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Dissertations / Theses on the topic 'Eleganz'

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Published: 4 June 2021

Last updated: 4 March 2023

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1

Hall, Linnea Suzanne. "Habitat selection by the elegant trogon (Trogon elegans) at multiple scales." Diss., The University of Arizona, 1996. http://hdl.handle.net/10150/187497.

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In this dissertation I discuss several facets of the ecology of the elegant trogon (Trogon elegans). In Chapter 1, I assessed habitat selection by the trogon from 1993 to 1995 at three spatial scales (those of the mountain and canyon, home range, and microsite scales). At the broadest (inter-mountain and inter-canyon) scale, trogons were positively associated with cover by sycamore, pinyon, and juniper vegetation, and the abundances of three bird species. At the intermediate scale, radio-tagged trogons in the Huachuca and Santa Rita mountains used both upland and riparian areas, and selectively used sites with dense vegetation within those areas. At the microsite scale, nest sites of trogons were primarily located in sycamore trees in riparian areas. Successful nests could be discriminated from unsuccessful nests on the basis of three variables. Adult trogons used trees that were mostly dead for several behaviors besides nesting, and males foraged from sycamore and oak trees. Across all three scales, trogons were associated with variables describing sycamores, junipers, pines, and oaks, indicating that these trees were important to elegant trogon habitat use in Arizona. In Chapter 2, I discussed the behavior and phenology of nesting elegant trogons in the Chiricahua, Huachuca, and Santa Rita mountains in 1993-1994. I described the average durations and characteristics of nest advertisement, incubation, brooding, nestling attendance, and fledgling attendance behaviors. Elegant trogons in Arizona had different behaviors from other members of Neotropical Trogonidae, especially in regards to their durations of incubation and feeding. In Chapter 3, I present analyses of disturbance records collected while observing trogons in 1993-1995, and the finding that elegant trogons did not react strongly to most contacts with humans. However, on some occasions trogons reacted long enough to humans to potentially impact their productivity at nest sites. Therefore, some protection of nesting trogons may be warranted. In general, management of trogons in Arizona will require consideration of whole watersheds, including the condition of riparian water tables and upland vegetation.

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2

Leff, Robert Daniel. "Elegant solutions." Thesis, Massachusetts Institute of Technology, 1997. http://hdl.handle.net/1721.1/10549.

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3

Tam, Chung Nga. "The role of ram-2 in Caenorhabditis elegans development /." View abstract or full-text, 2004. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202004%20TAM.

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Thesis (M. Phil.)--Hong Kong University of Science and Technology, 2004.
Includes bibliographical references (leaves 124-134). Also available in electronic version. Access restricted to campus users.

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4

Pierce-Shimomura, Jonathan Thomas. "Behavioral, neural and genetic analyses of chemotaxis in the nematode, Caenorhabditis elegans /." view abstract or download file of text, 2000. http://wwwlib.umi.com/cr/uoregon/fullcit?p9998044.

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Thesis (Ph. D.)--University of Oregon, 2000.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 113-123). Also available for download via the World Wide Web; free to University of Oregon users.

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5

Willis, John Henry. "Regulation of the cytoskeleton in the early Caenorhabditis elegans embryo /." view abstract or download file of text, 2004. http://wwwlib.umi.com/cr/uoregon/fullcit?p3136453.

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Thesis (Ph. D.)--University of Oregon, 2004.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 68-73). Also available for download via the World Wide Web; free to University of Oregon users.

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6

Leung, Benjamin Hong Nien. "Intestinal morphogenesis in the Caenorhabditis elegans embryo /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/5073.

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7

Ludewig, Hanno Andreas. "Nuclear receptor pathways in Caenorhabditis elegans: DIN-1, a DAF-12 coregulator of dauer diapause and developmental arrest." [S.l.] : [s.n.], 2003. http://www.diss.fu-berlin.de/2003/265/index.html.

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8

Wong, Yan Fung. "MAB-30 functions to maintain cell identity of sensory ray in C. elegans /." View abstract or full-text, 2008. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202008%20WONG.

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9

Garcez, Fernanda Rodrigues. "Limonóides e protolimonóides de Trichilia elegans ssp. Elegans A. Juss. (Meliaceae)." Universidade de São Paulo, 1997. http://www.teses.usp.br/teses/disponiveis/46/46135/tde-12112015-153501/.

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o presente trabalho teve como objetivo realizar o estudo químico das sementes de Trichilia elegans ssp. Elegans A. Juss. (coletadas no município de Corumbá, MS), visando o isolamento e identificação ou elucidação estrutural dos seus metabólitos secundários, particularmente limonóides. Da fase diclorometânica, obtida de uma partição efetuada com o extrato etanólico das sementes, foram isoladas, através de técnicas cromatográficas de separação (cromatografia em colunas de sílica gel, de Sephadex LH 20 e CLAE em fase reversa), dezoito substâncias, compreendendo: dois protolimonóides, onze limonóides com esqueleto do tipo obacunol (abertura dos anéis A e D), quatro com esqueleto do tipo ivorensato de metila (abertura dos anéis A, B e D) e 3β-O-β-D-glicopiranosilsitosterol. Todas as substâncias são inéditas, com exceção do esteróide glicosilado e de dois limonóides com esqueleto do tipo obacunol (kihadaninas A e B). As determinações estruturais foram efetuadas com base em dados espectroscópicos de RMN 1H e 13C, incluindo experimentos bidimensionais (COSY 1H-1H, COSY 1H-13C, HMQC, NOESY e HMBC); a partir de informações obtidas dos espectros de massas e na região do IV e através de dados de difração de raios-X. Quatro dos limonóides obtidos foram submetidos a um ensaio biológico de atividade antitumoral, utilizando-se linhagens mutantes de Saccharomyces cerevisiae, porém, mostraram-se inativos.
The present work describes the isolation and identification or structural elucidation of the chemical constituents of the seeds of Trichilia elegans ssp. Elegans A. Juss., collected in Corumbá, MS. From the dichloromethane solubles, obtained from partition of the ethanolic extract from the seeds, eighteen substances have been isolated, after a combination of column and flash chromatography on silica gel, gel filtration and reversed phase HPLC separations. The isolated substances have been characterized as two new protolimonoids, nine new obacunol- and four new methyl ivorensate-type limonoids, in addition to two known limonoids belonging to the obacunol group (kihadanins A and B) and 3-O-β-D-glucopyranosyl-sitosterol. The structures of these compounds have been established on the basis of 1D (1H, 13C) and 2D (1H-1H and 1H-13C COSY, HMQC, HMBC and NOESY) NMR spectroscopic techniques, IR and mass spectral data and X-ray crystallographic analyses. Four of the isolated limonoids have been tested against DNA reparr deficient mutants of Saccharomyces cerevisiae but, nevertheless, shown to be inactive.

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10

Choy, Robert Kwai Ming. "Worms on prozac : genetic and molecular analysis of fluoxetine resistance in the nematode Caenorhabditis elegans /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/5031.

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11

Severson, Aaron Frederick. "An investigation into the mechanism of cytokinesis in the Caenorhabditis elegans embryo /." view abstract or download file of text, 2001. http://wwwlib.umi.com/cr/uoregon/fullcit?p3018394.

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Thesis (Ph. D.)--University of Oregon, 2001.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 118-127). Also available for download via the World Wide Web; free to University of Oregon users.

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12

Williams, Corey L. "Analysis of cystic kidney disease-related genes in Caenorhabditis elegans." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2009p/williams.pdf.

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13

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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14

Dekkers, Martijn. "Plasticity in Caenorhabditis elegans." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2008. http://hdl.handle.net/1765/13961.

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15

Tighe-Pigott, Katharine. "THE ELEGANT UNIVERSE: STORIES." UKnowledge, 2018. https://uknowledge.uky.edu/english_etds/81.

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The Elegant Universe: Stories is a story collection featuring female characters unflinching in their self-appraisal, and wry in their humor, who explore the realities of their heterosexual relationships, particularly the weighty decision whether to have children or not in these dark and terrifying times. Sometimes funny, sometimes sad, the stories collected here explore the various, subtle modes of threat that are the palpable part of the experience of being a woman—not in society, or in the workplace, but primarily inside relationships with men. At the same time, the stories own that love can grow between men and women despite the near and present poison of misogyny. They own the miracle of motherhood while depicting the palpable fragility of new life and the proximity of mothers to unstoppable wreckage and ruin.

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16

Beurton, Flore. "Étude de l’interaction physique et fonctionnelle entre le complexe histone méthyltransférase SET-2/SET1 et le complexe histone déacétylase SIN-3S dans l’embryon de C. elegans." Thesis, Lyon, 2018. http://www.theses.fr/2018LYSEN017.

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Les complexes histones méthyltransférases SET1, hautement conservés de la levure aux mammifères, sont ciblés aux régions promotrices par la protéine CFP1/CXXC, résultant en l’implémentation de la méthylation de la lysine 4 de l’histone H3 (H3K4me), modification post-traductionnelle influençant l’expression des gènes selon le contexte chromatinien. La présence de plusieurs complexes SET1 distincts dans différents systèmes modèles eucaryotes a compliqué l’étude de leurs fonctions dans un contexte développemental. Caenorhabditis elegans contient une seule protéine homologue de SET1, SET-2, et d’uniques homologues des autres sous-unités du complexe, RBBP5, ASH2, WDR5, DPY30 et CFP1. Cependant, la composition biochimique du complexe n’a pas été décrite. En couplant des expériences de co-immunoprécipitation avec des analyses de spectrométrie de masse, j’ai identifié le complexe SET-2/SET1 dans les embryons de C. elegans. D’autre part, j’ai montré que le complexe SET-2/SET1 co-immunoprécipite aussi un autre complexe conservé modifiant la chromatine et j’ai mis en évidence les interactions mises en jeu entre ces deux complexes. Mon analyse génétique a démontré que les mutants de perte de fonction des sous-unités des deux complexes partagent des phénotypes communs, en cohérence avec des fonctions développementales communes. Le laboratoire a également entrepris des expériences de transcriptomique et d’immunoprécipitation de la chromatine montrant un nouveau rôle de CFP-1 dans le recrutement de ce complexe au niveau de sites spécifiques de la chromatine
The highly conserved SET1 family complexes are targeted by CFP1/CXXC protein to promoter regions through multivalent interactions to implement methylation of histone H3 Ly4 (H3K4me), a modification that correlates with gene expression depending on the chromatin context. The presence of distinct SET1 complexes in multiple eukaryotic model systems has hampered studies aimed at identifying the complete array of functions of SET1/MLL regulatory networks in a developmental context. Caenorhabditis elegans contains one SET1 protein, SET-2, one MLL-like protein, SET-16, and single homologs of RBBP5, ASH2, WDR5, DPY30 and CFP1. The biochemical composition of the complex however, has not been described. Through the use of co-immunoprecipitation coupled to mass spectrometry-based proteomics, I identified the SET-2/SET1 complex in C. elegans embryos. Most importantly, I showed that the SET-2/SET1 complex also co-immunoprecipitates another conserved chromatin-modifying complex and I highlighted the interactions involved between these two complexes. My genetic analysis revealed that loss of function mutants of the two complex subunits share common phenotypes, consistent with common developmental functions. The laboratory has also undertaken transcriptomic and chromatin immunoprecipitation experiments showing that CFP-1 has a role in the binding of this complex at specific chromatin regions

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17

Chen, Di. "Regulatory pathways controlling larval development in caenorhabditis elegans." Free to MU Campus, others may purchase, 2004. http://wwwlib.umi.com/cr/mo/fullcit?p3144405.

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18

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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19

Lakowski, Bernard C. "Genetic factors affecting life span in the nematode Caenorhabditis elegans." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0005/NQ44483.pdf.

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20

Felkai, Stephanie. "Phenotypic consequences of altering expression of the Caenorhabditis elegans timing gene clk-1." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=21551.

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clk-1 mutants of the nematode C. elegans have been phenotypically characterized in previous work and found to have decreased rates of development and of periodic adult behaviours, such as defecation, pumping and swimming (Wong et al., 1995). In this study, the defecation periods in older wild type and clk-1 mutant worms were found to be similar despite their differences in young adults. Transgenic strains which express high levels of clk-1 were characterized phenotypically. Over-expression of the clk-1 gene has no observed effect on physiological rates as measured conventionally in young adults but rather has an effect on defecation rates in an age-dependent manner. A proportion of ageing transgenic animals over-expressing clk-1 did not have decreased defecation period, as seen in ageing wild type and clk-1 mutants. This suggests that the action of CLK-1, which functions in controlling physiological rates, is reduced in older wild type worms. As previously characterized, clk-1 mutants have lengthened life spans compared to wild type (Wong et al., 1995). Consistent with this effect, we found transgenic strains with high clk-1 expression to have a shortened average life span. Furthermore, no effect on average life span was found in transgenic control strains in which clk-1 expression was not altered, confirming that the presence of the transgene and the phenotype marking its presence do not influence the observed effects in strains with high clk-1 expression. Together, the findings from both the studies on physiological rates and life span suggest that clk-1 plays a role in determining the rate at which worms age.

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21

Lemieux, Jason. "The Caenorhabditis elegans Clock gene gro-1 encodes a metazoan N6-( [delta]2) isopentenyl PPi: tRNA isopentenyl transferase /." Thesis, McGill University, 1999. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=21589.

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The Caenorhabditis elegans gene gro-1 belongs to the Clock group of genes. The four known genes making up this class are believed to be involved in a general mechanism acting to coordinate the time-dependent processes in the organism. Mutation of these genes alter the timing of many disparate processes. This results in the mean lengthening of embryonic and post-embryonic development, as well as in a lengthening of the periods of a number of adult behaviours including pharyngeal pumping, swimming and the defecation cycle. These mutants also exhibit a significantly increased life span. The gene gro-1 has been cloned and encodes a metazoan N6-(Delta2) isopentenyl PPi: tRNA isopentenyl transferase. In S. cerevisiae and bacteria this enzyme has been shown to modify tRNAs that code for codons begining with U. This modification consists of the isopentenylation of the adenine residue at position 37, adjacent to the anti-codon. Interestingly, gro-1 is the fifth member of an operon. Preliminary expression studies with GFP reporter constructs suggest that as in yeast, GRO-1 is expressed in the cytoplasm and mitochondria, as well as in the nucleus.

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22

Han, Dong 1970. "Identification and molecular genetic characterization of a coq-4 knockout mutation in Caenorhabditis elegans." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33769.

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In Caenorhabditis elegans, mutations in the clk-1 gene result in delayed embryonic and post-embryonic development, a slowing down of rhythmic behaviors and an extended life span. CLK-1 encodes the demethoxyubiquinone (DMQ or DMQn) hydroxylase in the ubiquinone (CoQ or Qn) biosynthesis pathway. Thus, clk-1 mutants produce DMQ instead of CoQ. In order to understand the relationship between the CoQ biosynthesis defect and the pleiotropic phenotype of clk-1 mutants, I isolated a deletion mutant, coq-4(qm143), in C. elegans. In Saccharomyces cerevisiae, mutants in COQ4, the coq-4 homologue, do not produce ubiquinone, like those in COQ7, the clk-1 homologue. coq-4(qm143) is a non-strict maternal-effect lethal mutation. Most of the progeny from a homozygous coq-4(qm143) hermaphrodite die during embryogenesis. However, homozygous coq-4(qm143) hermaphrodites from a heterozygous mother can develop and behave normally until adulthood. As adults, they become uncoordinated and paralytic, and are defective in egg-laying. Unlike hermaphrodites, homozygous coq-4(qm143) males are fully maternally rescued. The qm143 is a 1469 base pair deletion, which completely removes the coq-4 gene and does not affect the coding sequence of any other gene. By performing germline transformation, I also showed that the non-viable phenotype of coq-4 (qm143) is indeed due to the removal of the coq-4 gene itself. The preliminary study of COQ-4 expression pattern by using a COQ-4::GFP fusion protein indicates that COQ-4 is expressed in mitochondria of the worm.

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23

Meng, Yan 1972. "Genes that affect development and biological timing in Caenorhabditis elegans." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=31272.

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In an effort to find new genes involved in development and the biological timing, I carried out a new screen for viable maternal-effect mutations similar in protocol to the previous screen in which 24 such genes have been identified. I screened 10,600 genomes and isolated 6 slow-growing mutations and 5 behavioral and morphological mutations. Another maternal-effect slow-growing mutation is isolated from a screen for both maternal-effect and non maternal-effect slow development mutations. Genetic mapping suggests that none of the seven slow growing mutations corresponds to previously identified genes, so seven new clk genes (clk-4, clk-5, clk-6, clk-7 clk-8, clk-9, clk-10) have been identified. Because most identified clk genes (clk-2, clk-4 to clk-10 and gro-1) are defined by single allele, we believe that these genes have not yet been saturated. Mutants of seven new clk genes have typical Clk phenotypes: a mean lengthening of embryonic development, postembryonic development, defecation cycle and life span. As the screening procedure did not involve any measure of life span, it is suggested that slow life is sufficient for long life. As expected, all seven mutations can be maternally rescued.

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24

Wang, Ying. "Identification of a protein that interacts with Caenorhadbitis elegans CLK-2 in a yeast two-hybrid assay." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=19733.

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The gene clk-2 of C. elegans is required in both the germline and the soma, for subsequent embryonic viability, and for developmental and behavioural rates, respectively, clk-2 encodes a protein that is homologous to Tel2p in yeast, which is required for the telomere length regulation. It has been demonstrated that clk-2 affects telomere length also in worms and human cells. By now the exact biochemical function of CLK-2 is unknown. In order to shed light onto the function of the gene clk-2, a two-hybrid screen was carried out to identify the interactors of the protein CLK-2. A potential interactor of CLK-2, Y105C5B.19, was identified in the screen. Y105C5B.19 is a novel gene and does not have homologues in other species. Y105C5B.19 contains an MSP (major sperm protein) domain, therefore it is possible that it could be involved in the processes that regulate oocyte maturation, gonadal sheath contractions, or sperm mobility. Interestingly, given that clk-2 is required for subsequent embryogenesis at some point during a narrow time between the end of oocyte maturation and the 2-cell stage, it is tempting to speculate that the interaction between CLK-2 and Y105C5B.19 might be functionally relevant. The lethality of clk-2(qm37) mutants might result from delayed consequences of defects in ovulation and/or fertilization, and perhaps such defects could result from the disruption of the interaction between CLK-2 and Y105C5B.19. The amino acid substitution C772Y resulting from the clk-2(qm37) mutation was found to disrupt the interaction between CLK-2 and Y105C5B.19 in a two-hybrid assay, lending support to the idea that the interaction between CLK-2 and Y105C5B.19 takes place in vivo.

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Estevez, Annette Orene Zager. "The role of the daf-8 gene in Caenorhabditis elegans dauer larva development /." free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9841284.

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26

Goudeau, Jérôme. "Links between Germline and Longevity in Caenorhabditis elegans." Thesis, Lyon, École normale supérieure, 2011. http://www.theses.fr/2011ENSL0641.

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Un nouveau gène de la longévité ouvre de nouvelles pistes pour vieillir mieux. L'accroissement de la longévité induit par la suppression des tissus reproducteurs a été observé chez la drosophile et chez le ver. Chez ce dernier, l'opération lui donne 60% de vie en plus et lui permet un vieillissement harmonieux et en bonne santé. Les mécanismes moléculaires qui induisent cette réponse font l'objet d'intenses recherches. Certains gènes étaient déjà connus pour être associés à l'accroissement de la longévité des vers sans lignée germinale, et nous avons démontré l'existence d'une nouvelle voie impliquant le récepteur nucléaire NHR-80. Les nématodes dépourvus de lignée germinale et dont nhr-80 est muté ne voient pas leur longévité augmenter. En outre, la surexpression du gène allonge davantage leur durée de vie: elle est 150% plus longue que celle de leurs congénères sauvages. Cela démontre l'importance de ce récepteur nucléaire dont l'activation par une hormone encore inconnue enclenche l'expression ou la mise sous silence de centaines d'autres gènes. Notamment, nous avons montré que l'une des cibles de NHR-80, l'enzyme FAT-6 qui transforme l'acide stéarique en acide oléique est fondamentale, puisque les vers dépourvus de lignée germinale ne présentent plus aucun gain en longévité en l'absence de FAT-6. À terme, nous espérons pouvoir récapituler les effets de l'ablation de la lignée germinale chez un organisme fertile, c'est à dire, d'induire les réarrangements métaboliques qui ont lieu suite à cette opération afin d'en tirer les effets positifs sur la santé, sans affecter la reproduction
Discovery of a key longevity gene opens new perspectives for healthy aging.Increased longevity induced by reproductive tissues removal (germline ablation) is observed in the fly Drosophila melanogaster and in the worm Caenorhabditis elegans. In the latter, the operation increases lifespan by 60%, and enables the nematode to age harmoniously and in good health. The molecular mechanisms that induce this response are subject of intensive research. Our study reveals the existence of a new powerful longevity gene, nhr-80, which mediates this longevity effect. We have shown that inactivation of nhr-80 prevents lifespan increase. Furthermore, nhr-80 overexpression lengthens the nematodes' lifespan by 150%! nhr-80 encodes a nuclear receptor, which activation by a still unknown hormone controls the expression of hundreds of other genes. We showed that one of the critical NHR-80 targets, the enzyme FAT-6, which transforms stearic acid into oleic acid, is necessary to prolong lifespan since a mutation of the fat-6 gene suppresses the effects of germline ablation on longevity. The next step will be to determine how an increase in the level of oleic acid induces an adaptive response resulting in increased longevity. This research may lead to the exciting possibility of recapitulating the benefits of germline ablation in fertile animals; in other words, to activate the longevity effects normally triggered by germline ablation in order to fight, in one go, a host of diseases associated with aging, without affecting reproduction

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27

Goldmark, Jesse P. "How and why to stop and wait : a graduate education in mechanisms and benefits of suspended animation /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/5040.

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28

King, Kevin V. "Signaling components in development and life span determination in C. elegans /." free to MU campus, to others for purchase, 1998. http://wwwlib.umi.com/cr/mo/fullcit?p9901251.

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29

Schumacher, Björn. "The C. elegans p53 pathway." Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-19806.

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30

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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31

Ding, Mei. "Epidermal morphogenesis in Caenorhabditis elegans /." Diss., Digital Dissertations Database. Restricted to UC campuses, 2004. http://uclibs.org/PID/11984.

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32

Zhao, Beibei. "Genetic analysis of reversal behavior in C. elegans." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=19627.

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Caenorhabditis elegans" locomotion consists of long forward crawling interrupted by short spontaneous reversals. We identified several intrinsic and extrinsic variables that influence the reversal frequency. In particular, reversal frequency can be transiently suppressed by touch. The genes glr-1 and nmr-1, which encode subunits of AMPA- and NMDA-type glutamate receptors, play a central role in touch-induced reversal suppression. Thus, reversal behavior is a motor output reflecting the integration of sensory inputs that display a form of memory. Food has a dramatic effect on reversal frequency that depends on chemosensation. Wild-type worms dramatically reduce reversal frequency on food but chemosensory mutants do not. A null allele of eat-2, a gene necessary for the proper response to food, confers a hyperreversal phenotype. eat-2 also enhances dauer formation in a serotonin deficient genetic background. These phenotypes do not appear to result from the effect of eat-2 on eating efficiency.

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33

Kim, Dae Young 1968. "Role of cki-2 during development in C. elegans." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=102991.

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Rapid progress has been made toward understanding the significance of CDK inhibitor proteins (CKIs) in the regulation of cell cycle progression. The overall goal of this study has been targeted to further expand our knowledge of CKI function through the investigation of a previously uncharacterized CKI named cki-2 during development in C. elegans. The characterization of cki-2 using a reverse genetic approach called co-suppression has revealed a novel mechanism that cki-2 and its related cell cycle regulators are required for the appropriate elimination of centrioles during oogenesis. Loss of cki-2 in the germ line caused perdurance of centrioles into the one-cell embryo, resulting in supernumerary centrosomes and aberrant cell divisions in the first cell cycle. This was significantly suppressed by reduction of cyclin E and a Cdk2 homologue, indicating that these cell cycle regulators are involved in this critical developmental process. In order to further understand the function of cki-2, a yeast two-hybrid screen was conducted which allowed us to identify three CKI-2 interacting proteins: orthologues of PCNA (PCN-1), SUMO (SMO-1), and a RING finger protein called RNF-1. CKI-2 has functionally separable domains in its amino (Cyclin/Cdk binding)- and carboxy (PCNA binding)-terminus and they exert distinct roles in cell cycle progression. It was observed that CKI-2 is covalently modified by SUMO on its N-terminus and this causes CKI-2 to relocalize to thr nucleolus, which is associated with its rapid degradation. Since many RING finger proteins act as components of the multi-subunit E3 ubquitin ligases, we speculated that RNF-1 might be involved in the CKI-2 degradation. This possibility was tested by co-expression of RNF-1 with CKI-2, revealing that co-expression of RNF-1 suppresses the embryonic lethality caused by the CKI-2 overexpression and moreover, this is correlated with an increased rate of CKI-2 degradation. In addition, western blot analyses performed on different genetic backgrounds suggested that the CKI-2 degradation occurs in an ubiquitin-dependent manner through the proteasome-mediated proteolysis pathway. Furthermore, a yeast-based assay developed to test a possible role of SUMO in modulating the CKI-2/RNF-1 interaction demonstrated that SUMO may antagonize the interaction between CKI-2 and RNF-l, these highlighting an intriguing model that appropriate levels of CKI-2 are regulated through ubiquitin-dependent proteolysis mediated by RNF-l, and which maybe modulated by SUMO.

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Anvari, Sara. "Evaluation of virulence in wild type and pyrimidine auxotrophs of Pseudomonas aeruginosa using the eukaryotic model system Caenorhabditis elegans." Thesis, University of North Texas, 2004. https://digital.library.unt.edu/ark:/67531/metadc5561/.

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The human opportunistic pathogen, Pseudomonas aeruginosa PAO1, has been shown to kill the nematode Caenorhabditis elegans. C. elegans has been a valuable model for the study of bacterial pathogenesis, and has reinforced the notion that common virulence and host defense mechanisms exist. Recently, the pyrimidine pathway was shown to regulate virulence levels. Therefore, mutations in the pyrimidine pathway of PAO1 showed decrease virulence in the nematode. When starving the nematode, bacterial resistance was also shown to increase. It was hypothesized that starvation induced the DAF pathway, which regulates the transcription of genes involved with the antibacterial defense mechanism. Further research will be conducted to test this theory by performing RNAi experiments for the genes functioning in the antibacterial defense mechanism.

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35

Schackwitz, Wendy. "Genetic and neural processing of the dauer pheromone response in Caenorhabditis elegans /." Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/10280.

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36

Bringmann, Henrik Philipp. "Experiments concerning the mechanism of cytokinesis in Caenorhabditis elegans embryos." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2007. http://nbn-resolving.de/urn:nbn:de:swb:14-1170257008922-66010.

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In my thesis I aimed to contribute to the understanding of the mechanism of cytokinesis in C. elegans embryos. I wanted to analyze the relative contributions of different spindle parts – microtubule asters and the midzone - to cytokinesis furrow positioning. I developed a UV laser-based severing assay that allows the spatial separation of the region midway between the asters and the spindle midzone. The spindle is severed asymmetrically between one aster and the midzone. I found that the spindle provides two consecutive signals that can each position a cytokinesis furrow: microtubule asters provide a first signal, and the spindle midzone provides a second signal. The use of mutants that do not form a midzone suggested that the aster-positioned furrow is able to divide the cell alone without a spindle midzone. Analysis of cytokinesis in hypercontracile mutants suggests that the aster-positioned cytokinesis furrow and the midzone positioned furrow inhibit each other by competing for cortical contractile elements. I then wanted to identify the molecular pathway responsible for cytokinesis furrow positioning in response to the microtubule asters. To this end, I performed an RNAi screen, which identified a role for LET-99 in cytokinesis: LET-99 appeared to be required for aster-positioned cytokinesis but not midzone-positioned cytokinesis. LET-99 localizes as a cortical band that overlaps with the cytokinesis furrow. Mechanical displacement of the spindle demonstrated that the spindle positions cortical LET-99 at the site of furrow formation. The furrow localization of LET-99 depended on G proteins, and consistent with this finding, G proteins are also required for aster-positioned cytokinesis. (Anlage: Quick time movies, 466, 67 MB)

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37

Li, Shaolin 1973. "Genetic analysis of the initiation of postembryonic development in Caenorhabditis elegans." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33799.

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Initiation of postembryonic development is an important event for normal C. elegans development. Extrinsic factors affect development as well as intrinsic developmental cues. In order to investigate the molecular basis of initiation of postembryonic development, a genetic screen was performed to identify temperature-sensitive mutants that cannot initiate the cell divisions associated with postembryonic development at the restrictive temperature. Hydroxyurea (HU), a DNA replication inhibitor, was used as a tool to select against worms that initiate postembryonic cell divisions and/or the developmental program. 1,600,000 haploid genomes were screened, and 20 mutants have been isolated. 6 of them have been mapped to a relatively small genetic interval, and one inx-6 has been cloned and encodes an innexin family protein. Mutation of inx-6 caused abnormalities in pharyngeal pumping, resulting in worms that could not feed. The functions of a cyclin B homologue (ZC168.4) in postembryonic development have also been studied since cyclin B mutants also have postembryonic developmental arrest phenotype. Results indicate that zygotic expression of cyclin B is absolutely required for normal postembryonic development. Moreover, we found a novel function of this cyclin B homologue, which demonstrates an uncommon paternal effect required for spermatogenesis and/or fertilization.

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38

Camp, Darius. "Genetic characterization of clk genes." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=100781.

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clk-1 encodes an enzyme involved in the biosynthesis of ubiquinone (UQ), a redox active lipid that is found in all cellular membranes, including in the mitochondrial respiratory chain. In the nematode Caenorhabditis elegans clk-1 mutants display slow and deregulated physiological rates, including slow embryonic and post-embryonic development, retarded germline development, slow behaviours, and an increased lifespan. clk-1 slow germline development phenotype was previously linked to clk-1 altered ROS metabolism and its effect on lipid oxidization and the let-60/ras pathway. I have taken a genetic suppressor approach to further investigate the causes of the slow germline development phenotype of the clk-1 mutants.
Through this approach one mutant that suppresses the germline phenotype of clk-1 was identified. This suppressor, gsc-1(qm216), restored clk-1 germline development to slightly faster rates than wild type worms. This effect was specific to clk-1 and gsc-1 did not speed germline development rates in wild type worms. Furthermore, this effect appeared to be additive to lowering cholesterol levels but not to increasing cytoplasmic ROS levels. gsc-1 by itself appeared to have a deleterious effect on brood size and to increase lifespan. Neither of these effects were additive to the clk-1 phenotype and were therefore believed to affect similar mechanisms. The genetic mapping of gsc-1 precisely located the mutation to the center of chromosome II and linked it tightly to the lin-5 mutation. However, none of the transgenic lines managed to complement the gsc-1 mutation and its identity was not discovered.
In addition, to determine the role of reactive oxygen species (ROS) in the Clk phenotype, I have been analyzing all clk mutants (clk-1 to -10), by increasing ROS levels through the disruption of sod-1 and sod-2 genes, and scoring Clk phenotypes. I found that, although several clk mutants appear to have altered ROS levels, the phenomenon does not apply to all clk worms and does not correlate with lifespan. The disruption of either sod-1 or -2 affects growth and embryonic viability: sod-2 tends to exacerbate the mutant phenotypes, while sod-1 shows both weakly enhancing or weakly suppressing effects. Interestingly, only one mutant, clk-4, and only one phenotype of this mutant, slow post-embryonic development, is suppressed by sod-2 (but not sod-1). Furthermore, disrupting the expression of the sod-1 gene has only moderate or no effect on the lifespan of wild type worms, while sod-2 was shown to extend lifespan. On the whole, our results suggest that low superoxide levels do not participate in extending lifespan and are not the common process inducing the Clk phenotype in these mutants. Yet, several of the mutants analyzed have a dramatically increased lifespan and specifically behave like mutants which affect mitochondrial electron transport such as isp-1. Thus, our findings suggest that electron transport has a crucial role in longevity and developmental rates that is independent of superoxide generation.

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39

Wong, Anne. "Mutations in the clk-1 gene of Caenorhabditis elegans affect developmental and behavioural timing." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=22828.

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Five allelic, maternal-effect mutations which affect developmental and behavioral timing in Caenorhabditis elegans have been identified. They result in a mean lengthening of embryonic and post-embryonic development, the cell cycle period, and life span, as well as the periods of the defecation, swimming, and pumping cycles. These mutants also display a number of additional phenotypes related to timing. For example, the variability in the length of embryonic development is several times larger in the mutants than in the wild-type, resulting in the occasional production of mutant embryos developing more rapidly than the most rapidly-developing wild-type embryos. In addition, the duration of embryonic development and the length of the defecation cycle of the mutants, but not of the wild-type, depends on the temperature at which their parents were raised. Finally, individual variations in the severity of distinct mutant phenotypes are correlated in a counter-intuitive way. For example, the animals with the shortest embryonic development have the longest defecation cycle and those with the longest embryonic development have the shortest defecation cycle. Most of the features affected by these mutations are believed to be controlled by biological clocks, and we therefore call the gene defined by these mutations clk-1, for "abnormal function of biological clocks".

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40

Partridge, Frederick A. "Molecular genetic analysis of the caenorhabditis elegans gene bus-8." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670093.

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41

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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42

Leiers, Britta. "Funktionelle Charakterisierung von zwei stressinduzierbaren Glutathion-S-Transferasen in Caenorhabditis elegans." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=964982196.

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43

Bahrami, Masoud. "Molekularbiologische und röntgenmikroskopische Charakterisierung der Heterochromatinproteine des Nematoden Caenorhabditis elegans." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=963721623.

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44

Fröde, Stephan. "Drei neu identifizierte Gene in der Morphogenese von Caenorhabditis elegans: pcp-2, pcp-3 und gon-12 sind sowohl während dem dritten Larvalstadium, als auch im alternativen Dauerlarvenstadium aktiv und regulieren die Entwicklung reproduktiver Organe." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=967472156.

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45

Tsang, Shun-Wa. "Dissection of the molecular components required for caenorhabditis elegans sensory ray morphogenesis /." View abstract or full-text, 2006. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202006%20TSANG.

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46

Grill, Stephan W. "The mechanics of asymmetric spindle positioning in the Caenorhabditis elegans embryo." [S.l. : s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=964461773.

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47

Kollewe, Astrid. "Klonierung und Charakterisierung von Säugerhomologen des für die Muskelkontraktion relevanten Unc-93 aus Caenorhabditis elegans." [S.l. : s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=963204211.

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48

Seifert, Mark. "Der Tyraminrezeptor des Fadenwurms Caenorhabditis elegans (Maupas, 1900)." [S.l. : s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972134433.

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49

Isermann, Kerstin. "Die Peroxiredoxine des Nematoden Caenorhabditis elegans (MAUPAS, 1900)." [S.l. : s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972505784.

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50

Meissner, Barbara. "Phenotype analysis of Caenorhabditis elegans lacking the intestinal peptide transporter." [S.l. : s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972045376.

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