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1
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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2
Ou, Gangwei. "Human intestinal epithelial cells in innate immunity : interactions with normal microbiota and pathogenic bacteria". Doctoral thesis, Umeå : Umeå University, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-18388.
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3
Benner, Jacqueline [Verfasser], Hannelore [Akademischer Betreuer] Daniel, Dirk [Akademischer Betreuer] Haller e Michael [Akademischer Betreuer] Schemann. "Amino acid homeostasis in Caenorhabditis elegans lacking the intestinal peptide transporter PEPT-1 and identification of PEPT-1 modulator proteins / Jacqueline Benner. Gutachter: Hannelore Daniel ; Dirk Haller ; Michael Schemann. Betreuer: Hannelore Daniel". München : Universitätsbibliothek der TU München, 2011. http://d-nb.info/1056935480/34.
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4
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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5
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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6
Harrington, Laura Susanna. "Investigating the function of centaurin proteins from 'Caenorhabditis elegans'". Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421653.
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7
Nettell, Julia Joy. "Studies of the Rh (Rhesus)-related proteins in Caenorhabditis elegans". Thesis, University of Bristol, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340354.
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8
Stear, Jeffrey Hamilton. "Studies of chromosome structure and movement in C. elegans /". Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/5056.
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9
Yigit, Erbay. "The Argonaute Family of Genes in Caenorhabditis Elegans: a Dissertation". eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/328.
Testo completoAbstract (sommario):
Members of the Argonaute family of proteins, which interact with small RNAs, are the key players of RNAi and other related pathways. The C. elegans genome encodes 27 members of the Argonaute family. During this thesis research, we sought to understand the functions of the members of this gene family in C. elegans. Among the Argonaute family members, rde-1 and alg-1/2have previously been shown to be essential for RNAi and development, respectively. In this work, we wanted to assign functions to the remaining members of this large family of proteins.
Here, we describe the phenotype of 31 deletion alleles representing all of the previously uncharacterized Argonaute members. In addition to rde-1, our analysis revealed that two other Argonaute members csr-1 and prg-1 are also essential for development. csr-1 is partially required for RNAi, and essential for proper chromosome segregation. prg-1, a member of PIWI subfamily of Argonaute genes, exhibits reduced brood size and temperature-sensitive sterile phenotype, implicating that it is required for germline maintenance.
Additionally, we showed that RDE-1 interacts with trigger-derived sense and antisense siRNAs (primary siRNAs) to initiate RNAi, while several other Argonaute proteins, SAGO-1, SAGO-2, and perhaps others, functioning redundantly, interact with amplified siRNAs (secondary siRNAs) to mediate downstream silencing. Moreover, our analysis uncovered that another member of Argonaute gene family, ergo-1, is essential for the endogenous RNAi pathway.
Furthermore, we built an eight-fold Argonaute mutant, MAGO8, and analyzed its developmental phenotype and sensitivity to RNAi. Our analysis revealed that the genes deleted in the MAGO8 mutant function redundantly with each other, and are required for RNAi and the maintenance of the stem cell totipotency.
10
Tenlen, Jennifer R. "Linking PAR polarity proteins to cell fate regulation : analysis of MEX-5 localization in Caenorhabditis elegans embryos /". Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/5009.
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11
Round, Elaine Kay. "Identification and analysis of G-protein pathway control in the Caenorhabditis elegans defecation motor program /". Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/10283.
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12
Ghosh, Shipa Rani. "Identifying and characterising novel sarcomeric proteins in the nematode Caenorhabditis elegans". Thesis, University of Leeds, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493551.
Testo completoAbstract (sommario):
In the past, the sarcomeric proteins of Caenorhabditis elegans were identified primarily by screening mutated worms for defects in locomotion. This approach excluded the identification of those proteins which are part of the sarcomeric structure, but nevertheless are not essential for the structural integrity and function of the muscle.
13
Hockertz, Michael Karl. "Characterization of the 16 kDalton heat shock proteins of Caenorhabditis elegans". Thesis, University of British Columbia, 1991. http://hdl.handle.net/2429/29877.
Testo completoAbstract (sommario):
The 16 kDa heat shock proteins of C. elegans have been partially purified and characterized using antipeptide antibodies and standard chromatographic techniques. Based upon the sequences of the previously isolated hsp16 genes, peptides were synthesized against which polyclonal antibodies were produced in rabbits. The antibodies were used to detect fractionated hspl6 by the western blot technique and to purify hsp16 by affinity chromatography.
The specificity of the anti-peptide antibodies indicated that the four hsp16 genes may encoded both 16 kDa and the 18 kDa polypeptides. The latter were previously thought to be derived from distinct genes. Two-dimensional gel electrophoresis showed that the 16 kDa hsps exist in multiple isoforms, probably due to their posttranslational modification. Hsp16 was purified by affinity chromatography with immobilized antibody to a C-terminal 36 residue peptide of hsp16-2. The hspl6s did not bind to the antibody in a low salt buffer, but did so in the presence 4M urea. Hsp16 was fractionated by hydroxylapatite and gel exclusion chromatography and shown to exist as a large reasonably uniform complex of 460±55 kDa.Medicine, Faculty of
Biochemistry and Molecular Biology, Department of
Graduate
14
Ren, Zhiji. "Identification and Characterization of MicroRNA Modulators in Caenorhabditis Elegans: A Dissertation". eScholarship@UMMS, 2002. http://escholarship.umassmed.edu/gsbs_diss/835.
Testo completoAbstract (sommario):
MicroRNAs (miRNAs) are endogenous non-coding small RNAs that posttranscriptionally regulate gene expression primarily through binding to the 3’ untranslated region (3’UTR) of target mRNAs, and are known to play important roles in various developmental and physiological processes. The work presented in this thesis was centered on understanding how Caenorhabditis elegans miRNAs are modulated by genetic, environmental, or physiological factors and how these small RNAs function to maintain the robustness of developmental processes under stressful conditions.
To identify modulators of the miRNA pathway, I developed sensitized genetic backgrounds that consist of a panel of miRNA gene mutants and miRNA biogenesis factor mutants with partially penetrant phenotypes. First, I found that upon infection of Caenorhabditis elegans with Pseudomonas aeruginosa, an opportunistic pathogen of diverse plants and animals, let-7 family miRNAs are engaged in reciprocal regulatory interactions with the p38 MAPK innate immune pathway to maintain robust developmental timing despite the stress of pathogen infection. These let-7 family miRNAs, along with other developmental timing regulators, are also integrated into innate immune regulatory networks to modulate immune responses. Next, I demonstrated that loss-of-function mutations of Staufen (stau-1), a double-stranded RNA-binding protein, increase miRNA activity for several miRNA families, and this negative modulation of Staufen on miRNA activity acts downstream of miRNA biogenesis, possibly by competing with miRNAs for binding to target mRNA 3’UTRs.
In summary, these studies provide a better understanding on how miRNAs are modulated by various environmental and cellular components, and further support the role of the miRNA pathway in conferring robustness to developmental processes under these perturbations.
15
Ren, Zhiji. "Identification and Characterization of MicroRNA Modulators in Caenorhabditis Elegans: A Dissertation". eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/835.
Testo completoAbstract (sommario):
MicroRNAs (miRNAs) are endogenous non-coding small RNAs that posttranscriptionally regulate gene expression primarily through binding to the 3’ untranslated region (3’UTR) of target mRNAs, and are known to play important roles in various developmental and physiological processes. The work presented in this thesis was centered on understanding how Caenorhabditis elegans miRNAs are modulated by genetic, environmental, or physiological factors and how these small RNAs function to maintain the robustness of developmental processes under stressful conditions.
To identify modulators of the miRNA pathway, I developed sensitized genetic backgrounds that consist of a panel of miRNA gene mutants and miRNA biogenesis factor mutants with partially penetrant phenotypes. First, I found that upon infection of Caenorhabditis elegans with Pseudomonas aeruginosa, an opportunistic pathogen of diverse plants and animals, let-7 family miRNAs are engaged in reciprocal regulatory interactions with the p38 MAPK innate immune pathway to maintain robust developmental timing despite the stress of pathogen infection. These let-7 family miRNAs, along with other developmental timing regulators, are also integrated into innate immune regulatory networks to modulate immune responses. Next, I demonstrated that loss-of-function mutations of Staufen (stau-1), a double-stranded RNA-binding protein, increase miRNA activity for several miRNA families, and this negative modulation of Staufen on miRNA activity acts downstream of miRNA biogenesis, possibly by competing with miRNAs for binding to target mRNA 3’UTRs.
In summary, these studies provide a better understanding on how miRNAs are modulated by various environmental and cellular components, and further support the role of the miRNA pathway in conferring robustness to developmental processes under these perturbations.
16
Winkelbauer, Marlene Elizabeth. "Elucidating the role of nephronophthisis proteins utilizing Caenorhabditis elegans as a model". Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/winkelbauer.pdf.
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17
Bagijn, Marloes Pauline. "Genetic and functional characterization of the Piwi proteins and piRNAs of Caenorhabditis elegans". Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609250.
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18
Shamalnasab, Mehrnaz. "Conserved Role of Acyl-CoA Binding Proteins in Life Span Regulation". Thesis, Lyon, École normale supérieure, 2012. http://www.theses.fr/2012ENSL0790.
Testo completoAbstract (sommario):
Depuis une vingtaine d’années, il est possible d’allonger la durée de vie génétiquement. Nombre d’études réalisées sur des espèces allant de la levure aux primates, ont permis d’identifier des cascades de signaux intracellulaires ayant un impact sur la longévité et la qualité du vieillissement. Il est important de noter que certaines de ces interventions réduisent considérablement l’incidence de cancers et de maladies liées au vieillissement chez les mammifères. Ceci témoigne des liens existant entre vieillissement et carcinogénèse et il probable que le développement de stratégies pharmacologiques ayant pour cible le vieillissement se révèlent efficaces contre les maladies du vieillissement comme le cancer, la maladie d’Alzheimer ou de Parkinson. Nous avons criblé la banque de mutants de Saccharomyces cerevisiae pour identifier des mutations génétiques qui augmentent la durée de vie. La plupart des gènes identifiés se sont révélés conservés puisqu’ils influencent aussi la longévité chez C. elegans. La protéine de liaison à l’acyl-CoA (ACBP) est une petite protéine (10 kDa) qui se lie avec une haute affinité aux chaîne d’acyl-CoA esters (moyennes et longues) et les transporte vers les sites de consommation de l'acyl-CoA. ACBP est hautement conservée parmi les espèces eucaryotes et joue un rôle important dans la biosynthèse des lipides et le trafic vésiculaire. Chez Saccharomyces cerevisiae, la délétion d’ACBP (ACB1) entraîne une augmentation de la longévité et favorise la résistance au stress. Pour tester si l’impact d’ACBP sur la longévité s'étend aux eucaryotes supérieurs, nous avons exploré le lien entre les gènes codant pour des ACBPs chez Caenorhabditis elegans et la longévité en utilisant l’ARN interfèrent. Chez C. elegans, sept paralogues ACBP ont été identifiés, qui sont exprimés dans différents tissus. Nous avons constaté que la réduction de l'expression de maa-1 (codant une ACBP associée aux membranes) prolonge la durée de vie des vers sauvages. Nos résultats démontrent que: 1) une perte de fonction de maa-1 entraîne une résistance au superoxyde, 2) et aux événements protéotoxiques telle que l'agrégation protéique associées aux maladies neurodégénératives comme la maladie de Huntington. Enfin, nous avons montré que l'activité du facteur de transcription HIF-1 (hypoxia inducible factor-1) contribue à la longévité causée par la mutation maa-1. En effet, la délétion du gène hif-1 annule complètement l’augmentation de la longévité causée par maa-1Understanding the aging process, its regulation, and how to delay it has become a priority for an increasing number of scientists worldwide. The principal reason for this is that it is becoming more and more evident that anti-aging interventions may be effective against age-related diseases such as cancer, cardiovascular, and neurodegenerative diseases. Simple model organisms such as Caenorhabditis elegans and Saccharomyces cerevisiae have been instrumental to identify the principal genes implicated in aging whose role has turned out to be conserved in mammals. The project presented here has originated from a genome-wide screen performed in S. cerevisiae that has led to discover several novel life span-regulatory genes whose deletion prevents aging. One of these genes encodes for Acyl-CoA binding protein (ACBP). ACBP is a small (10 kDa) protein that binds medium- and long-chain fatty acyl-CoA esters with high affinity and transports them to acyl-CoA consuming processes. ACBP is highly conserved among eukaryotic species and plays important roles in lipid biosynthesis and vesicle trafficking. In S. cerevisiae, lack of ACBP (Acb1) extends longevity and promotes stress resistance. To test whether the life span-regulatory role of ACBP extends to higher eukaryotes, we explored the link between the C. elegans ACBP genes and longevity by RNAi screening. In C. elegans, seven ACBP paralogs have been identified, which are expressed in different tissues. We found that reducing the expression of maa-1 (encoding a membrane associated ACBP) extended the longevity of wild-type worms. Our results show that 1) a loss of function maa-1 mutant is resistant to the superoxide-generating agent paraquat and 2) reduction of maa-1 expression increases resistance to the proteotoxicity associated with the aggregation of the Huntington's disease-associated polyQ peptide. The activity of the anti-aging transcription factor HIF-1 (hypoxia inducible factor-1) contributes to the extended longevity caused by lack of maa-1. The effect of MAA-1 loss on longevity was fully reverted by the deletion of the hif-1 gene
19
Ao, Wanyuan. "Caenorhabditis elegans UNC-45 defines a novel class of myosin-associated proteins". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ60271.pdf.
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20
Brunquell, Jessica. "Uncovering Transcriptional Activators and Targets of HSF-1 in Caenorhabditis elegans". Scholar Commons, 2017. http://scholarcommons.usf.edu/etd/6686.
Testo completoAbstract (sommario):
In order to survive, cells must be able to cope with a variety of environmental stressors. The heat shock response (HSR) is a pro-survival mechanism employed by cells in response to protein denaturing stress, such as heat. Since its discovery in 1960, the heat shock response has been found to be regulated by the transcription factor heat shock factor 1 (HSF1). During periods of increased stress, HSF1 undergoes a multi-step process of activation that involves homotrimerization, DNA-binding, and post-translational regulatory modifications, all of which ultimately function to control the transcription of chaperone genes. These chaperone genes encode molecular chaperone proteins which function to promote survival during stress by restoring protein homeostasis to the cell. Although HSF1 is classically studied for its role in regulating the HSR, HSF1 also has roles in regulating metabolism, development, and longevity. Studies in the nematode Caenorhabditis elegans demonstrate the HSF1 homolog, HSF-1, as a global regulator of gene expression that has both stress-dependent and -independent functions. Modulating HSF1 activity therefore has implications beyond stress-induced processes, and has been suggested as a promising therapeutic target for diseases of aging and protein dysfunction.
We were interested in determining regulators of the HSR using C. elegans as a model to test for effects on proteostasis and longevity. In these studies, we observed the effects of compound treatment (Chapters 1 and 2), genetic manipulation (Chapters 3 and 4), and environmental stimuli (Chapters 5 and 6), on the HSR in C. elegans. In Chapters 1 and 2, we describe our findings that treatment with the DNA synthesis inhibitor Fluorodeoxyuridine, and treatment with coffee and caffeine, enhance the heat shock response and improve proteostasis in aging worms in an HSF-1-dependent manner. In Chapters 3 and 4, we uncovered that negative regulation of the HSR by the cell cycle and apoptosis regulator CCAR2 is conserved in C. elegans, and is mediated by the CCAR2 ortholog, LST-3. We also uncovered that negative regulation of the HSR by LST-3 requires the SIRT1 homolog Sir-2.1, and knockdown of LST-3 via lst-3 RNAi works through Sir-2.1 to enhance stress-resistance, fitness, proteostasis and longevity. In Chapters 5 and 6, we describe the global impact of HSF-1 in regulating transcriptional processes during a heat stress. The profiling of global HSF-1 mRNA and miRNA targets has allowed us to uncover a heat-dependent and -independent role for HSF-1 in regulating gene expression to impact stress-resistance, proteostasis, and longevity. Altogether, these studies demonstrate the impact of compound treatment, genetic manipulation, and environmental stimuli on the heat shock response, while also uncovering global stress-dependent and -independent roles for HSF-1. This work therefore provides insight into various methods of activating the HSR by modulating HSF-1 activity, and uncovering global HSF-1 target genes, which may be useful for designing therapeutic treatment strategies for diseases of protein dysfunction.
21
Kolasinska-Zwierz, Paulina Maria. "Global distribution of three modifications of histone H3 and the chromatin proteins HPL-2 and LIN-13 in C. elegans and the implications for chromatin-related processes". Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609189.
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22
Woo, Wei-Meng. "Roles of epidermal cytoskeleton and extracellular matrix proteins in Caenorhabditis elegans embryonic morphogenesis /". Diss., Digital Dissertations Database. Restricted to UC campuses, 2005. http://uclibs.org/PID/11984.
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23
Sultan, Roxana. "Interactions between two Caenorhabditis elegans sex-determining proteins, HER-1 and TRA-2A". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0019/MQ54124.pdf.
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24
Rao, Wei. "A proteomic analysis of lipid raft and GPI anchored proteins in Caenorhabditis elegans". Thesis, University of Leeds, 2010. http://etheses.whiterose.ac.uk/2240/.
Testo completoAbstract (sommario):
Glycosylphosphatidylinositol (GPI) anchored proteins are a unique group of membrane proteins found on the surface and certain intracellular compartments of eukaryotic cells. They are bound to the membrane by a GPI moiety and have a number of important functions, including digestion, endocytosis and signal transduction. GPI anchored proteins also reside within lipid rafts, which are microdomains on the phospholipid bilayer composed of sphingolipids and cholesterol. Rafts are thought to be capable of forming semi-stable “islands”of lipids and proteins that act as a platform for a number of important cellular processes, such as T-cell activation, caveolin mediated endocytosis and protein compartmentalisation. The majority of research into rafts has been carried out in single cellular organisms or cell cultures, and their importance within development has been poorly understood. In this project a proteomic analysis of lipid raft and GPI anchored proteins was made for the proteome of the model organism Caenorhabditis elegans. We found a total of 327 predicted GPI anchored proteins from the C. elegans genome via a novel four-program prediction method and validated three of those proteins with mass spectrometric (MS) identification. The GPI biosynthesis pathway genes of C. elegans were also elucidated via a bioinformatics search. 41 lipid raft proteins were identified using MS, which accounts for the largest number of such proteins found in the worm. This project will hopefully become a starting point for the research of GPI anchored proteins and lipid rafts within the nematode, and shine a light on the properties of these important classes of proteins within the context of a developmentally complex organism.
25
Vipavee, Anupunpisit Otsuka Anthony John. "Expression and characterization of the unc-104 kinesin-related protein from Caenorhabditis elegans". Normal, Ill. Illinois State University, 1996. http://wwwlib.umi.com/cr/ilstu/fullcit?p9633415.
Testo completoAbstract (sommario):
Thesis (Ph. D.)--Illinois State University, 1996.Title from title page screen, viewed May 26, 2006. Dissertation Committee: Anthony J. Otsuka (chair), Herman E. Brockman, Alan J. Katz, David F. Weber, Brian J. Wilkinson. Includes bibliographical references (leaves 177-191) and abstract. Also available in print.
26
Gaudet, Jeffrey P. C. "Molecular analysis of the role of the FEM proteins in Caenorhabditis elegans sex determination". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0023/NQ49947.pdf.
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27
Aspbury, Robert Allen. "Fatty acylation and isoprenylation of cellular proteins in the free-living nematode Caenorhabditis elegans". Thesis, University of Liverpool, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364150.
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Dietz, Sabrina Franziska [Verfasser]. "Identification and characterization of novel telomere binding proteins in Caenorhabditis elegans / Sabrina Franziska Dietz". Mainz : Universitätsbibliothek der Johannes Gutenberg-Universität Mainz, 2021. http://d-nb.info/1236341260/34.
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29
Khandekar, Anagha. "Age-related Changes in the Neuronal Architecture of Caenorhabditis Elegans: A Dissertation". eScholarship@UMMS, 2010. http://escholarship.umassmed.edu/gsbs_diss/798.
Testo completoAbstract (sommario):
Though symptoms such as loss of vision, decline in cognition and memory are evident during aging, the underlying processes that affect neuronal function during aging are not well understood. Unlike changes in other tissues and organs, age-related changes in the nervous system affect the overall physical, mental as well as social state of human beings. To start elucidating the molecular mechanisms underlying normal age-dependent brain decline, we have characterized structural neuronal changes occurring during Caenorhabditis elegans aging. Our analysis reveals distinct neuronal alterations that arise with age and that the types of changes and their age of onset are neuronal-type specific, highlighting the differential susceptibility of neurons to the stresses of life. We also find that these age-dependent neuronal changes are largely uncoupled from lifespan. As a first step towards understanding the neuropathological conditions manifested during senescence, we have characterized the role of the neuronal maintenance gene sax-7/L1CAM in normal C. elegans aging. Our comparison of age-related structural changes in the wild-type nervous system with that of sax-7 mutants, indicates that loss of function of sax-7 results in accelerated neuronal deterioration that mimics alterations occurring during normal aging. Conversely, overexpressing wild-type copies of SAX-7 delays some of the neuronal changes that accompany normal aging, indicating that SAX-7 plays a neuroprotective role. Additionally we find that x mechanical stress from body movements impacts the neuronal changes during adulthood. Taken together, our results give an entry point into the mechanisms of age-related neuroanatomical changes and neuronal protection.
30
Khandekar, Anagha. "Age-related Changes in the Neuronal Architecture of Caenorhabditis Elegans: A Dissertation". eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/798.
Testo completoAbstract (sommario):
Though symptoms such as loss of vision, decline in cognition and memory are evident during aging, the underlying processes that affect neuronal function during aging are not well understood. Unlike changes in other tissues and organs, age-related changes in the nervous system affect the overall physical, mental as well as social state of human beings. To start elucidating the molecular mechanisms underlying normal age-dependent brain decline, we have characterized structural neuronal changes occurring during Caenorhabditis elegans aging. Our analysis reveals distinct neuronal alterations that arise with age and that the types of changes and their age of onset are neuronal-type specific, highlighting the differential susceptibility of neurons to the stresses of life. We also find that these age-dependent neuronal changes are largely uncoupled from lifespan. As a first step towards understanding the neuropathological conditions manifested during senescence, we have characterized the role of the neuronal maintenance gene sax-7/L1CAM in normal C. elegans aging. Our comparison of age-related structural changes in the wild-type nervous system with that of sax-7 mutants, indicates that loss of function of sax-7 results in accelerated neuronal deterioration that mimics alterations occurring during normal aging. Conversely, overexpressing wild-type copies of SAX-7 delays some of the neuronal changes that accompany normal aging, indicating that SAX-7 plays a neuroprotective role. Additionally we find that x mechanical stress from body movements impacts the neuronal changes during adulthood. Taken together, our results give an entry point into the mechanisms of age-related neuroanatomical changes and neuronal protection.
31
Auclair, Melissa M. "A Genetic Analysis of Genomic Stability in Caenorhabditis Elegans: A Dissertation". eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/345.
Testo completoAbstract (sommario):
In humans, Bloom’s Syndrome is caused by a mutation of the RecQ helicase BLM. Patients with Bloom’s Syndrome exhibit a high amount of genomic instability which results in a high incidence of cancer. Though Bloom’s Syndrome has been intensively studied, there are still many questions about the function of BLM which need to be answered. While it is clear that loss of BLM increases genomic instability, the other effects of genomic instability on the organism aside from cancer such as a potential effect on aging, have yet to be elucidated.
In Chapter II, I identify new phenotypes in the C. elegans ortholog of BLM, him-6. him-6 mutants have an increased rate of cell death, a mortal germ line phenotype, and an increased rate of mutations. Upon further examination of the mutator phenotype, it was determined that the increased rate of mutations was caused by small insertions and deletions. The mutator phenotype identified in him-6 mutants closely mimics the cellular phenotype seen in Bloom’s Syndrome cells. This indicates that HIM-6 may behave in a similar fashion to BLM. In addition to the mutator phenotype, it was found that loss of him-6causes a shortened life span. This may provide evidence that there is a link between genomic stability and aging.
In Chapter III, I identify a new role for the transcription factor DAF-16. DAF-16 in C. elegans has been intensively studied and regulates a wide variety of pathways. In this chapter, I demonstrate via the well established unc-93 assay that loss of daf-16 causes a subtle mutator phenotype in C. elegans. This indicates that DAF-16 may play a role in suppression of spontaneous mutation. When I examined other classic genomic instability phenotypes, I found at 25°C, the number of progeny in the DAF-16 mutants was significantly reduced compared to wild type worms. Additionally, I demonstrate daf-16(mu86)has a cell death defect.
This study identifies several new phenotypes caused by a loss of him-6. These phenotypes provide further evidence that loss of him-6 causes genomic instability. In addition, this study also demonstrates that him-6 has a shortened life span which may be due to genomic instability. Secondly, this study identifies a new role for DAF-16 in preventing the occurrence of spontaneous mutations. This may indicate a novel function for DAF-16 in maintaining genomic stability.
32
Park, Frederick D. "Establishment of POP-1 asymmetry, a binary code for cell fate decisions in C. elegans /". Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/4992.
Testo completo
33
Russnak, Roland Hans. "Structure, expression and evolution of the 16 kilodalton heat shock protein gene family of C. elegans". Thesis, University of British Columbia, 1986. http://hdl.handle.net/2429/27521.
Testo completoAbstract (sommario):
Sequences coding for three related 16 kd heat shock proteins (hsps) of the nematode Caenorhabditis elegans were isolated and characterized. The extensive accumulation of hsp16 mRNA during heat stress facilitated the identification of two cDNAs, CEHS48 and CEHS41, which encoded hsp16 variants. These plasmids were selected by their ability to hybridize to mRNA which directed the synthesis of hspl6 in vitro, and were further characterized by sequence analysis.
Two-dimensional gel electrophoresis of hspl6 synthesized in vitro from mRNA selected by hybridization to either of the cDNAs under conditions of low stringency revealed the existence of at least five electrophoretic variants with significantly different isoelectric points.
The above cDNAs were used as specific probes to isolate recombinant bacteriophage containing C. elegans genomic DNA. Overlapping phage clones were used to define a region of approximately 30 kilobases. The genes coding for hsp16-48, previously identified by cDNA cloning, and for another 16 kd hsp designated hspl6-l were characterized by DNA sequencing. These two genes were arranged in a head-to-head orientation. Both the coding and flanking regions of these genes were located within a 1.9 kb region which was duplicated exactly to form a perfect 3.8 kb inverted repeat structure. This structure ended in unusual G + C-rich sequences 24 bp in length. The identity of the two arms of the inverted repeat at the nucleotide sequence level implied that the duplication event may have occurred relatively recently in evolution. Alternatively, gene conversion between the two modules could have maintained homology between the two gene pairs. Comparison of the hsp16-48 gene with its corresponding cDNA revealed the presence of a single, short intron. An intron of comparable length and in an analogous position was also found in the hsp16-1 gene. The introns separated variable and conserved regions within the amino acid sequences of the encoded heat shock proteins. A domain of approximatey 80 amino acids is contained within the conserved second exon and is homologous to a similar region in the small hsps of Drosophila, Xenopus, soybean and man as well as the a-crystallin protein of the vertebrate lens.
Each hsp16 gene contained a TATA box upstream of the start of transcription. Promoter sequences, which have been shown to be required for heat inducibility in various systems, were located upstream of either TATA box
Northern blot analysis showed that the hsp16-48 and hsp16-1 genes are expressed at levels approximately 20 - 40 fold lower than two closely related genes, hsp16-41 and hsp16-2, upon temperature elevation.Medicine, Faculty of
Biochemistry and Molecular Biology, Department of
Graduate
34
King, Skylar Dawn. "Ceramide Biosynthesis and NEET Proteins Impact Development, Function, and Maintenance of the Caenorhabditis elegans Germline". Thesis, University of North Texas, 2019. https://digital.library.unt.edu/ark:/67531/metadc1538805/.
Testo completoAbstract (sommario):
I used the C. elegans genetic model to examine the role of ceramide biosynthesis (sphingolipid pathway) and iron regulation and found that each process impacts germline development and function. Using a sphingolipid specific antibody mAb15B4, I found that sphingolipids are associated with germ granules (P granules) within C. elegans and zebrafish; thus, suggesting conservation of macromolecules associated with germ granules. Phenotype analysis of ceramide biosynthesis mutants in C. elegans revealed that this pathway is essential for normal germline function in the aging adult hermaphrodite; specifically, precocious germline senescence was observed. Furthermore, I found that disruption of ceramide biosynthesis, via the hyl-2 deletion mutation, negatively impacts mAb15B4 localization at the P granules. Through genetic suppression analysis, I determined that insulin signaling and lipid biosynthesis can modulate the mAb15B4 localization to P granules. Additional, phenotype analysis showed that ceramide biosynthesis dysfunction decreased fecundity, and led to germline structure defects and uterine tumors. Through suppression analysis, I determined that modulation of the insulin signaling pathway suppressed the precocious germline senescence due to ceramide biosynthesis dysfunction. Since the presence of uterine tumors is associated with reproductive senescence I concluded that ceramide biosynthesis has a role in germline maintenance in the aging of the germline (germline senescence).
The other important fate of a germ cell is programmed cell death. Apoptosis, which occurs through a highly conserved molecular pathway, is a normal component of growth and homeostatic processes. I used C. elegans to gain a greater understanding of the cisd gene function. The C. elegans genome has three previously uncharacterized cisd genes which code for CISD-1 (homology to vertebrate mitoNEET/CISD1 and NAF-1/CISD2) and CISD-3.1 and CISD-3.2 (homology to vertebrate Miner2/CISD3). I determined that independent disruption of the cisd genes resulted in a significant increase in the number of cell corpses within the adult hermaphrodite germline. Genetic analysis was used to examine the dysfunction of cisd-1 relative to the cell death canonical pathway genes. The increased gamete cell death in the cisd-1 hermaphrodite is suppressed by the ced-9 (Bcl-2 homolog) gain-of-function and requires functional CED-3 (caspase) and CED-4 (APAF). Additionally, the increased germ cell programmed cell death is facilitated by the pro-apoptotic, CED-9-binding protein, CED-13. Further analysis of the cisd gene family members show that cisd-3.2 dysfunction leads to germline defects and reproductive dysfunction, suggesting defects in germline stem cell proliferation. Expression analysis using the cisd promoters to drive fluorescent protein reporters showed that the cisd gene family is expressed in various tissues including the germline; fusion protein analysis showed that CISD-3 is mitochondrial localized. I propose that cisd-3.2 germline defects are a result of abnormal mitochondrial function.
Combined, this work is significant because it identifies sphingolipids as a new component of embryonic P granules, a role for ceramide biosynthesis in reproductive senescence, and places the cisd gene family members as regulators of physiological germline programmed cell death acting through CED-13 and the core apoptotic machinery. Furthermore, it is the first study to show that a CISD3 protein family member is required for normal germline function. These findings support the idea that ceramide biosynthesis and iron regulation are core components in germline development and function.
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Joswala, Swetha Ramani. "INVESTIGATION INTO THE MEIOTIC ROLES OF COHESIN AND CENTROMERE PROTEINS IN CAENORHABDITIS ELEGANS". Cleveland State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=csu1611678282003653.
Testo completo
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Lublin, Alex Louis. "The pumilio proteins PUF-5 and PUF-6/7/10 are necessary for repression of C. Elegans notch/glp-1 during late oogenesis (or not all that glitters is GLD-1) /". Connect to full text at ProQuest Digital Dissertations. IP filtered, 2005.
Cerca il testo completoAbstract (sommario):
Thesis (Ph.D. in Cell and Developmental Biology) -- University of Colorado at Denver and Health Sciences Center, 2005.Typescript. Includes bibliographical references (leaves 82-86). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
37
Pagano, John M. Jr. "RNA Recognition by the Caenorhabditis elegans Embryonic Determinants MEX-5 and MEX-3: A Dissertation". eScholarship@UMMS, 2010. https://escholarship.umassmed.edu/gsbs_diss/486.
Testo completoAbstract (sommario):
Post-transcriptional regulation of gene expression is a mechanism that governs developmental and cellular events in metazoans. In early embryogenesis, transcriptionally quiescent cells depend upon maternally supplied factors such as RNA binding proteins and RNA that control key decisions. Morphogen gradients form and in turn pattern the early embryo generating different cell types and spatial order. In the nematode Caenorhabditis elegans, the early embryo relies upon several RNA binding proteins that control mRNA stability, translation efficiency, and/or mRNA localization of cell fate determinants essential for proper development.
MEX-5 and MEX-3 are two conserved RNA-binding proteins required to pattern the anterior/posterior axis and early embryo. Mutation of either gene results in a maternal effect lethal phenotype with proliferating posterior muscle into the anterior blastomeres (Muscle EXcess). Several cell-fate determinants are aberrantly expressed in mex-5 and mex-3 embryos. Both proteins are thought to interact with cis-regulatory elements present in 3’-UTRs of target RNAs controlling their metabolism. However, previous studies failed to demonstrate that these proteins regulate maternal transcripts directly.
This dissertation presents a thorough assessment of the RNA binding properties of MEX-5 and MEX-3. Quantitative biochemical approaches were used to determine the RNA binding specificity of both proteins. MEX-5 has a relaxed specificity, binding with high affinity to linear RNA containing a tract of six or more uridines within an eight-nucleotide window. This is very different from its mammalian homologs Tristetraprolin (TTP) and ERF-2. I was able to identify two amino acids present within the MEX-5 RNA binding domain that are required for the differential RNA recognition observed between MEX-5 and TTP. MEX-3 on the other hand is a specific RNA binding protein, recognizing a bipartite element with flexible spacing between two four-nucleotide half-sites. I demonstrate that this element is required for MEX-3 dependent regulation in vivo. Previous studies only identify a small number of candidate regulatory targets of MEX-5 and MEX-3. The defined sequence specificity of both proteins is used to predict new putative targets that may be regulated by either protein. Collectively, this study examines the RNA binding properties of MEX-5 and MEX-3 to clarify their role as post-transcriptional regulators in nematode development.
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Youds, Jillian L. "Roles of the DOG-1 and JRH-1 helicase-like proteins in DNA repair in Caenorhabditis elegans". Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/2832.
Testo completoAbstract (sommario):
Helicases perform vital roles in the cell by unwinding D N A to make it accessible for the
essential processes of replication, transcription and repair. In Caenorhabditis elegans, the DOG-
1 helicase-like protein is required for polyG/polyC-tract (G/C-tract) maintenance, as dog-l
animals have a mutator phenotype characterized by deletions that initiate in G/C-tracts. DOG-1
may unwind secondary structures that form in polyguanine D N A during lagging strand
replication. In order to more completely understand the role of dog-1, genetic interactors were
identified, dog-1 functionally interacts with the him-6/BLM helicase. Absence of
recombinational repair-implicated proteins in the dog-1 background, including HIM-6/BLM,
RAD-51, BRD-1/BARD1 and HIM-9/XPF, as well as the trans-lesion synthesis polymerases
polKMD po/7 increased the frequency of animals with G/C-tract deletions, indicating that these
pathways are important mechanisms for repair at G/C-tracts in the absence of DOG-1. These
data support the hypothesis that persisting D N A secondary structures can cause replication fork
stalling, which can be resolved by deletion-free or deletion-prone mechanisms.
DOG-1 has highest sequence identity to human BR1P1/FANCJ, which is mutated in
patients from the Fanconi Anemia (FA) subgroup J. D N A damage sensitivity experiments
indicated that, like chicken F A N C J cells, dog-1 mutants were not significantly sensitive to DNA
damage from X-ray or UV-irradiation, but were extremely hypersensitive to the D N A interstrand
cross-linking agent UVA-activated trimethylpsoralen. Thus, DOG-1 appears to have a
conserved role in cross-link repair and is the C. elegans F A N C J homolog. Characterization of
the dog-1/FANCJ-relatsd helicase, Jrh-1, revealed that mutants for this putative helicase are
moderately sensitive to cross-linking agents, dog-1 jrh-1 double mutants displayed a synthetic
lethal phenotype characterized by excessive recombination intermediates and mitotic catastrophe
in the germline. However, absence of JRH-1 did not have any effect on G/C-tract deletions,
indicating that JRH-1 does not have a redundant function with DOG-1 at G/C-tracts. Absence of
JRH-1 reduced the fitness of eTl and nTl translocation hétérozygotes, but not translocation
homozygotes, jrh-1 was synthetically lethal with him-6/BLM and with the endonuclease mus-81,
suggesting a possible role for JRH-1 in regulating the balance between different types of repair.
39
Narasimhan, Sri Devi. "Converging Pathways in the Regulation of Longevity and Metabolism in Caenorhabditis Elegans: A Dissertation". eScholarship@UMMS, 2010. https://escholarship.umassmed.edu/gsbs_diss/509.
Testo completoAbstract (sommario):
The lifespan of an organism is determined by a complex array of genetic, environmental and nutritional factors. Yet single gene manipulations have been shown to significantly extend lifespan in several model organisms. Of all the genes that have been studied thus far, components of the insulin/IGF-1 signaling (IIS) pathway have emerged as the most robust regulators of longevity. In addition, IIS also regulates development, energy metabolism and the response to stress in a conserved manner. In Caenorhabditis elegans, signaling through this pathway is initiated by activation of the insulin/IGF-1 receptor tyrosine kinase DAF-2, which then activates a PI3-kinase signaling pathway involving additional downstream serine/threonine kinases such as PDK-1, AKT-1, AKT-2 and SGK-1. The concerted action of these kinases results in the negative regulation of the single FOXO transcription factor homolog DAF-16. Under reduced signaling conditions, active DAF-16 is able to translocate into the nucleus and regulate the expression of hundreds of genes regulating longevity, stress resistance, metabolism and development.
The PTEN phosphatase homolog DAF-18, which antagonizes IIS at the level of PI3-kinase, is a major negative regulator of the pathway. However, not much was known about additional phosphatases that negatively regulated the kinases in the pathway. Dephosphorylation is a critical regulatory mechanism by which cellular signaling homeostasis is maintained. Aberrant hyper-activation of growth factor signaling pathways, including IIS, has been implicated in several cancers. In addition, deregulation of IIS is also closely linked to Type II diabetes. Therefore, the identification phosphatases that balance kinase activity will provide a better understanding of the regulation of the IIS pathway under normal as well as disease conditions. A directed RNAi screen using dauer diapause was conducted in our lab to identify serine/threonine phosphatases that modulated IIS. My work in the Tissenbaum Lab has primarily focused on characterization of the top three candidates from this screen, the genes pptr-1, pdp-1 and fem-2. From these studies, we have also uncovered novel crosstalk between the IIS and TGF-β signaling pathways.
In Chapter 2, we demonstrate that PPTR-1, a PP2A phosphatase regulatory subunit negatively regulates the IIS pathway by modulating AKT-1 dephosphorylation. PPTR-1 modulates several outputs of IIS similar to DAF-18. In addition, PPTR-1 co-localizes and physically interacts with its substrate, AKT-1. PPTR-1 modulates dephosphorylation of AKT-1 at a conserved threonine site and we show the molecular conservation of this interaction in mammalian adipocytes. Ultimately, this negative regulation by PPTR-1 results in increased DAF-16 nuclear localization and transcriptional activity.
Next, in Chapter 3, we show how PDP-1 is a novel link between the IIS and TGF-β signaling pathways. Similar to DAF-18 and PPTR-1, PDP-1 regulates multiple outputs of the IIS pathway and promotes DAF-16 activity. Interestingly, PDP-1 acts at the level of DAF-8 and DAF-14, two R-SMAD proteins that function in a TGF-β pathway. Our data suggests that PDP-1 may negatively regulate TGF-β signaling to downregulate the expression of several insulin(s). Without the insulin ligands, there is less activation of the IIS pathway, and DAF-16 is more active, thereby promoting transcription of genes that act to enhance longevity and stress resistance.
In Chapter 4, we investigate possible crosstalk between IIS and the TGF-β signaling pathways, as the latter was previously considered as a parallel independent pathway. From our studies on PDP-1, we knew that this phosphatase, despite acting in the TGF-β pathway, was a robust modulator of multiple outputs of IIS. Using double mutant combinations as well as RNAi we unravel complex and extensive crosstalk between the two pathways. Importantly, our results suggest that DAF-16 is likely to be the most downstream component of the two pathways.
In Chapter 5, we describe genetic characterization of fem-2, and its regulation of the IIS pathway. RNAi of fem-2 results in robust suppression of dauer formation, similar to pptr-1 and pdp-1 RNAi but this phenotype is only observed in the e1370 allele of daf-2. While knockdown of pptr-1 and pdp-1 suppress dauer formation of additional alleles of daf-2, fem-2 RNAi has no effect. These results reveal a complex genetic interaction between fem-2 and the daf-2 receptor.
Taken together, our results identify several novel regulators of IIS that modulate this pathway by distinct mechanisms.
40
Rupert, Peter Benjamin. "Structure determination of the SKN-1 DNA binding domain complex /". view abstract or download file of text, 1999. http://wwwlib.umi.com/cr/uoregon/fullcit?p9947981.
Testo completoAbstract (sommario):
Thesis (Ph. D.)--University of Oregon, 1999.Typescript. Includes vita and abstract. Includes bibliographical references (leaves 96-106). Also available for download via the World Wide Web; free to University of Oregon users. Address: http://wwwlib.umi.com/cr/uoregon/fullcit?p9947981.
41
Mickey, Katherine Morgan. "Cell-cell interactions and the specification of cell fates during C. elegans embryogenesis /". Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/5043.
Testo completo
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Arda, H. Efsun. "C. Elegans Metabolic Gene Regulatory Networks: A Dissertation". eScholarship@UMMS, 2010. https://escholarship.umassmed.edu/gsbs_diss/479.
Testo completoAbstract (sommario):
In multicellular organisms, determining when and where genes will be expressed is critical for their development and physiology. Transcription factors (TFs) are major specifiers of differential gene expression. By establishing physical contacts with the regulatory elements of their target genes, TFs often determine whether the target genes will be expressed or not. These physical and/or regulatory TF-DNA interactions can be modeled into gene regulatory networks (GRNs), which provide a systems-level view of differential gene expression. Thus far, much of the GRN delineation efforts focused on metazoan development, whereas the organization of GRNs that pertain to systems physiology remains mostly unexplored.
My work has focused on delineating the first gene regulatory network of the nematode Caenorhabditis elegans metabolic genes, and investigating how this network relates to the energy homeostasis of the nematode. The resulting metabolic GRN consists of ~70 metabolic genes, 100 TFs and more than 500 protein–DNA interactions. It also includes novel protein-protein interactions involving the metabolic transcriptional cofactor MDT-15 and several TFs that occur in the metabolic GRN. On a global level, we found that the metabolic GRN is enriched for nuclear hormone receptors (NHRs). NHRs form a special class of TFs that can interact with diffusible biomolecules and are well-known regulators of lipid metabolism in other organisms, including humans. Interestingly, NHRs comprise the largest family of TFs in nematodes; the C. elegans genome encodes 284 NHRs, most of which are uncharacterized. In our study, we show that the C. elegans NHRs that we retrieved in the metabolic GRN organize into network modules, and that most of these NHRs function to maintain lipid homeostasis in the nematode. Network modularity has been proposed to facilitate rapid and robust changes in gene expression. Our results suggest that the C. elegans metabolic GRN may have evolved by combining NHR family expansion with the specific modular wiring of NHRs to enable the rapid adaptation of the animal to different environmental cues.
43
Carroll, Bryan Thomas. "Characterization of Stomatin Suppressors ssu-1 AND ssu-2". Connect to text online, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1121454937.
Testo completo
44
Pratumtip, Boontrakulpoontawee Otsuka Anthony John. "The caenorhabditis elegans unc-44 ankyrin gene wild-type, mutant, and revertant gene structures and transcripts /". Normal, Ill. Illinois State University, 1995. http://wwwlib.umi.com/cr/ilstu/fullcit?p9603515.
Testo completoAbstract (sommario):
Thesis (Ph. D.)--Illinois State University, 1995.Title from title page screen, viewed May 2, 2006. Dissertation Committee: Anthony J. Otsuka (chair), Herman E. Brockman, David W. Borst, H. Tak Cheung, Radheshyam K. Jayaswal. Includes bibliographical references (leaves 170-187) and abstract. Also available in print.
45
Zhang, Liang. "Systematic analysis of Caenorhabditis elegans miRNA functions through two GW182 family proteins: AIN-1 and AIN-2". Connect to online resource, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3315811.
Testo completoAbstract (sommario):
Thesis (Ph.D.)--University of Colorado at Boulder, 2008.Source: Dissertation Abstracts International, Volume: 69-08, Section: B, page: 4578. Adviser: Min Han. Includes supplementary digital materials.
46
Vaitkevičius, Karolis. "Effects of Vibrio cholerae protease and pigment production on environmental survival and host interaction /". Umeå : Univ, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1474.
Testo completo
47
Power, Rowena Suzanne. "The application of a transgenic strain of the nematode Caenorhabditis elegans to the biomonitoring of metal polluted soil". Thesis, University of Nottingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310841.
Testo completo
48
Vasale, Jessica J. "Roles of Cellular RNA-Dependent RNA Polymerases in Endogenous Small RNA Pathways in Caenorhabditis elegans: A Dissertation". eScholarship@UMMS, 2010. https://escholarship.umassmed.edu/gsbs_diss/481.
Testo completoAbstract (sommario):
The RNA interference (RNAi) pathway in Caenorhabditis elegans is a two-step, small RNA-mediated silencing pathway. Unlike in other organisms, Dicer processing of double-stranded RNA into small interfering (si) RNAs is not sufficient in worms to induce gene silencing. The activity of cellular RNA-dependent RNA polymerase (RdRP) is necessary to synthesize a secondary pool of siRNAs, which interact with a unique class of Argonaute proteins to form the functional effector complexes that mediate silencing. The aims of this thesis were to: 1) characterize the role of RdRP family members in endogenous small RNA biogenesis; 2) identify the Argonaute proteins that interact with RdRP-dependent small RNAs; and 3) investigate the biological function of RdRP-dependent small RNA pathways in C. elegans.
In this thesis, I describe genetic, deep sequencing, and molecular studies, which identify 22G-RNAs as the most abundant class of endogenous small RNA in C. elegans. The 22G-RNAs resemble RdRP-dependent secondary siRNAs produced during exogenous RNAi, in that they possess a triphosphorylated 5’ guanine residue and exhibit a remarkable strand bias at target loci. Indeed, I show that 22G-RNAs are dependent on the activity of the RdRPs RRF-1 and EGO-1 and function in multiple distinct endogenous small RNA pathways. Interestingly, I have found that RRF-1 and EGO-1 function redundantly in the germline to generate 22G-RNAs that are dependent on and interact with members of an expanded family of worm-specific Argonaute (WAGO) proteins. The WAGO/22G-RNA pathway appears to be a transcriptome surveillance pathway that silences coding genes, pseudogenes, transposons, and non-annotated, or cryptic, transcripts. In contrast, I have found that EGO-1 alone is required for the biogenesis of a distinct class of 22G-RNAs that interact with the Argonaute CSR-1. Surprisingly, the CSR-1/22G-RNA pathway does not appear to silence its targets transcripts. Instead, the CSR-1/22G-RNA pathway is essential for the proper assembly of holocentric kinetochores and chromosome segregation.
Lastly, I show that a third endogenous small RNA pathway, the ERI pathway, is a two-step silencing pathway that requires the sequential activity of distinct RdRPs and Argonautes. In the first step of this pathway, the RdRP, RRF- 3, is required for the biogenesis of 26G-RNAs that associate with the Argonaute, ERGO-1. In the second step, RRF-1 and EGO-1 generate 22G-RNAs that associate with the WAGO Argonautes.
This work demonstrates how several C. elegans small RNAs pathways utilize RdRPs to generate abundant populations of small RNAs. These distinct categories of small RNAs function together with specific Argonaute proteins to affect gene expression, to play essential roles in development, and in the maintenance of genome and transcriptome integrity.
49
Kelley, Joanna L. "Adaptive evolution : from genome-wide scans to biological significance /". Thesis, Connect to this title online; UW restricted, 2008. http://hdl.handle.net/1773/10256.
Testo completo
50
Bowman, Richard. "Regulation of synaptonemal complex assembly through nuclear import and loading of cohesins and SYP-2 proteins in Caenorhabditis elegans". Thesis, University of Iowa, 2017. https://ir.uiowa.edu/etd/5915.
Testo completoAbstract (sommario):
The synaptonemal complex is a complex of proteins that connect homologous chromosomes, allowing genetic recombination to occur during meiosis in C. elegans. It is made up of lateral element proteins that assemble along each pair of sister chromatids and central region proteins that extend from, and join, each homolog. Here we aimed at understanding how synaptonemal complex activity is regulated through the study of nuclear import and isoform of its structural protein SYP-2. AKIR-1 is a protein with a previously identified meiotic role in the unloading of the Synaptonemal Complex (SC) Central Region (CR) proteins from the short arms of bivalent chromosomes exiting diakinesis. A Yeast-2-hybrid (Y2H) screen for additional proteins that interact with AKIR-1 found a potential interaction with the α-importin IMA-2. The efficient transfer of proteins from the cytoplasm into a meiotic nucleus in C. elegans is dependent on the activity of α- and β-importins. The α-importins associate to both cargo proteins and β-importins forming a complex that transits into the nucleus. Once inside the nucleus, the complex is disassembled and the importin complex is cycled back into the cytoplasm for reuse. Based on this, a double AKIR-1 and IMA-2 mutant was created to determine what role this interaction has in C. elegans meiosis. We found the first evidence of a role for AKIR-1 in the meiotic nuclear import and chromatin loading of meiotic cohesin complex proteins. We identified a meiotic phenotype in the double mutant akir-1(gk528);ima-2(ok256) that was not apparent in either of the akir-1(gk528) or ima-2(ok256) single mutants in which neither the cohesin REC-8 or the lateral element protein HTP-3 did not associate with chromatin normally, instead forming aggregates with which the central region SYP proteins co-localized. Additionally, we found that the pairing center protein HIM-8 was not being efficiently transported into the nucleus, localizing to the nuclear envelope instead of chromatin, as well as in cytoplasmic poly complexes (PCs). This loss of efficient import and localization resulted in morphological changes in the gonad as well. The gonad of akir-1;ima-2 contained significantly fewer nuclei and did not have a transition zone. We saw an increase in recombination intermediaries represented by RAD-51 foci, an ssDNA associating protein, in late pachytene. This increase indicated a lack of synapsis and crossover formation.
We also examined the effect of a hypomorph of syp-2 on the proper assembly of the synaptonemal complex. The hypomorph displayed similar embryonic lethality to that of the syp-2 null mutant. However, unlike the null mutant, the syp-2 hypomorph showed a partial assembly of CR proteins. We also found an increased incidence of recombination intermediaries compared to the syp-2 null mutant, indicating hat DSB repair pathway is altered in this mutant.
Autophagy is a regulator of aging in many organisms, including C. elegans, as well as functioning in the immune response pathway and muscle protein degradation. AKIRIN has been shown to have myriad roles in the soma in other model animals, and can be found in nearly every tissue. It has been shown to coordinate neural development and skeletal muscle differentiation, migration, and repair across multiple species. AKIRIN also acts as a cofactor in chromatin and cytoskeleton remodeling, gene transcription, and mediates interactions between the Twist transcription factor and Brahma. My research found the first evidence for a role of AKIR-1 in autophagosome inhibition after finding a significant increase in autophagosome puncta in the transgenic akir-1(gk529)::mCherry;LGG-1 mutants. We also found increased muscle deterioration and decreased motility in the akir-1(gk528) mutant, suggesting a role for AKIR-1 in actin filament maintenance. To test that association, we created a double mutant with akir-1(gk528);sma-1(ru18), a SMAD protein found in the apical membrane cytoskeleton, and that is required for body elongation in C. elegans. Our research provided evidence of AKIR-1 operating in a parallel pathway to SMA-1 as the double mutant displayed an additive reduction in body length.