Relevant bibliographies by topics / C. elegans

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'C. elegans'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 March 2025

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Journal articles on the topic "C. elegans"

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Sarkar, Ramin. "Treatment Analysis for Alzheimer’s Disease using Caenorhabditis Elegans as a Model." International Journal of Advanced Pharmaceutical Sciences and Research 4, no. 4 (June 30, 2024): 29–34. http://dx.doi.org/10.54105/ijapsr.a4057.04040624.

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Alzheimer's Disease, a progressive neurodegenerative condition lacking a definitive and guaranteed treatment, prompts critical investigation for effective remedies to manage its behavioral and cognitive impact. Herbal extracts like Ginkgo Biloba, Lion's Mane, Basil, and Sage present potential options to alleviate plaque build-up caused by Alzheimer's. This study aims to identify the most efficacious herbal extract for treating Alzheimer's, using aged Caenorhabditis elegans (C. elegans) as a model organism. The hypothesis states that treated C. elegans will exhibit increased behavioral movement and altered molecular effects compared to the untreated C. elegans. The Independent Variable consists of the various extracts fed to the C. elegans. The Dependent Variables consist of the C. elegan's behavioral abilities (speed, responsiveness, foraging) and C. elegan’s molecular effects measured by protein concentration. The Control Variable is the untreated aged C. elegan’s behavioral movement and molecular effects. Data was collected using WormLab and molecular assays to validate and determine the treatment's effectiveness. Through ANOVA testing, statistically significant differences emerged in four out of five measured tests, rejecting the null hypothesis more often than accepting it. Results from data indicate Ginkgo Biloba extract as the best extract, due to displaying increased speed, responsiveness, and foraging ability in C.elegans compared to other extracts and untreated C. elegans.This suggests Ginkgo Biloba as a highly possible treatment option.
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McKay, Renée M., James P. McKay, Leon Avery, and Jonathan M. Graff. "C. elegans." Developmental Cell 4, no. 1 (January 2003): 131–42. http://dx.doi.org/10.1016/s1534-5807(02)00411-2.

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Fodor, András. "Sydney Brenner ötven éve „mutatta be” a C. eleganst a genetikusoknak." Magyar Tudomány 186, no. 1 (January 24, 2025): 83–90. https://doi.org/10.1556/2065.186.2025.1.10.

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A Genetics folyóiratban ötven évvel ezelőtt (1974) jelent meg két későbbi Nobel-díjas (Sydney Brenner, Sir John Sulston) brit tudós ikerközleménye („A C. elegans genetikája”, „A C. elegans örökítőanyaga” címekkel), melynek tudománytörténeti jelentősége volt, amit az is bizonyít, hogy a C. eleganson dolgozó kutatók nyerték el a 2024-es fiziológiai és orvostudományi Nobel-díjat. Ez adta az alkalmat, hogy a Brenner- laboratóriumban a C. elegans hőskorában vendégkutatóként dolgozó magyar genetikus felidézze a kutatások lényegét és légkörét.
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SUGI, Takuma. "C. elegans Memory." Seibutsu Butsuri 52, no. 3 (2012): 144–45. http://dx.doi.org/10.2142/biophys.52.144.

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Chamberlin, Helen M. "C. elegans select." Nature Methods 7, no. 9 (September 2010): 693–95. http://dx.doi.org/10.1038/nmeth0910-693.

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Pettitt, Jonathan. "C. elegans II." Trends in Cell Biology 8, no. 2 (February 1998): 92. http://dx.doi.org/10.1016/s0962-8924(98)80022-6.

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Neff, Ellen. "C. elegans HeALTH." Lab Animal 49, no. 8 (July 23, 2020): 221. http://dx.doi.org/10.1038/s41684-020-0609-y.

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GENGYO, Keiko, Yasuhiro HATA, and Hiroaki KAGAWA. "Handling of C. elegans." Seibutsu Butsuri 27, no. 1 (1987): 42–45. http://dx.doi.org/10.2142/biophys.27.42.

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Starich, Todd, Melissa Sheehan, Joy Jadrich, and Jocelyn Shaw. "Innexins in C. elegans." Cell Communication & Adhesion 8, no. 4-6 (January 2001): 311–14. http://dx.doi.org/10.3109/15419060109080744.

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Weitzman, Jonathan B. "CDK7 in C. elegans." Genome Biology 3 (2002): spotlight—20020418–01. http://dx.doi.org/10.1186/gb-spotlight-20020418-01.

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Dissertations / Theses on the topic "C. elegans"

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Gerrits, Daphne D. "Tyrosinases of C. elegans." Thesis, University of Edinburgh, 1998. http://hdl.handle.net/1842/14890.

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The cuticle of C. elegans is extensively cross-linked by covalent disulphide bridges, tyrosine bonds and possibly glutamyl-lysine bonds. Four genes predicted to be involved in the formation of tyrosine bonds have been identified in C. elegans. tyr-1 and tyr-2 map to chromosome III, tyr-3 and tyr-4 map to chromosome I. These encode tyrosinase-like enzymes. The tyrosinase genes are very similar in structure: all genes have two Cu active sites (CuA and CuB), predicted secretory leader peptides and sxc domains (found in other proteins from C. elegans and Toxocara canis). tyr-1 has an additional polyglutamine region which may be involved in protein-protein interactions. A set of cDNAs prepared from a synchronous population of worms, harvested at two hour intervals through the lifecycle, starting shortly after hatching, was used in semi-quantitative fluorescent PCR. Steady state levels of tyr-1, -2 and -4 genes are upregulated at each moult, suggesting their involvement in the synthesis of the new cuticle. tyr-3 transcripts could not be detected in this set of cDNAs, however it was isolated from a population of worms enriched in males. Studies using lacZ- and GFP-reporter genes driven by promoter fragments of the tyrosinase genes showed that tyr-4 and tyr-1 are expressed in specific subsets of hypodermal cells. In addition tyr-1 is expressed in the vulval cells. tyr-2 was found to be expressed only faintly in hypodermal cells, and showed strong expression in the uterine cells. No expression of tyr-3 was observed. These data imply that tyrosinases are not only involved of cross-linking of cuticular proteins, but are probably also involved in the generation of the egg shell.
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Schumacher, Björn. "The C. elegans p53 pathway." Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-19806.

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Gustafson, Megan Alyse. "Serotonin signaling in C. elegans." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/40957.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2007.
Includes bibliographical references.
Wild-type animals that have been acutely food deprived slow their locomotory rate upon encountering bacteria more than do well-fed animals. This behavior, called the enhanced slowing response, is partly serotonin (5-HT) dependent. Animals mutant for the 5-HT reuptake transporter gene mod-5 slow even more than wild-type animals because endogenous 5-HT activity is potentiated. This behavior, called the hyperenhanced slowing response, can be suppressed by mutations in genes that encode proteins important for 5-HT signaling, like the 5-HT receptor encoded by mod-1 and the Ga subunit of a G protein encoded by goa-1. This ability to suppress indicates that these genes likely act downstream of or in parallel to one or more 5-HT synapse(s) that mediate(s) the enhanced slowing response. To find genes that play a role in 5-HT signaling, we screened for suppressors of the 5-HT hypersensitivity of mod-5. We found at least seven alleles of goa-i and at least two alleles of mod-1. This shows that our screen is able to target genes that play a role in endogenous 5-HT signaling. We identified two alleles of the FMRFamide-encoding gene fp-1, which was known to mediate paralysis in exogenous 5-HT. We showed that loss-of-function mutations in flp-1 confer an enhanced slowing response defect. We also identified an allele of abts-1, which encodes a bicarbonate transporter, and showed that it has defects in cholinergic signaling. We identified three mutants that show linkage to LG I, four to II, three to V and one to X, most of which display defects consistent with a role in 5-HT signaling.
(cont.) We used a candidate gene approach to find that deletions in ser-4, which encodes a metabotropic 5-HT receptor, confer 5-HT resistance. ser-4 acts redundantly with the ionotropic 5-HT receptor mod-1 to suppress the hyperenhanced slowing response of mod-5. Our genetic analysis suggests that ser-4 acts in a pathway with goa-1, in parallel to mod-1. We found that the enhanced slowing response defect of flp-1 is primarily due to its defect in transmitting a 5-HT signal and that flp-1 likely acts downstream of ser-4 and mod-1.
by Megan Alyse Gustafson.
Ph.D.
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Barry, Nicholas C. (Nicholas Craig). "Tools for connectomics in C. elegans." Thesis, Massachusetts Institute of Technology, 2018. http://hdl.handle.net/1721.1/120687.

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Thesis: S.M., Massachusetts Institute of Technology, School of Architecture and Planning, Program in Media Arts and Sciences, 2018.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 43-46).
Efforts to model computation in biological neural networks require knowledge of the structure of the network, the dynamics that play across it, and a network simple enough to be tractable to our incipient analyses. The simplicity of the 302-node nervous system of the nematode C. elegans and its transparency have made it an attractive model organism in neuroscience for several decades. Indeed, Caenorhabditis elegans has long been touted as the only species for which the connectome is known, reconstructed by hand from electron micrographs. However, while the number and identity of neurons in C. elegans appears fixed across animals, the variability in the connections between them has not been sufficiently characterized by the above efforts, which examined only a handful of animals and required many years of human labor. Such a characterization, and, moreover, an ability to accurately assess shifts in these neural graphs on timescales compatible with the pace and statistical rigor of scientific research would significantly accelerate efforts to understand neural computation. This thesis lays the groundwork for the development of such a framework. The expansion microscopy tissue preparation platform provided the basis for the set of experiments described within, in which strategies for molecular annotation of C. elegans and the subsequent protocols for readout are examined.
by Nicholas C Barry.
S.M.
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Zhang, Xing. "Exploring fungal virulence using C. elegans." Thesis, Aix-Marseille, 2020. http://theses.univ-amu.fr.lama.univ-amu.fr/200924_ZHANG_406xehco6dvggp718z420kj_TH.pdf.

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Parmi les candidats figuraient plusieurs entérotoxines thermolabiles, une famille de protéines qui est élargie dans le génome de D. coniospora par rapport à d'autres champignons pathogènes. Nous nous sommes concentrés sur 3 (DcEntA-C). L'expression de DcEntA et de DcEntB, mais pas de DcEntC, rendait les vers malades et plus sensibles à l'infection. Normalement, l'infection par D. coniospora provoque l'induction de l'expression de gènes codant des peptides antimicrobiens des familles nlp et cnc. Il est intéressant de noter que l'expression de la seule entérotoxine DcEntA a bloqué la transcription des gènes nlp et cnc. DcEntA a agi en inhibant la translocation nucléaire du facteur de transcription STAT STA-2, nécessaire à l'expression des gènes de défense. Nous avons démontré que cet effet était spécifique car DcEntA a induit une forte expression d'un gène inductible par une infection indépendante de STA-2. En revanche, les vers exprimant l'entérotoxine DcEntB présentaient une élévation de l'expression de nlp-29 dépendante de STA-2. DcEntB est localisé au niveau du nucléole et affecte la taille et la morphologie du nucléole. La base moléculaire de ces différences et l'importance relative de ces facteurs au cours de l'infection ont été étudiées en détail. Notre résultat révélé la complexité des stratégies de virulence fongique. Globalement, en disséquant le mode d'action des différents facteurs de virulence, cette étude nous a permis de mieux comprendre la pathogénie fongique et la course évolutive entre l'hôte et l'agent pathogène
Among the candidates were several heat-labile enterotoxins, a protein family that is expanded in the genome of D. coniospora compared to other pathogenic fungi. We focused on 3 (DcEntA-C). Expression of DcEntA and DcEntB, but not DcEntC made worms sick and more susceptible to infection. Normally, D. coniospora infection provokes the induction of expression of antimicrobial peptide genes of the nlp and cnc families. Interestingly, expression of the single enterotoxin DcEntA blocked the transcription of both nlp and cnc genes. DcEntA acted by inhibiting the nuclear translocation of the STAT transcriptional factor STA-2, required for defence gene expression. We demonstrated that this effect was specific as DcEntA induced high expression of a STA-2-independent infection-inducible gene. In contrast, worms expressing the enterotoxin DcEntB exhibited a STA-2 dependent elevation of nlp-29 expression. DcEntB was localized to the nucleolus and affected nucleolus size and morphology. The molecular basis of these differences and the relative importance of these factors during infection was explored in detail. Our result revealed the complexity of fungal virulence strategies. Overall, by dissecting the mode of action of different virulence factors, this study allowed us to understand better fungal pathogenesis and the evolutionary arms race between host and pathogen
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Boyle, Jordan Hylke. "C. elegans locomotion : an integrated approach." Thesis, University of Leeds, 2009. http://etheses.whiterose.ac.uk/1377/.

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he popular model organism Caenorhabditis elegans is a tiny nematode worm with a largely invariant nervous system, consisting of exactly 302 neurons with known connectivity. Moreover, the behavioural roles of many of these neurons have been uncovered using experimental techniques including targeted cell killing and genetic mutations. The result is an organism in which the locomotion subsystem is mapped at cellular resolution. Despite its small size and the apparent simplicity of the underlying nervous system, the worm is capable of a surprisingly rich repertoire of behaviours including navigation and foraging, mating, learning, and even rudimentary social behaviour. Indeed, this humble worm provides us with the first tangible possibility of understanding the complex behaviours of an organism from the genetic level, right up to the system level. The focus of this thesis on the locomotion system is motivated at least in part by the fact that most, if not all, of the worm’s behaviours are mediated by some form of locomotion. The main objective of this thesis is to help elucidate the mechanisms underlying C. elegans forward locomotion. In pursuit of this goal I apply an integrated methodology that emphasises collaboration between modellers like myself and experimentalists, ensuring that models are grounded in the biological reality and experiments are well designed and poignant. In contrast to previous models of C. elegans forward locomotion, the starting point of this investigation is the realization that the ability of the worm to locomote through a variety of different physical environments can shed light on the mechanism of neural and neuromuscular control of this behaviour. This work therefore begins with the presentation of several stand-alone studies, both theoretical and experimental, aimed at answering a number of preliminary questions. These include the development of a suitable model of the worm’s low Reynolds number physical environments; a preliminary study of the importance of body physics on the kinematics of locomotion; an electrophysiological modelling study of the worm’s body wall muscles; and an experimental investigation of the worm’s locomotion in different environments, ranging from liquid to dense gels. These results lead to a new perspective on the worm’s locomotion. Indeed, the conventional wisdom is that two kinematically distinct C. elegans locomotion behaviours – swimming in liquids and crawling on dense gel-like media – correspond to distinct locomotory gaits. By analysing the worm’s motion through these different media, we reveal a smooth modulation of the undulations from swimming to crawling, marked by a linear relationship between key locomotion metrics. These results point to a single locomotory gait, governed by the same underlying control mechanism. The core of this thesis is an integrated neuromechancial model of C. elegans forward locomotion. This model incorporates the results of the preliminary investigation of muscle, body and locomotion properties. The neural circuitry is grounded in the literature but simplified to a set of repeating units. Neuronal properties are modelled at different levels of abstraction, with a proof-of-concept continuous model that is used to ground assumptions in physiological data, and a simplified binary model that is then used to study the locomotion control in detail. A key property of the motor neurons in both these models is their bistable response, inspired by a recent publication demonstrating such properties in other motor neurons. Interestingly, the model is quite different to any that have come before, both in terms of its underlying neural dynamics and the behaviours that it addresses. The key achievement of this model is its ability to qualitatively and quantitatively account for locomotion across a range of media from water to agar, as well as in more complex (heterogeneous) environments. One particularly interesting result is the demonstration that a proprioceptive oscillatory mechanisms can account not only for the generation of the body undulation, but also the observed modulation in response to the changing physical environments. Indeed, this model lacks any form of centrally generated nervous system control. Finally, the model makes a number of important predictions about neuronal functions, synaptic functions and the proprioceptive response to different physical environments. A number of experiments and experimental designs are suggested to test these predictions. Preliminary experimental results are then presented to address each of these predictions. To date, these results all appear to validate the model and uncover new information about the locomotion system, hence demonstrating the power of the holistic, integrated methodology of this work. Specifically I address the role of the inhibitory D-class neurons and find evidence suggesting that they are part of the core circuit for forward locomotion, but that the phenotype associated with their removal only manifests strongly in less resistive (more fluid) media. Furthermore, I shed light on the relative roles of neural and muscle inhibition and suggest that it may be an absence of neural inhibition that underlies the forward locomotion defect of GABA defective worms.
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Mendenhall, Alexander R. "Genetic Mechanisms for Anoxia Survival in C. Elegans." Thesis, University of North Texas, 2008. https://digital.library.unt.edu/ark:/67531/metadc9062/.

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Oxygen deprivation can be pathological for many organisms, including humans. Consequently, there are several biologically and economically relevant negative impacts associated with oxygen deprivation. Developing an understanding of which genes can influence survival of oxygen deprivation will enable the formulation of more effective policies and practices. In this dissertation, genes that influence adult anoxia survival in the model metazoan system, C. elegans, are identified and characterized. Insulin-like signaling, gonad function and gender have been shown to influence longevity and stress resistance in the soil nematode, C. elegans. Thus, either of these two processes or gender may influence anoxia survival. The hypothesis that insulin-like signaling alters anoxia survival in C. elegans is tested in Aim I. The hypotheses that gonad function or gender modulates anoxia survival are tested in Aim II. Insulin-like signaling affects anoxia survival in C. elegans. Reduction of insulin-like signaling through mutation of the insulin-like receptor, DAF-2, increases anoxia survival rates in a gpd-2/3 dependent manner. The glycolytic genes gpd-2/3 are necessary for wild-type response to anoxia, and sufficient for increasing anoxia survival through overexpression. Gonad function and gender both affect anoxia survival in C. elegans. A reduction of ovulation and oocyte maturation, as measured by oocyte flux, is associated with enhanced anoxia survival in all cases examined to date. Reduction of function of several genes involved in germline development and RTK/Ras/MAPK signaling reduce ovulation and oocyte maturation while concurrently increasing anoxia survival. The act of mating does not influence anoxia survival, but altering ovulation through breeding or chemical treatment does. The male phenotype also increases anoxia survival rates independent of genotype. These studies have identified and characterized over ten different genotypes that affect adult survival of anoxia in C. elegans. Before these studies were conducted, there were no genes known to influence adult anoxia survival in C. elegans. Furthermore, these studies have begun to uncouple mechanisms of longevity and stress resistance.
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Ellis, Gregory Cody. "Regulation of polarity during C. elegans embryogenesis /." view abstract or download file of text, 2002. http://wwwlib.umi.com/cr/uoregon/fullcit?p3072580.

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Thesis (Ph. D.)--University of Oregon, 2002.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 90-98). Also available for download via the World Wide Web; free to University of Oregon users.
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Choi, Seungwon. "Regulation of Behavioral Arousal in C. elegans." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:10808.

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Animals undergo periods of behavioral quiescence and arousal in response to environmental, circadian, or developmental cues. During larval molts, C. elegans undergoes a period of profound behavioral quiescence termed lethargus. Locomotion quiescence during lethargus was abolished in mutants lacking a neuropeptide receptor (NPR-1), and was reduced in mutants lacking NPR-1 ligands (FLP-18 and -21). Wild type strains are polymorphic for the npr-1 gene, and their lethargus behavior varies correspondingly. Locomotion quiescence and arousal were mediated by decreased and increased secretion of an arousal neuropeptide (PDF-1) from central neurons. PDF receptors (PDFR-1) expressed in peripheral mechanosensory neurons enhanced touch-evoked calcium transients. Thus, a central circuit stimulates arousal from lethargus by enhancing the sensitivity of peripheral mechanosensory neurons in the body. These results define a circuit mechanism controlling a developmentally programmed form of quiescence.
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Feng, Ying. "Study of glucose transporters in C. elegans." Thesis, University of Bath, 2010. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.537773.

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The calorie restriction (CR) and insulin/IGF-I-like signalling (IIS) are two pathways regulating the lifespan of C. elegans. Recent studies showed that glucose restriction extends the lifespan of C. elegans while excessive glucose shortens the lifespan of the worms. The first step of the glucose metabolism is the transport of glucose across the plasma membrane by the glucose transporters. The work described in this thesis aims to identify glucose transporters in C. elegans and to provide a primary investigation of the in vitro and in vivo function of the identified glucose transporter. Nine putative transporters have been cloned and expressed. Out of the nice cloned putative transporters in the C. elegans genome, H17B01.1 (H17) only is identified as a fully functional glucose transporter using an oocyte expression system in which glucose transport activity is directly measured. The two transcripts of H17 are both capable of transporting glucose with high affinity, as well as transporting trehalose. Heterologous expression of H17 in mammalian CHO-T cells suggests that the protein is localised both on the plasma membrane and in the cytosol. In vitro studies of H17 show that the protein does not respond to insulin stimulation when expressed in mammalian CHO-T cell and rat primary adipocyte systems. In vivo functional studies using H17 RNAi indicate that the worm’s lifespan is not affected by the H17 knockdown. However, glucose metabolism of C. elegans (as measured by glucose oxidation to CO2 and incorporation into fat reserves) is influenced by the decreased expression of H17, especially in the daf-2 mutant strain, e1370. However, the increase of glucose metabolism caused by H17 knockdown observed in daf-2 mutant is inhibited in the age-1 and akt-1 mutant strains. The findings reported in this thesis suggest that the H17 glucose transporter may play an important role glucose metabolism in C. elegans and that this transport and metabolism is influenced by insulin receptor activity and serine kinase cascades.
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Books on the topic "C. elegans"

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Kevin, Strange. C. elegans. New Jersey: Humana Press, 2006. http://dx.doi.org/10.1385/1597451517.

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Haspel, Gal, and Anne C. Hart, eds. C. elegans. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2181-3.

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Biron, David, and Gal Haspel, eds. C. elegans. Totowa, NJ: Humana Press, 2015. http://dx.doi.org/10.1007/978-1-4939-2842-2.

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F, Altun Zeynep, ed. C. elegans atlas. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2008.

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L, Riddle Donald, ed. C. elegans II. Plainview, N.Y: Cold Spring Harbor Laboratory Press, 1997.

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A, Hope Ian, ed. C. elegans: A practical approach. Oxford: Oxford University Press, 1999.

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Olsen, Anders, and Matthew S. Gill, eds. Ageing: Lessons from C. elegans. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-44703-2.

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1955-, Strange Kevin, ed. C. elegans: Methods and applications. Totowa, N.J: Humana Press, 2006.

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Eric, Aamodt, ed. The neurobiology of C. elegans. San DIego, Ca: Elsevier Academic Press, 2006.

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Schedl, Tim, ed. Germ Cell Development in C. elegans. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-4015-4.

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Book chapters on the topic "C. elegans"

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Viswanathan, Mohan, and Heidi A. Tissenbaum. "C. elegans Sirtuins." In Sirtuins, 39–56. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-637-5_3.

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Xiao, Rui, and X. Z. Shawn Xu. "C. elegans TRP Channels." In Transient Receptor Potential Channels, 323–39. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0265-3_18.

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Olsen, Anders, James N. Sampayo, and Gordon J. Lithgow. "Aging in C. elegans." In Aging of Organisms, 163–99. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-017-0671-1_7.

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Crook, Matt, Avni Upadhyay, and Wendy Hanna-Rose. "Necrosis in C. elegans." In Methods in Molecular Biology, 171–82. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-383-1_13.

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Park, Byung-Jae, Jin Il Lee, and Joohong Ahnn. "Calreticulin in C. elegans." In Calreticulin, 248–57. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9258-1_22.

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Zhang, Yue, and William B. Mair. "Dietary Restriction in C. elegans." In Healthy Ageing and Longevity, 355–91. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-44703-2_16.

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Eastburn, Dennis J., and Min Han. "Ras Signaling in C. Elegans." In RAS Family GTPases, 199–225. Dordrecht: Springer Netherlands, 2006. http://dx.doi.org/10.1007/1-4020-4708-8_9.

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Durbin, Richard. "Nematode C. elegans, Nervous System." In Comparative Neuroscience and Neurobiology, 82–83. Boston, MA: Birkhäuser Boston, 1988. http://dx.doi.org/10.1007/978-1-4899-6776-3_33.

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Wood, Jordan F., and Denise M. Ferkey. "GRK Roles in C. elegans." In Methods in Pharmacology and Toxicology, 283–99. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3798-1_13.

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Sugi, Takuma. "Genome Editing of C. elegans." In Methods in Molecular Biology, 389–96. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3016-7_29.

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Conference papers on the topic "C. elegans"

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Baskota, Anuj, Hsin-Yun Chang, Amaresh Chaturbedi, Justin Kuo, Serhan Ardanuc, Siu Sylvia Lee, and Amit Lal. "Modeling and Imaging of GHz Ultrasonic Impedance of C. elegans." In 2024 IEEE Ultrasonics, Ferroelectrics, and Frequency Control Joint Symposium (UFFC-JS), 1–4. IEEE, 2024. https://doi.org/10.1109/uffc-js60046.2024.10794041.

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Machado, Pedro, John Wade, and T. M. McGinnity. "Si elegans: FPGA hardware emulation of C. elegans nematode nervous system." In 2014 Sixth World Congress on Nature and Biologically Inspired Computing (NaBIC). IEEE, 2014. http://dx.doi.org/10.1109/nabic.2014.6921855.

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Fontaine, Ebraheem, Joel Burdick, and Alan Barr. "Automated Tracking of Multiple C. Elegans." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.260657.

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Fontaine, Ebraheem, Joel Burdick, and Alan Barr. "Automated Tracking of Multiple C. Elegans." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.4398256.

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Costalago Meruelo, Alicia, Pedro Machado, Kofi Appiah, and T. Martin McGinnity. "Si elegans: A Computational Model of C. elegans Muscle Response to Light." In Symposium on Neuro-Bio-Inspired Computation and Architectures. SCITEPRESS - Science and and Technology Publications, 2015. http://dx.doi.org/10.5220/0005712201210126.

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Machado, Pedro, John Wade, and T. M. Mcginnity. "Si elegans - Computational Modelling of C. elegans Nematode Nervous System using FPGAs." In Special Session on Neuro-Bio-Inspired Computation and Architectures. SCITEPRESS - Science and and Technology Publications, 2014. http://dx.doi.org/10.5220/0005169301690176.

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Johari, S., V. Nock, and W. Wang. "PDMS micropillars for C. elegans force measurement." In 2016 IEEE International Conference on Semiconductor Electronics (ICSE). IEEE, 2016. http://dx.doi.org/10.1109/smelec.2016.7573578.

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Hsieh, Ting-Yu, and Yuan Luo. "HLSM for live C. elegans (Conference Presentation)." In Photosensitive Materials and their Applications, edited by Robert R. McLeod, Yasuo Tomita, John T. Sheridan, and Inmaculada Pascual Villalobos. SPIE, 2020. http://dx.doi.org/10.1117/12.2554508.

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Vidal, Marc. "Toward a proteome atlas for C. Elegans." In the sixth annual international conference. New York, New York, USA: ACM Press, 2002. http://dx.doi.org/10.1145/565196.565237.

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Adams, Kevin, Roger Mailler, and Michael W. Keller. "Adhesion of C. Elegans to Agar Surfaces." In ASME 2012 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/imece2012-89670.

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The surface adhesion between C. elegans and the agar plates on which they are commonly grown has yet to be accurately quantified. C. elegans are a scientifically important species of nematode whose simple structure allowed the first mapping of the complete nervous system in a multicellular organism. One of the current topics of research in the C. elegans community is the investigation of neuronal function in locomotion. Models of locomotion are used in these studies to aid in determination of the functions of specific neurons involved in locomotion. The adhesion force plays a critical role in developing these models. This paper presents the experimental determination of the adhesion energy of a representative sample of C. elegans. Adhesion energy was determined by a direct pull-off technique. In this approach, nematodes are anesthetized to prevent movement and secured to a small load cell before an agar plate is slowly brought into contact with the specimen and then removed. The maximum tensile force is then fit to a JKR-type adhesion model, which assumes that the nematode is a cylinder in order to determine the adhesion energy. Repeated adhesions are also investigated to determine the importance of drying on the measured adhesion force.
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Reports on the topic "C. elegans"

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Mellies, Jay L. C. elegans as a Model for EPEC Infection. Fort Belvoir, VA: Defense Technical Information Center, November 2005. http://dx.doi.org/10.21236/ada441203.

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Padgett, Richard W. Cell Cycle Regulation by TGFb Signaling in C. elegans. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada398212.

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Padgett, Richard. Cell Cycle Regulation by TGFb Signaling in C. elegans. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada390936.

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Ling Hsiao, Ray, Yu Wei Lin, and Chiang Yun Chen. Supplementary Information of Innovative Observation of a 266-nm Laser Inhibiting Egg Laying in Caenorhabditis elegans. Science Repository, July 2022. http://dx.doi.org/10.31487/j.acr.2022.02.04.sup.

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Infrared laser as a heat source could induce gene expression by activating heat promoter genes in Caenorhabditis elegans, as previously reported. In this study, we innovatively used a 266-nm laser to irradiate C. elegans for only one second and observed a significant inhibition of the overall number of eggs laid (P < 0.0001) and the first day egg laying (P=0.005). This is the first study to establish how light with a wavelength of 266-nm can influence a life activity such as laying eggs in C. elegans.
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Sternberg, Paul W. Identification of Novel Candidate Tumor Suppressor Genes Using C. elegans as a Model. Fort Belvoir, VA: Defense Technical Information Center, November 1996. http://dx.doi.org/10.21236/ada323557.

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Sternberg, Paul W. Identification of Novel Candidate Tumor Suppressor Genes Using C. elegans as a Model. Fort Belvoir, VA: Defense Technical Information Center, December 1997. http://dx.doi.org/10.21236/ada344938.

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Sternberg, Paul W. Identification of Novel Candidate Tumor Suppressor Genes Using C. elegans as a Model. Fort Belvoir, VA: Defense Technical Information Center, November 1999. http://dx.doi.org/10.21236/ada391240.

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Spencer, Andrew G. Characterization of sur-2, a Novel Ras-Mediated Signal Transduction Component in C. elegans. Fort Belvoir, VA: Defense Technical Information Center, April 2000. http://dx.doi.org/10.21236/ada381285.

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Negrete, Oscar A., Catherine Branda, Jasper O. E. Hardesty, Mark David Tucker, Julia N. Kaiser, Carol L. Kozina, and Gabriela S. Chirica. A C. elegans-based foam for rapid on-site detection of residual live virus. Office of Scientific and Technical Information (OSTI), February 2012. http://dx.doi.org/10.2172/1035339.

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Fraser, Andrew, and Julie Ahringer. Characterization of Two C. Elegans Homologuses of Oncogenic Inhibitor of Apoptosis Proteins (IAPs) and Identification of Interacting Genes. Fort Belvoir, VA: Defense Technical Information Center, September 2000. http://dx.doi.org/10.21236/ada393958.

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