, Animal/*physiology; Body Temperature Regulation/physiology; Caenorhabditis elegans/*enzymology/genetics; Caenorhabditis elegans Proteins/genetics/*metabolism; Diacylglycerol Kinase/genetics/*metabolism; Gene Expression Profiling; Mutation; Neurons/enzymology; Thermosensing/*physiology  
  Abstract A memory of prior thermal experience governs Caenorhabditis elegans thermotactic behavior. On a spatial thermal gradient, C. elegans tracks isotherms near a remembered temperature we call the thermotactic set-point (T(S)). The T(S) corresponds to the previous cultivation temperature and can be reset by sustained exposure to a new temperature. The mechanisms underlying this behavioral plasticity are unknown, partly because sensory and experience-dependent components of thermotactic behavior have been difficult to separate. Using newly developed quantitative behavioral analyses, we demonstrate that the T(S) represents a weighted average of a worm's temperature history. We identify the DGK-3 diacylglycerol kinase as a thermal memory molecule that regulates the rate of T(S) resetting by modulating the temperature range of synaptic output, but not temperature sensitivity, of the AFD thermosensory neurons. These results provide the first mechanistic insight into the basis of experience-dependent plasticity in this complex behavior.  
  Call Number Serial 1679  
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Author (up) Hamada, T.; Sakube, Y.; Ahnn, J.; Kim, D.H.; Kagawa, H. file  url
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  Title Molecular dissection, tissue localization and Ca2+ binding of the ryanodine receptor of Caenorhabditis elegans Type Journal Article
  Year 2002 Publication Journal of Molecular Biology Abbreviated Journal J Mol Biol  
  Volume 324 Issue 1 Pages 123-135  
  Keywords Amino Acid Sequence; Animals; Binding Sites; Caenorhabditis elegans/genetics/*metabolism; Caenorhabditis elegans Proteins/genetics/*metabolism; Calcium/*metabolism; Cross Reactions; Gene Expression Regulation, Developmental; Molecular Sequence Data; Muscles/*metabolism; Mutation; Recombinant Proteins/genetics/immunology/metabolism; Ryanodine Receptor Calcium Release Channel/genetics/immunology/*metabolism; Sequence Homology, Amino Acid  
  Abstract The ryanodine receptor of Caenorhabditis elegans (CeRyR) which contains 5,071 amino acid residues, is encoded by a single gene, ryr-1/unc-68. The unc-68(kh30) mutation, isolated in an animal showing abnormal response to the anesthetic ketamine, has the substitution Ser1444Asn in CeRyR, predicted to be a phosphorylation site. To elucidate the function of the region of CeRyR, and to determine the localization of CeRyR in this animal, ten region-peptides were produced in Escherichia coli by using expression plasmids and eight antisera were raised against these fusion peptides. One antibody against the region corresponding to the kh30 mutation site enabled detection of CeRyR from mutant animals both in Western analysis and in situ. Specificity of this antiserum was demonstrated using Western analysis, which showed the full size and the partial size bands in wild-type and in the Tc1-induced deletion mutant animals, respectively, but no corresponding bands in unc-68 null mutant animals. CeRyR was detected in I-bands of muscle sarcomeres by double immunostaining. CeRyR was found in the body wall, pharyngeal, vulval, anal and sex muscles of adult worms and also found to be present in embryonic muscle, but not in non-muscle cells. Two EF-hand motifs and the C terminus were demonstrated to be Ca(2+) binding regions. On the basis of these results, we propose a model for the functional domains of CeRyR, which agrees well with the model of mammalian skeletal RyR, which is based on proteolysis and cross-linking analysis. We discuss the usefulness and limitations of the molecular dissection approach, which uses peptides and peptide-specific antibodies to determine the local structure and function of individual domains within a large molecule.  
  Call Number Serial 447  
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Author (up) Kampkotter, A.; Timpel, C.; Zurawski, R.F.; Ruhl, S.; Chovolou, Y.; Proksch, P.; Watjen, W. file  url
openurl 
  Title Increase of stress resistance and lifespan of Caenorhabditis elegans by quercetin Type Journal Article
  Year 2008 Publication Comparative Biochemistry and Physiology. Part B, Biochemistry & Molecular Biology Abbreviated Journal Comp Biochem Physiol B Biochem Mol Biol  
  Volume 149 Issue 2 Pages 314-323  
  Keywords Animals; Antioxidants/pharmacology; Biological Availability; Caenorhabditis elegans/drug effects/*physiology; Caenorhabditis elegans Proteins/genetics/metabolism; Gene Expression Regulation, Enzymologic/drug effects; Immunity, Innate/*drug effects; Longevity/*drug effects; Oxidative Stress/*drug effects; Quercetin/pharmacokinetics/*pharmacology; Signal Transduction/drug effects; Superoxide Dismutase/genetics; Tissue Distribution; Transcription Factors/metabolism  
  Abstract The health beneficial effects of a diet rich in fruits and vegetables are, at least in part, attributed to polyphenols that are present in many herbal edibles. Although many in vitro studies revealed a striking variety of biochemical and pharmacological properties data about the beneficial effects of polyphenols in whole organisms, especially with respect to ageing, are quite limited. We used the well established model organism Caenorhabditis elegans to elucidate the protective effects of quercetin, the main representative of the flavonol class of polyphenols, in vivo. Quercetin is taken up by the worms, enhanced the resistance to oxidative stress and prolonged the mean lifespan of C. elegans by 15%. Quercetin was shown to be a strong radical scavenger possibly explaining the observed down-regulation of mitochondrial manganese superoxide dismutase by a reduced need for this antioxidant enzyme for maintenance of cellular redox homeostasis. Quercetin treatment also led to a translocation of the C. elegans FoxO transcription factor DAF-16 into the nucleus, a state often correlated with stress response and longevity. According to our results we suggest that the protective and life prolonging action of quercetin is not only due to its strong antioxidant capacity but may also be mediated by modulation of signalling pathways.  
  Call Number Serial 1023  
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Author (up) Materi, W.; Pilgrim, D. file  url
openurl 
  Title Novel Caenorhabditis elegans unc-119 axon outgrowth defects correlate with behavioral phenotypes that are partially rescued by nonneural unc-119 Type Journal Article
  Year 2005 Publication Genesis (New York, N.Y. : 2000) Abbreviated Journal Genesis  
  Volume 42 Issue 2 Pages 104-116  
  Keywords Animals; Axons/*ultrastructure; *Behavior, Animal; Caenorhabditis elegans/genetics/*growth & development; Caenorhabditis elegans Proteins/genetics/*physiology; Exons; Gene Transfer Techniques; Green Fluorescent Proteins/analysis/genetics; Introns; Muscles/innervation; Mutation; Nerve Tissue Proteins/genetics/*physiology; Neurons, Afferent/*cytology; Phenotype  
  Abstract UNC-119 function is necessary for the correct development of the Caenorhabditis elegans nervous system. Worms mutant for unc-119 exhibit nervous system structural defects, including supernumerary axon branches, defasciculated nerve fibers, and choice point errors. Axons of both mechanosensory (ALM) and chemo- sensory (ASI) neurons have elongation defects within the nerve ring. Expressing unc-119 cDNA in mechanosensory neurons rescues the elongation defect of ALM axons, but expression in ASI neurons does not rescue ASI axon elongation defects. Neither gross movement nor dauer larva formation defects are rescued in either case. However, expressing a construct including introns under the control of the same promoters results in substantial rescue of phenotypic defects. In these cases reporter expression expands to tissues outside those specified by the promoter, notably into head muscles. Surprisingly, expressing an unc-119 cDNA construct under the control of a muscle-specific promoter fully rescues the dauer formation defect and substantially rescues movement. Thus, although UNC-119 normally acts in a cell-autonomous fashion, the cell-nonautonomous rescue of neural function suggests that it either acts at the cell surface or that it can be transported into the cell from the extracellular environment and play its normal role.  
  Call Number Serial 1004  
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