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1
Cheng, Albert Wu. "Characterization of irx-1 transcription factor in C. elegans male sensory ray development /." View abstract or full-text, 2007. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202007%20CHENG.
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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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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.
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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.
4
De, Bono Mario Godwin. "Studies on the regulation and evolution of tra-1, the terminal somatic sex determining gene in Caenorhabditis elegans." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321108.
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White, Arron D. "The role of the C. elegans transcription factor LIN-11 in cell fate specification." Scholarly Commons, 2000. https://scholarlycommons.pacific.edu/uop_etds/533.
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Vulval differentiation in Caenorhabditis elegans is a well characterized developmental system in which three vulval precursor cells divide, generating the 22 nuclei that form the functional wild type vulva. Additionally, the combined formation of the vulva and the uterus is a model for organogenesis. Hermaphrodites homozygous for a lin-11 mutation are unable to form a functional vulva due to abnormal mitotic divisions in two of the three vulval precursor cells that contribute cells to the vulva.
Laser microsurgery was used to ablate the two abnormal vulval precursor cells and other vulval precursor cells that could take on their developmental fate. These cells were believed to be responsible for the inability of hermaphrodites homozygous for a lin- 11 mutation to form a functional vulva. The results show that ablated hermaphrodites homozygous for a lin-11 mutation are rarely able to lay eggs, suggesting that there are other defects in the egg-laying apparatus in addition to the vulval precursor cells.
To ensure that the ablated animals did not form a functional vulva and fail to lay eggs due to defects in the neurons regulating egg-laying, ablated lin-11 mutant animals were exposed to serotonin, imipramine or nicotine. These drugs are able to induce egglaying in wild type and ablated wild type animals. Ablated hermaphrodites homozygous for a lin-11 mutation exposed to the drug treatments were not able to lay eggs. Therefore, the abnormal secondary cells are not entirely responsible for the lack of a functional vulva and the inability to lay eggs, suggesting that either uterine cells or other vulval cells are also abnormal.
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Meisel, Kacey Danielle. "Characterization of lin-42/period transcriptional regulation by the Ikaros/hunchback-family transcription factor ZTF-16 in Caenorhabditis elegans." Thesis, Virginia Tech, 2013. http://hdl.handle.net/10919/23130.
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The gene lin-42 is an ortholog of the mammalian period gene, a component of the circadian pathway that converts environmental stimuli into behavioral and physiological outputs over 24 hours. Mammalian period also regulates adult stem cell differentiation, although this function is poorly understood. The structure, function and expression of lin-42 are all similar to period. Therefore, we are studying lin-42 regulation and function during C. elegans larval development as a model for understanding period control of mammalian stem/progenitor cell development. Previous work has shown that ZTF-16 is a regulator of lin-42 transcription. The lin-42 locus encodes three isoforms, and we have characterized lin-42 isoform specific regulation by ZTF-16 through phenotypic assays and analysis of transcriptional reporter strains. Our data show that ZTF-16 regulates the cyclic expression of lin-42A and lin-42B during larval development. However, ztf-16 is not expressed during the adult stage and does not regulate lin-42C, which is expressed only in adults and may be responsible for the circadian functions of lin-42. We also show that ztf-16 reduction-of-function mutations phenocopy loss-of- function phenotypes of the lin-42A/B isoforms. Finally, we have found that deletion of a putative ZTF-16 transcription factor binding site within the lin-42BC promoter abolishes tissue-specific expression patterns. Together, these data indicate that ZTF-16 is required to regulate the expression of lin-42A/B during C. elegans development, and may do this by direct binding to the lin-42BC promoter. Our findings pave the way for testing the possible regulation of period expression by HIL-family transcription factors in mammalian tissues.
Master of Science
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Grove, Christian A. "A Multiparameter Network Reveals Extensive Divergence Between C. elegans bHLH Transcription Factors: A Dissertation." eScholarship@UMMS, 2009. https://escholarship.umassmed.edu/gsbs_diss/441.
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It has become increasingly clear that transcription factors (TFs) play crucial roles in the development and day-to-day homeostasis that all biological systems experience. TFs target particular genes in a genome, at the appropriate place and time, to regulate their expression so as to elicit the most appropriate biological response from a cell or multicellular organism. TFs can often be grouped into families based on the presence of similar DNA binding domains, and these families are believed to have expanded and diverged throughout evolution by several rounds of gene duplication and mutation. The extent to which TFs within a family have functionally diverged, however, has remained unclear. We propose that systematic analysis of multiple aspects, or parameters, of TF functionality for entire families of TFs could provide clues as to how divergent paralogous TFs really are.
We present here a multiparameter integrated network of the activity of the basic helix-loop-helix (bHLH) TFs from the nematode Caenorhabditis elegans. Our data, and the resulting network, indicate that several parameters of bHLH function contribute to their divergence and that many bHLH TFs and their associated parameters exhibit a wide range of connectivity in the network, some being uniquely associated to one another, whereas others are highly connected to multiple parameter associations.
We find that 34 bHLH proteins dimerize to form 30 bHLH dimers, which are expressed in a wide range of tissues and cell types, particularly during the development of the nematode. These dimers bind to E-Box DNA sequences and E-Box-like sequences with specificity for nucleotides central to and flanking those E-Boxes and related sequences.
Our integrated network is the first such network for a multicellular organism, describing the dimerization specificity, spatiotemporal expression patterns, and DNA binding specificities of an entire family of TFs. The network elucidates the state of bHLH TF divergence in C. elegans with respect to multiple functional parameters and suggests that each bHLH TF, despite many molecular similarities, is distinct from its family members. This functional distinction may indeed explain how TFs from a single family can acquire different biological functions despite descending from common genetic ancestry.
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Johnson, Ryan William. "Genetic Regulation of Caenorhabditis Elegans Post-Embryonic Development Involving the Transcription Factors EGL-38, VAB-3, and LIN-14." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1213060175.
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White, Arron D. "The role of the C. elegans transcription factor LIN-11 in cell fate specification : a thesis." Scholarly Commons, 2001. https://scholarlycommons.pacific.edu/uop_etds/533.
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Vulval differentiation in Caenorhabditis elegans is a well characterized developmental system in which three vulval precursor cells divide, generating the 22 nuclei that form the functional wild type vulva. Additionally, the combined formation of the vulva and the uterus is a model for organogenesis. Hermaphrodites homozygous for a lin-11 mutation are unable to form a functional vulva due to abnormal mitotic divisions in two of the three vulval precursor cells that contribute cells to the vulva.
Laser microsurgery was used to ablate the two abnormal vulval precursor cells and other vulval precursor cells that could take on their developmental fate. These cells were believed to be responsible for the inability of hermaphrodites homozygous for a lin- 11 mutation to form a functional vulva. The results show that ablated hermaphrodites homozygous for a lin-11 mutation are rarely able to lay eggs, suggesting that there are other defects in the egg-laying apparatus in addition to the vulval precursor cells.
To ensure that the ablated animals did not form a functional vulva and fail to lay eggs due to defects in the neurons regulating egg-laying, ablated lin-11 mutant animals were exposed to serotonin, imipramine or nicotine. These drugs are able to induce egglaying in wild type and ablated wild type animals. Ablated hermaphrodites homozygous for a lin-11 mutation exposed to the drug treatments were not able to lay eggs. Therefore, the abnormal secondary cells are not entirely responsible for the lack of a functional vulva and the inability to lay eggs, suggesting that either uterine cells or other vulval cells are also abnormal.
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Oh, Seung Wook. "Regulation of Life Span by DAF-16/Forkhead Transcription Factor in Caenorhabditis elegans: A Dissertation." eScholarship@UMMS, 2005. https://escholarship.umassmed.edu/gsbs_diss/22.
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The insulin/IGF-1 signaling pathway plays a pivotal role in life span regulation in diverse organisms. In Caenorhabditis elegans, a PI 3-kinase signaling cascade downstream of DAF-2, an ortholog of the mammalian insulin and insulin-like growth factor-1 (IGF-1) receptor, negatively regulates DAF-16/forkhead transcription factor. DAF-16 then regulates a wide variety of genes involved in longevity, stress response, metabolism and development. DAF-16 also receives signals from other pathways regulating life span and development. However, the precise mechanism by which DAF-16 directs multiple functions is poorly understood.
First, in Chapter II, we demonstrate that JNK is a novel positive regulator of DAF-16 in both life span regulation and stress resistance. Our genetic analysis suggests that the JNK pathway acts in parallel with the insulin-like signaling pathway to regulate life span and both pathways converge onto DAF-16. We also show that JNK-1 directly interacts with and phosphorylates DAF-16. Moreover, in response to heat stress, JNK-1 promotes the translocation of DAF-16 into thc nucleus. Our findings define a novel interaction between the stress response pathway (JNK) and the master regulator of life span (DAF-16), and provide a mechanism by which JNK regulates longevity and stress resistance.
Next, in Chapter III, we focus on the downstream targets of DAF-16. Here, we used a modified chromatin immunoprecipitation (ChIP) method to identify direct target promoters of DAF-16. We cloned 103 target sequences containing consensus DAF-16 binding sites and randomly selected 33 targets for further analysis. The expression of majority of these genes is regulated in a DAF-16-dependent manner. Moreover, inactivation of more than 50% of these genes significantly altered DAF-16-dependent functions such as longevity, fat storage and dauer diapause. Our results show that the ChIP-based cloning strategy leads to greater enrichment of DAF-16 target genes, compared to previous studies using DNA micro array or bioinformatics. We also demonstrate that DAF-16 is recruited to multiple promoters to coordinate regulation of its downstream target genes.
In summary, we identified the JNK signaling pathway as a novel input into DAF-16 to adapt animals to the environmental stresses. We also revealed a large number of novel outputs of DAF-16. Taken together, these studies provide insight into the complex regulation by DAF-16 to control diverse biological functions and eventually broaden our understanding of aging.
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Auclair, Melissa M. "A Genetic Analysis of Genomic Stability in Caenorhabditis Elegans: A Dissertation." eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/345.
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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.
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Elewa, Ahmed M. "POS-1 Regulation of Endo-mesoderm Identity in C. elegans: A Dissertation." eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/711.
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How do embryos develop with such poise from a single zygote to multiple cells with different identities, and yet survive? At the four-cell stage of the C. elegans embryo, only the blastomere EMS adopts the endo-mesoderm identity. This fate requires SKN-1, the master regulator of endoderm and mesoderm differentiation. However, in the absence of the RNA binding protein POS-1, EMS fails to fulfill its fate despite the presence of SKN-1. pos-1(-) embryos die gutless. Conversely, the RNA binding protein MEX-5 prevents ectoderm blastomeres from adopting the endo-mesoderm identity by repressing SKN-1. mex-5(-) embryos die with excess muscle at the expense of skin and neurons.
Through forward and reverse genetics, I found that genes gld-3/Bicaudal C, cytoplasmic adenylase gld-2, cye-1/Cyclin E, glp-1/Notch and the novel gene neg-1 are suppressors that restore gut development despite the absence of pos-1. Both POS-1 and MEX-5 bind the 3’UTR of neg-1 mRNA and its poly(A) tail requires GLD-3/2 for elongation. Moreover, neg-1 requires MEX-5 for its expression in anterior ectoderm blastomeres and is repressed in EMS by POS-1. Most neg-1(-) embryos die with defects in anterior ectoderm development where the mesoderm transcription factor pha-4 becomes ectopically expressed. This lethality is reduced by the concomitant loss of med- 1, a key mesoderm-promoting transcription factor.
Thus the endo-mesoderm identity of EMS is determined by the presence of SKN- 1 and the POS-1 repression of neg-1, whose expression is promoted by MEX-5. Together they promote the anterior ectoderm identity by repressing mesoderm differentiation. Such checks and balances ensure the vital plurality of cellular identity without the lethal tyranny of a single fate.
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Elewa, Ahmed M. "POS-1 Regulation of Endo-mesoderm Identity in C. elegans: A Dissertation." eScholarship@UMMS, 2014. https://escholarship.umassmed.edu/gsbs_diss/711.
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How do embryos develop with such poise from a single zygote to multiple cells with different identities, and yet survive? At the four-cell stage of the C. elegans embryo, only the blastomere EMS adopts the endo-mesoderm identity. This fate requires SKN-1, the master regulator of endoderm and mesoderm differentiation. However, in the absence of the RNA binding protein POS-1, EMS fails to fulfill its fate despite the presence of SKN-1. pos-1(-) embryos die gutless. Conversely, the RNA binding protein MEX-5 prevents ectoderm blastomeres from adopting the endo-mesoderm identity by repressing SKN-1. mex-5(-) embryos die with excess muscle at the expense of skin and neurons.
Through forward and reverse genetics, I found that genes gld-3/Bicaudal C, cytoplasmic adenylase gld-2, cye-1/Cyclin E, glp-1/Notch and the novel gene neg-1 are suppressors that restore gut development despite the absence of pos-1. Both POS-1 and MEX-5 bind the 3’UTR of neg-1 mRNA and its poly(A) tail requires GLD-3/2 for elongation. Moreover, neg-1 requires MEX-5 for its expression in anterior ectoderm blastomeres and is repressed in EMS by POS-1. Most neg-1(-) embryos die with defects in anterior ectoderm development where the mesoderm transcription factor pha-4 becomes ectopically expressed. This lethality is reduced by the concomitant loss of med- 1, a key mesoderm-promoting transcription factor.
Thus the endo-mesoderm identity of EMS is determined by the presence of SKN- 1 and the POS-1 repression of neg-1, whose expression is promoted by MEX-5. Together they promote the anterior ectoderm identity by repressing mesoderm differentiation. Such checks and balances ensure the vital plurality of cellular identity without the lethal tyranny of a single fate.
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Jia, Hongtao. "Characterization of multiple functions of EGL-38, a Pax2/5/8-related protein in Caenorhabditis elegans." Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1199121386.
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Martinez, Natalia Julia. "Delineating the C. elegans MicroRNA Regulatory Network: A Dissertation." eScholarship@UMMS, 2009. https://escholarship.umassmed.edu/gsbs_diss/411.
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Metazoan genomes contain thousands of protein-coding and non-coding RNA genes, most of which are differentially expressed, i.e., at different locations, at different times during development, or in response to environmental signals. Differential gene expression is achieved through complex regulatory networks that are controlled in part by two types of trans-regulators: transcription factors (TFs) and microRNAs (miRNAs). TFs bind to cis-regulatory DNA elements that are often located in or near their target genes, while microRNAs hybridize to cis-regulatory RNA elements mostly located in the 3’ untranslated region (3’UTR) of their target mRNAs.
My work in the Walhout lab has centered on understanding how these trans-regulators interact with each other in the context of gene regulatory networks to coordinate gene expression at the genome-scale level. Our model organism is the free-living nematode Caenorahbditis elegans, which possess approximately 950 predicted TFs and more than 100 miRNAs
Whereas much attention has focused on finding the protein-coding target genes of both miRNAs and TFs, the transcriptional networks that regulate miRNA expression remain largely unexplored. To this end, we have embarked in the task of mapping the first genome-scale miRNA regulatory network. This network contains experimentally mapped transcriptional TF=>miRNA interactions, as well as computationally predicted post-transcriptional miRNA=>TF interactions. The work presented here, along with data reported by other groups, have revealed the existence of reciprocal regulation between these two types of regulators, as well as extensive coordination in the regulation of shared target genes. Our studies have also identified common mechanisms by which miRNAs and TFs function to control gene expression and have suggested an inherent difference in the network properties of both types of regulators.
Reverse genetic approaches have been extensively used to delineate the biological function of protein-coding genes. For instance, genome-wide RNAi screens have revealed critical roles for TFs in C. elegans development and physiology. However, reverse genetic approaches have not been very insightful in the case of non-coding genes: A single null mutation does not result in an easily detectable phenotype for most C. elegans miRNA genes. To help delineate the biological function of miRNAs we sought to determine when and where they are expressed. Specifically, we generated a collection of transgenic C. elegans strains, each containing a miRNA promoter::gfp (Pmir::gfp) fusion construct. The particular pattern of expression of each miRNA gene should help to identify potential genetic interactors that exhibit similar expression patterns, and to design experiments to test the phenotypes of miRNA mutants.
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Liu, Jing. "Biochemical and structural studies of key components in the Wnt signaling pathway /." Thesis, Connect to this title online; UW restricted, 2008. http://hdl.handle.net/1773/5685.
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Stempor, Przemyslaw. "Relationships between chromatin features and genome regulation." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/288630.
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Regulation of gene expression is an essential process for all living organisms. Transcriptional regulation, associated with chromatin, is governed by: (1) DNA sequence, which creates regulatory sites (promoters, enhancers and silencers), where sequence motifs and features (e. g. CpG) can attract transcription factors (TFs) and influence chromatin structure or RNA polymerase II (Pol II) binding, initiation and elongation; (2) non-sequence, epigenetic factors - histone modifications, TF binding, chromatin remodelling (histone placement, eviction and reconstitution), and non-coding RNA regulation. These factors interact with each other, creating a complex network of interactions. In this thesis I describe computational studies of heterochromatin factors in regulation of gene and repeat expression, an analysis of active regulatory elements, and global analyses of big datasets in C. elegans. I first show that a team of heterochromatin factors - HPL-2/HP1, LIN-13, LIN-61, LET-418/Mi-2, and H3K9me2 histone methyltransferase MET-2/SETDB1 - collaborates with piRNA and nuclear RNAi pathways to silence repetitive elements and protect the germline. I also found that the TACBGTA motif is particularly enriched on repeats and heterochromatin factors binding sites, and that repeat elements are derepressed in the soma during normal C. elegans ageing. I then describe the work on active regulatory regions. I show that CFP-1/CXXC1 binds CpG dense, nucleosome depleted promoters and, along SET-2, is required for H3K4me3 deposition at these loci. Using expression profiling I determined that the majority of CFP-1 binding targets are not significantly mis-regulated in cfp-1 mutants, but are weakly upregulated in bulk analyses. I also show that CFP-1 functionally interacts with the Sin3S/HDAC complex. In cfp-1 mutant I observed both loss and gain of SIN-3 binding, depending on chromatin context. Finally, I performed a data driven study on a large collection of ChIP-seq profiles using non-parametric sparse factor analyses (NSFA) and compared it to other, unsupervised machine learning algorithms. This study uncovered interactions and structure in genomic datasets. In addition, I present a collection of computational tools and methods I developed to facilitate processing, storage, retrieval, annotation, and analyses of large datasets in genomics.
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McElwee, Joshua J. "A comparative analysis of transcriptional alterations in long-lived insulin/IGF-1-like signaling mutants in Caenorhabditis elegans and Drosophila melanogaster /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/4982.
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Unhavaithaya, Yingdee. "Conserved Nucleosome Remodeling/Histone Deacetylase Complex and Germ/Soma Distinction in C. elegans: A Dissertation." eScholarship@UMMS, 2003. https://escholarship.umassmed.edu/gsbs_diss/239.
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A rapid cascade of regulatory events defines the differentiated fates of embryonic cells, however, once established, these differentiated fates and the underlying transcriptional programs can be remarkably stable. Here, we describe two proteins, MEP-1, a novel protein, and LET-418/Mi-2, both of which are required for the maintenance of somatic differentiation in C. elegans. MEP-1 was identified as an interactor of PIE-1, a germ-specific protein required for germ cell specification, while LET-418 is a protein homologous to Mi-2, a core component of the nuc1eosome remodeling/histone deacetylase (NuRD) complex. In animals lacking MEP-1 and LET-418, germline-specific genes become derepressed in somatic cells, and Polycomb group (PcG) and SET domain-related proteins promote this ectopic expression. We demonstrate that PIE-1 forms a complex with MEP-1, LET-418, and HDA-1. Furthermore, we show that the overexpression of PIE-1 can mimic the mep-1/let-418 phenotype, and that PIE-1 can inhibit the Histone deacetylase activity of the HDA-1 complex in COS cells. Our findings support a model in which PIE-1 transiently inhibits MEP-1 and associated factors to maintain the pluripotency of germ cells, while at later times MEP-1 and LET-418 remodel chromatin to establish new stage- or cell-type-specific differentiation potential.
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Bordet, Guillaume. "Rôle des facteurs chromatiniens PRC1 dans la robustesse des programmes de différenciation neuronaux chez C. elegans." Thesis, Aix-Marseille, 2017. http://www.theses.fr/2017AIXM0341.
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L’acquisition et le maintien de l’identité d’un neurone sont assurés par des facteurs de transcription terminaux exprimés durant toute la vie du neurone. Cependant le processus d’expression génique peut être très bruité. L’objectif de mon projet de thèse est de déterminer comment un neurone peut acquérir et maintenir son identité de manière fiable malgré ce bruit intrinsèque, en utilisant le modèle C. elegans. En combinant des techniques récentes d’ingénierie du génome par CRISPR et des méthodes d’imagerie quantitative in vivo, j’ai observé que l’expression endogène des facteurs de transcription terminaux est fortement bruitée. J’ai également établi que des mutations dans le complexe chromatinien PRC1 induisent une perte stochastique de l’identité de certains neurones au cours du temps. Le complexe PRC1 agit directement au sein des neurones. Il affecte le niveau d’initiation de l’expression des facteurs de transcription terminaux durant l’embryogenèse ainsi que la fiabilité de la maintenance de leur expression aux stades larvaires et adultes. En conclusion, mon travail suggère que le complexe PRC1 joue un rôle important dans la protection des neurones contre le bruit génique, les aidant ainsi à acquérir et maintenir de manière fiable leur identitéThe acquisition and maintenance of neuronal identity is driven by terminal transcription factors expressed throughout the life of the neuron. However, the gene expression process can be noisy. The aim of my PhD work is to determine how a neuron can acquire and maintain its identity in a reliable manner despite this intrinsic noise, using C. elegans as a model system. Combining recent techniques of genome engineering by CRISPR with in vivo quantitative imaging, I observed that the endogenous expression of terminal transcription factors is highly noisy. I also established that mutations in the chromatin complex PRC1 induce a stochastic loss of the identity of some neurons over time. The PRC1 complex directly acts in the neurons. It affects the levels of initiation of the terminal transcription factors during embryogenesis as well as the reliability of their maintenance at larval and adult stages. To conclude, my work suggests that the PRC1 complex plays an important role to protect neurons against gene expression noise, helping them to acquire and maintain their identity in a reliable manner
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Tabuchi, Tomoko M. "Chromosome-Biased Binding and Function of C. elegans DRM Complex, and Its Role in Germline Sex-Silencing: A Dissertation." eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/538.
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DRM is a conserved transcription factor complex that includes E2F/DP and pRB family proteins and plays important roles in the cell cycle and cancer. Recent work has unveiled a new aspect of DRM function in regulating genes involved in development and differentiation. These studies, however, were performed with cultured cells and a genome-wide study involving intact organisms undergoing active proliferation and differentiation was lacking. Our goal was to extend the knowledge of the role of DRM in gene regulation through development and in multiple tissues. To accomplish this, we employed genomic approaches to determine genome-wide targets of DRM using the nematode Caenorhabditis elegans as a model system. In this dissertation, I focus on the DRM component LIN-54 since it was proposed to exhibit DNA-binding activity. First, we confirmed the DNA-binding activity of C.elegans LIN-54 in vivo, and showed it is essential to recruit the DRM complex to its target genes. Next, chromatin immunoprecipitation and gene expression profiling revealed that LIN-54 controls transcription of genes implicated in cell division, development and reproduction. This work identified an interesting contrast in DRM function in soma vs. germline: DRM promotes transcription of germline-specific genes in the germline, but prevents their ectopic expression in the soma. Furthermore, we discovered a novel characteristic of DRM, sex chromosome-biased binding and function. We demonstrated that C. elegans DRM preferentially binds autosomes, yet regulates X-chromosome silencing by counteracting the H3K36 histone methyltransferase MES-4. By using genomics, cytology, and genetics, we defined DRM as an important player in the regulation of germline X-chromosome gene expression, and addressed molecular mechanisms vii behind the antagonistic interactions between DRM and MES-4. I present a model to explain the interplay of DRM and MES-4, and propose a novel function of DRM and MES-4 in maintaining proper chromosome gene expression dosage. This work extends our knowledge of the conserved roles of DRM in development, and provides a new view of differing DRM functions in soma versus germline. Furthermore, we defined a novel chromosome-specific aspect of DRM-mediated regulation.
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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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Choy, Siu Wah. "Characterization of a transcriptional repressor complex and mab-21 interacting genes in male sensory ray patterning of C. elegans /." View abstract or full-text, 2006. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202006%20CHOY.
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Ho, Siu-hong. "Characterization of the transcriptional regulation of C. elegans mab-21 gene and its genetic partner, a sin3-like gene /." View Abstract or Full-Text, 2002. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202002%20HO.
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Thesis (Ph. D.)--Hong Kong University of Science and Technology, 2002.Includes bibliographical references (leaves 175-187). Also available in electronic version. Access restricted to campus users.
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Kulkarni, Madhura. "Role of ubiquitination in (Caenorhabditis elegans) development and transcription regulation during spermatogenesis." College Park, Md.: University of Maryland, 2008. http://hdl.handle.net/1903/8612.
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Thesis (Ph. D.) -- University of Maryland, College Park, 2008.Thesis research directed by: Dept. of Cell Biology & Molecular Genetics. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
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Sharpe, Helen E. "Interconnections between pre-mRNA processing events and transcription in the nematode Caenorhabditis elegans." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497450.
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Padvitski, Tsimafei. "Integrative analysis of age-related changes in the transcriptome of Caenorhabditis elegans." Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-11825.
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Ageing is difficult to study because of the complexity and multi-factorial nature of traits that result from a combination of environmental, genetic, epigenetic and stochastic factors, each contributing to the overall phenotype. In light of this challenge, transcriptomic studies of aging organisms are of particular interest, since transcription is an intermediate step that links genotype and phenotype. In recent years microarrays have been widely used for elucidation of changes that occur with age in the transcriptome in Caenorhabditis elegans. However, different microarray studies of C. elegans report sets of differentially expressed genes of varying consistence, with different functional annotations. Failures to find a consistent set of transcriptomic alterations may reflect the absence of a specific genetic program that would guide age-related changes but may also, to some extent, be a consequence of a small sample sizes and a lack of study power in transcriptomic researches. To tackle this issue we analyzed RNA sequences of samples from a time-series experiment of normal aging of C. elegans, performing the first, to our knowledge, NGS-based study of such kind. As a result, evidences were collected that promote a union of two competing theories: the theory of DNA damage accumulation and the theory of programmed aging. Next, we applied two alternative methods, namely the Short Time-series Expression Mining and the Network Smoothing algorithm, in order to obtain and analyze sets of genes that represent distinct modules of age-related changes in the transcriptome. Besides characterization of age-related changes, we were also interested in assessment and validation of the Network Smoothing algorithm. Generally, results of clustering of smoothed scores are consistent with results of short time-series clustering, allowing robust elucidation of functions that are perturbed during aging. At the last phase of the project we questioned if observed changes in the transcriptome can be controlled by specific transcription factors. Thus we used Chip-seq data to predict plausible transcription factor regulators of gene sets obtained using time series clustering and Network smoothing. On the one hand, all predicted transcription factors had documented relevance to aging. On the other hand, we did not achieve gene set specific prediction of transcription factors. In fact, genes with the opposite dynamics were predicted to respond to the same transcription factors. To summarize, we characterized in details age-related changes in the transcriptome of C. elegans, validated the performance of the Network Smoothing algorithm and showed that integration of gene expression with Chip-seq data allows to predict transcription factors that are capable to modulate the lifespan of C. elegans.
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Williams, Joseph Paul. "Sequencing and annotation of potential cis-acting transcription elements in the emb-9 gene promoter of caenorhabditis elegans /." MSU Only Available Electronically, 2009. http://purl.missouristate.edu/etd/Williams.Joseph-2009-SP.
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Nguyen, Lamtho Laura T. "Isolation and characterization of CEABF-1, the ABF-1 homolog in C. elegans." Scholarly Commons, 2003. https://scholarlycommons.pacific.edu/uop_etds/578.
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The basic helix-loop-helix (bHbH) family-of transcription factors is important in many developmental and regulatory pathways such as cellular proliferation and differentiation, lineage commitment, sex determination, neurogenesis, myogenesis, hematopoeisis and pancreatic development. The free-living nematode Caenorhabdits elegans is an important model organism. Genetics studies of a gene in nematodes help us to better understand the functioning of hornologs in more complex organisms. These studies investigate the nematode homolog of ABF-1, CeABF-1, and its potential role in the development of C. elegans. The BLAST Database (http://www.ncbi.nlm.nih.gov) predicted a bHLH protein in C. elegans, located on cosmid ZK682.4, of 170 amino acids with an overall 51% similarity to human ABF-1. Importantly, it had a 72% similarity to human ABF-1 within the bHLH domain. Genomic and eDNA clones of CeABF-1 were isolated using whole nematodes and PCR methods. Clones were constructed that would allow us to use green fluorescent protein (GFP) to localize CeABF-1 expression. We also used RNA interference to determine the function of CeABF-1. No obvious phenotype was observed in nematodes unable to produce the CeABF-1 protein. Preliminary studies suggest that CeABF-1 is not an essential gene for development in C. elegans. Constructs were also made for protein induction and antibody studies. Further studies are necessary to determine how CeABF-1 is involved in nematode development and its interaction with other proteins.
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Weick, Eva-Maria. "Genetic and functional characterisation of piRNA pathway factors in Caenorhabditis elegans." Thesis, University of Cambridge, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708028.
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Wilkins, Annekathrin. "Factors influencing the dispersal of Pseudomonas fluorescens NZI7 by Caenorhabditis elegans." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:6bf58183-f197-490d-86d4-633ae8d46c06.
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Caenorhabditis elegans is a natural predator of the mushroom pathogen Pseudomonas fluorescens NZI7. The bacterial mechanisms for reducing predation by the nematode through the secretion of secondary metabolites have been described, but not yet fully explored. The behaviour of nematodes is influenced by the different factors produced by the pseudomonads. In this thesis we develop a range of assays to link the behaviour of C. elegans to these factors to identify their role in bacteria-nematode interactions. We show that these factors play two distinct roles: they may either repel nematodes, or harm them. This permits the classification of mutants of P. fl. NZI7 lacking these factors as either attractive, edible or both. Many studies of C. elegans behaviour have demonstrated that the nematode can distinguish between different food sources. Our results show two distinct types of response: chemotaxis drives the response to attractive or repellent stimuli, and nematodes also show a choice behaviour that is independent of chemotaxis. This choice behaviour is determined by bacterial edibility and requires nematodes to come into contact with the bacteria. This contact is the foundation of the bacterial dispersal by nematodes. By making use of the luminescence property of the available bacterial mutants, we demonstrate an intimate link between the behaviour of C. elegans and the success with which bacteria are disseminated: if nematodes are induced to regularly leave a bacterial colony, whether through their genotype or the low edibility of the food, then they will spread bacteria effectively. Throughout this thesis, we use computational simulations based on a hybrid cellular automaton model to represent the nematode-bacteria interactions. These simulations recreate the observed behaviour of the system, thus they help to confirm our hypotheses and establish the fundamental aspects of the interactions between the two species.
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Zechner, Kerstin. "3' end processing and RNA polymerase II transcription termination in protein coding genes in the nematode C. elegans." Thesis, University of Oxford, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.564397.
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In all organisms studied so far, the recognition of a functional poly(A) site is essential for RNA polymerase II termination at the end of nearly all genes transcribed by this enzyme (Whitelaw and Proudfoot, 1986; Guo et al., 1995; Birse et al. 1997). A number of eukaryotes have some of their genes organised in polycistronic structures which resemble bacterial operons (Davis and Hodgson, 1997; Ganot et al., 2004; Spieth et al. 1993), and in C. elegans, approximately 20% of all genes are contained within these operon-like structures (Blumenthal et al., 2002). Here, functional poly(A) sites will be synthesised and recognised by RNA polymerase II at the end of each gene within the operon, however termination of the polymerase only occurs at the final gene of the polycistronic transcription unit In these studies, we analyse the halting of RN A polymerase II transcription at the end of monocistronic genes and furthermore observe how premature RNA polymerase II termination is prevented during polycistronic transcription in the nematode C. elegans. We predominantly make use of reverse transcriptase PCR-based techniques to examine these mechanisms. We show that a large increase in pre-mRNAs stretching into the 3' flank of genes can be detected in worms depleted of the riboexonuclease XRN-2, indicating that this enzyme may have a possible role in RNA pol II termination and 3' end formation in C. elegans. Furthermore, we provide evidence that the polymerase can read into telomeric structures in the nematode. Also, we demonstrate that an RNAi-mediated knockdown of the UI-70K subunit of the UI snRNP causes a drop in polycistronic transcripts, providing a link between cis- splicing and the prevention of premature RNA polymerase II termination at operon-internal poly(A) sites. Finally, we illustrate that operon-internal poly(A) sites are capable of directing efficient 3' end formation outside of a polycistronic background. Together, these findings provide valuable insights into the mechanisms involved in directing or preventing premature RNA polymerase II transcription termination at C. elegans poly(A) sites.
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Jia, Kailiang. "Daf-9, a cytochrome P450 regulating C. elegans larval development and adult longevity /." free to MU campus, to others for purchase, 2000. http://wwwlib.umi.com/cr/mo/fullcit?p9998488.
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Fontrodona, Montals Laura. "A comprehensive functional study of Caenorhabditis elegans rsr-2 uncovers a new link between splicing and transcription." Doctoral thesis, Universitat Autònoma de Barcelona, 2012. http://hdl.handle.net/10803/117661.
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Durant el transcurs d’un rastreig a gran escala per RNA d’interferència (iARN) en Caenorhabditis elegans, el gen rsr-2 va ser identificat com a interactor genètic del gen lin-35 Retinoblastoma, l’homòleg de la família humana de Retinoblastoma. El gen rsr-2 és l’ortòleg de la proteina humana d’splicing SRm300/SRRM2. A diferència del seu ortòleg en llevat Cwc21, rsr-2 és essencial per la viabilitat. Degut a que la forta inactivació d’rsr-2 produeix uns fenotips molt severs, hem aprofitat l’efecte lleu que produeix l’ARN interferent a través de l’aliment per estudiar les funcions d’rsr-2 durant el desenvolupament.
Els assatjos d’iARN d’rsr-2 juntament amb anàlisis d’epistàsia genètica situen rsr-2 en la via de la determinació sexual de la línia germinal. Tot i així, tiling arrays d’animals rsr-2(iARN) no han revelat defectes significatius en l’splicing. Gràcies a experiments d’immunofluorescència, hem observat que un anticòs específic per RSR-2 co-localitza amb cromatina en nuclis de cèl·lules de la línia germinal. Interessantment, experiments d’immunoprecipitació de cromatina i seqüenciació massiva (ChIP-Seq) han desvetllat que RSR-2 co-precipita cromatina seguint un patró similar al de l’ARN polimerassa II. Aquests experiments de ChIP-Seq també han fet palès que RSR-2 és reclutada a la cromatina d’un mode que és independent de l’splicing i suggereixen que RSR-2 podria desenvolupar un rol de regulador transcripcional. Addicionalment, hem explorat els transcriptomes d’animals rsr-2(iARN) i prp-8(iARN) en estadi de larva 3 (L3), fet que ens ha permès classificar rsr-2 com a un factor d’splicing no essencial. Conjuntament, el nostre estudi mostra que RSR-2 és una proteina multifuncional que regula el desenvolupament de Caenorhabditis elegans influenciant, i probablement acoblant, els processos d’splicing i transcripció.During the course of a large scale interference RNA (RNAi) screen in Caenorhabditis elegans, rsr-2 was identified as a genetic interactor of lin-35 Rb, the homolog of human Retinoblastoma. The rsr-2 gene encodes the ortholog of the human spliceosomal protein SRm300/SRRM2. In contrast to its yeast ortholog Cwc21, rsr-2 is essential for viability. Since strong inactivation of rsr-2 produces severe phenotypes, we took advantage of the mild effect of RNAi by feeding to study functions of rsr-2 during development. rsr-2 RNAi assays and genetic epistasis analysis locate rsr-2 within the germ line sex determination pathway but tiling arrays of rsr-2(RNAi) animals do not disclose significant splicing defects. By inmunofluorescence, we observe that an antibody specific for RSR-2 co-localizes with chromatin in germ line nuclei. Interestingly, ChIP-Seq experiments reveal that RSR-2 co-precipitates chromatin in a pattern similar to that of RNA Polymerase II. These ChIP-Seq assays also evidenced a splicing-independent recruitment of RSR-2 to chromatin and suggest that RSR-2 could have a role in regulating transcription. Moreover, we have explored the transcriptomes of rsr-2(RNAi) and prp-8(RNAi) L3 worms by RNA-Seq, which classified rsr-2 as a non-essential splicing factor. Altogether, our study shows that RSR-2 is a multifunctional protein that regulates development by influencing, and probably coupling, splicing and transcription.
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Mergoud, dit Lamarche Adeline. "Étude des modifications sub-cellulaires associées au vieillissement musculaire chez Caenorhabditis elegans-Rôle du facteur de transcription UNC-120/SRF." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1114.
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Le vieillissement s'accompagne d'une perte progressive de la masse et de la fonction musculaire, appelée sarcopénie. Différents mécanismes ont été proposés pour expliquer la sarcopénie. Cependant, la majorité d'entre eux ont été identifiés dans le contexte d'une atrophie induite expérimentalement (par dénervation, immobilisation, jeûne...) ou via des études corrélatives chez l'homme. Ainsi nous ne connaissons pas aujourd'hui l'importance et la chronologie de ces facteurs dans le contexte du vieillissement physiologique. Caenorhabditis elegans est un organisme modèle de référence pour les études de longévité. Grâce aux outils génétiques disponibles chez le nématode C. elegans, des voies moléculaires, qui contrôlent la longévité et dont le rôle est conservé chez les mammifères, ont pu être identifiées, comme la voie du récepteur de l'insuline/IGF-1. Toutefois le vieillissement musculaire a été très peu étudié dans cet organisme.Le premier objectif de mon projet de thèse était de décrire chez C. elegans les changements subcellulaires qui sont associés la perte de mobilité avec l'âge afin d'identifier des biomarqueurs potentiels du vieillissement musculaire. Le deuxième objectif était d'utiliser ces biomarqueurs comme outil pour identifier des gènes modificateurs de la sarcopénie. Nous avons ainsi pu mettre en évidence une diminution de l'expression de gènes impliqués dans la structure et la fonction musculaire très tôt au cours de la vie adulte. Ce phénotype est suivi par une fragmentation progressive des mitochondries puis une accumulation de vésicules d'autophagie. Ces biomarqueurs ont été utilisés pour tester le rôle potentiel, dans le maintien du muscle, de facteurs impliqués dans la différenciation musculaire au cours de l'embryogenèse.L'ensemble des résultats obtenus nous permettent de proposer un modèle selon lequel le facteur de transcription unc-120, orthologue du Serum Response Factor, agirait en aval de la voie de signalisation de l'insuline/IGF-1 dans le contrôle des différents biomarqueurs du vieillissement musculairesAging is accompanied by a progressive loss of muscle mass and function, named sarcopenia. Different mechanisms have been proposed to explain it. Furthermore most of them have been identified in the context of an experimental induced atrophy (by denervation, immobilization, fasting...) or via correlative studies in humans. Thus today we do not know the importance and chronology of these factors in the context of physiological aging. Caenorhabditis elegans is a reference model organism for longevity studies. Thanks to genetics tools available for the nematode C. elegans, evolutionarily conserved molecular pathways, which control longevity, have been identified, such as the Insulin/IGF-1 receptor pathway. However muscle aging has been very poorly studied in this organism. The first aim of my thesis project was to describe, in C. elegans, subcellular changes that are associated with mobility loss with age in order to determine potential biomarkers of muscle aging. The second aim was to use these biomarkers as tools to identify genes able to modify sarcopenia. Specifically, we could highlight a decrease of expression of genes involved in muscle mass and function very early during adulthood. This phenotype is followed by a gradual mitochondrial fragmentation then an accumulation of autophagic vesicles.These biomarkers have been used to test the potential role in muscle maintenance, of factors involved in muscle differentiation during embryogenesis. Altogether these results suggest a model in which the transcription factor unc-120, ortholog of Serum Response Factor, would act downstream in the insulin/IGF-1 signalization pathway on the control of the different biomarkers of muscle aging
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Hanafi, Jasmin. "Identifying factors involved in chromosome movement during prophase I of meiosis in Caenorhabditis elegans." Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=121248.
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Meiosis is a reductional cell division that produces haploid gametes and uniquely allows the introduction of genetic diversity via crossover recombination between homologous chromosomes. Any defect during this process could lead to the non disjunction of chromosomes, which in turn leads to aneuploidy in the resulting progeny, a condition that is generally lethal but in certain cases results in serious developmental abnormality. In C. elegans, at the onset of meiosis, chromosomes condense and cis-acting regions near each chromosome end called pairing centers recruit zinc-finger proteins which help chromosomes associate with nuclear envelope bridge proteins. These bridge proteins are in turn linked to the cytoskeleton network. This association is important to facilitate chromosome clustering and homology search. Once chromosomes are properly homologously paired, the process of division continues until eventually four haploid cells are produced. Though the successful coordination and regulation of each step in meiosis is critical for the survival of a species, many components of the process remain unclear. During prophase I, chromosome movement resulting in proper homologous pairing is controlled and regulated in a manner that is not well understood. The objective of my research therefore, is to try and identify factors involved in this chromosome movement. To do this, a candidate RNAi screen of 482 genes was conducted and 156 genes were positively identified as having a lack of chromosome movement. Since any mistakes in pairing and subsequent stabilization of homologous chromosomes could lead to non disjunction and possible embryonic lethality (emb) from loss of an autosome or a high incidence of males (him) from loss of the X chromosome, positive candidates were also screened for emb and him. Of the 156 positive candidates, 24 were also positive for emb and 1 was additionally positive for him. These candidates present many possibilities for further validation and characterization in future projects.La méiose est une division cellulaire réductionnelle qui produit des gamètes haploïdes et permet d'une façon unique l'introduction de diversité génétique à travers la recombinaison entre les chromosomes homologues. Tout problème dans le processus peut causer une impossibilité de séparation entre les chromosomes, ce qui à son tour cause l'aneuploïdie dans la génération suivante, une condition qui est généralement mortelle, mais résulte en anomalie dans le développement dans certains cas. Les chromosomes de C. elegans, au tout début de la méiose, se condensent et les régions "cis" à la fin de chaque chromosome appelées centres paires recrutent les protéines avec des doigts de zinc qui aident les chromosomes associer avec le pont de protéines sur l'enveloppe nucléaire. Le pont est connecté au réseau cytosquelette. Cette association est importante pour la facilitation du regroupement des chromosomes et la recherche de chromosomes homologues. À la retrouvaille des chromosomes homologues, le processus de division continue jusqu'à ce que quatre cellules haploïdes soient produites. Même si le succès de la coordination de chaque étape de la méiose est critique pour la survie des espèces, certain détails du processus restent inconnus.Durant la prophase I, le mouvement des chromosomes qui résulte dans le propre couplement des chromosomes homologues est contrôlé et régulé d'une manière encore inconnue. L'objectif de mes recherches est donc d'identifier des facteurs associés dans ledit mouvement des chromosomes. Pour accomplir ce but un écran de ARNi avec 482 gènes comme candidates a été mené et 156 gènes ont été positivement identifiés pour une manque de mouvement des chromosomes. Comme tout problème de formation des couples de chromosomes ainsi que dans la stabilisation des chromosomes homologues qui suit peut causer de la non-disjonction et possible mort embryonnaire (emb) suite à la perte d'un autosome ou une haute incidence de males (him) causé par la perte du chromosome X, les candidats out aussi été examinés pour emb et him. Des 156 candidats positifs, 24 ont aussi été positifs pour emb et un candidat a été additionnellement positif pour him. Ces candidats se présentent comme une source de futures recherches de validation ainsi que de caractérisation.
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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.
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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.
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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.
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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;
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Kagias, Konstantinos. "Analysis of chromatin factors during an in vivo cell reprogramming event in C. Elegans." Strasbourg, 2009. http://www.theses.fr/2009STRA6242.
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Nous étudions les mécanismes sous-tendant la reprogrammation de l’identité cellulaire. Nous avons établi un nouveau modèle où la reprogrammation d’une cellule différenciée en un autre type cellulaire différencié peut être suivie in vivo. Ainsi nous nous concentrons, chez le nématode C. Elegans, sur le cas de la cellule “Y”, une cellule épithéliale qui forme, avec 5 autres cellules, le rectum au début du développement. Cette cellule se détache ensuite et devient un motoneurone appelé “PDA”. Mon projet de thèse a consisté à examiner le rôle de facteurs chromatiniens impliqués dans ce processus. Cit_af ref_bf(Ng, 2008 ref_num2226)ref_af Nous avons initié un crible génétique ciblé par interférence à l’ARN afin d’identifier les activités de remodelage de la chromatine qui sont importantes pour initier la reprogrammation de la cellule rectale Y. Nous avons ainsi identifié le gène egl-27. L’homologue humain, MTA1, est un membre de plusieurs complexes altérant la chromatine. De façon intéressante, MTA1 interagit physiquement avec le facteur de liaison à l’ADN SALL4cit_af ref_bf(Liang, 2008 ref_num2191)ref_af ; or nous avons précédemment montré que SALL4/SEM-4 affecte une étape précoce de la transformation de Y en PDA. Cit_af ref_bf(Tsubooka, 2009 ref_num1943)ref_af Nous avons trouvé que SEM-4 et EGL-27 colocalisent dans le noyau et peuvent être coprécipités. Nos résultats montrent que ces 2 facteurs coopèrent dans différent processus de plasticité cellulaire. Nous avons par ailleurs identifié des interacteurs génétiques de egl-27. Nos expériences d’épistasie nous permettent de postuler une cascade génétique qui contrôlerait les premières étapes de la transformation de Y en PDA, et dont de nombreux membres ont une fonction conservée au cours de l’évolution dans le maintien de la plasticité cellulaireWe study the mechanisms underlying the reprogramming of a cell identity. We have established a new model where the reprogramming of a differentiated cell into another differentiated cell can be followed in vivo. We focus on the ‘Y’ cell in C. Elegans, a rectal epithelial cell which forms, with 5 other cells, the rectum in the embryo and early larvae. Later, this cell retracts and becomes the motor neuron ‘PDA’. My thesis project examines the role of chromatin factors implicated in this process. We have conducted an RNAi screen to identify the chromatin remodelling activities that are important for the initiation of the reprogramming of ‘Y’ rectal cell. We identified this way the gene egl-27. Its human homologue, MTA1, is a member of several chromatin remodelling complexes and, interestingly, it physically interacts with the transcription factor SALL4, which we have previously shown to affect the early steps of Y-to-PDA transformation. We found that SEM-4 and EGL-27 colocalize in the nucleus of cells and that they co-precipitate. Our results show that these two factors are involved in the regulation of multiple cellular plasticity events. We have also identified genetic interactors of egl-27 and our epistatic analysis has allowed us to postulate a genetic cascade that controls the initial steps of Y-to-PDA transformation. Accordingly, the members of this cascade appear to have a conserved function in cellular plasticity during the evolution
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Raman, Indu. "Functional tests of winged-helix transcription factors for metabolic adaptation in C. elegans." Ann Arbor, Mich. : ProQuest, 2007. 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:1445925.
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Thesis (M.S. in Molecular and Cellular Biology)--S.M.U., 2007.Title from PDF title page (viewed Mar. 18, 2008). Source: Masters Abstracts International, Volume: 46-01 Adviser: James A. Waddle. Includes bibliographical references.
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Li, Xin. "Signal transduction pathways and their regulation of transcriptional factors during C. elegans development." Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1228090565.
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Sleiman, Sama. "Study of the role of pax transcription factors and SP-related factors in C. Elegans organ development." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1198630665.
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Rodrigues, Ricardo José Cordeiro Machado [Verfasser]. "Searching and characterizing novel 21U RNA biogenesis factors in Caenorhabditis elegans / Ricardo José Cordeiro Machado Rodrigues." Mainz : Universitätsbibliothek Mainz, 2019. http://d-nb.info/1194968724/34.
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LaRue, Bobby Lee Jr. "Genetic and Environmental Factors that Mediate Survival of Prolonged Oxygen Deprivation in the Nematode Caenorhabditis Elegans." Thesis, University of North Texas, 2010. https://digital.library.unt.edu/ark:/67531/metadc103350/.
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Ischemic events of even a very short duration are not tolerated Ill in humans. The human cost of ischemia, when looked at as combined cardiovascular disease, dwarfs all other causes of death in the United States. Annually, CVD kills as many people in the US as does cancer, chronic lower respiratory disease, accidents, and diabetes mellitus combined. In 2005 (the latest year for which final statistics are available), CVD was responsible for 864,480 deaths or 35.3 percent of total deaths for the year. In my study, I have used the nematode Caenorhabditis elegans to determine genetic and environmental modulators of oxygen deprivation a key component of ischemia. I have found that animals with mutations in insulin like signaling pathways, neuronal function, electron transport chain components, germline function, and animals that are preconditioned by being raised on a diet of E. coli HT115 bacteria at 25°C have an enhanced ability to survive long-term (>72 hours) anoxia (<.005 kPa O2) at 20°C. The enhanced anoxia survival phenotype partially correlates with increased levels of carbohydrate stores in the nematodes. Suppression of this enhanced anoxia survival phenotype is possible by altering expression of the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase, the FOXO transcription factor DAF-16, and 5’-AMP kinase.
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Casadio, Angela. "Identification and characterisation of novel factors involved in the nonsense-mediated mRNA decay (NMD) pathway." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/22897.
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Nonsense mediated mRNA decay (NMD) is a surveillance mechanism that targets transcripts containing premature stop codons (PTCs) for degradation, and that also regulates up to 10% of the whole transcriptome. During the course of my PhD I set out to identify novel NMD factors by performing a genome-wide RNA interference (RNAi) screen in a transgenic strain of Caenorhabditis elegans carrying an NMD reporter. I identified five novel proteins that are putative NMD factors in worms: NGP-1, NPP-20, AEX-6, PBS-2 and NOAH-2. Knock-down of these proteins led to severe developmental defects: worms were either arrested during various larval stages or died prematurely. The only exception was AEX-6, the knockdown of which led to a milder phenotype. Homology analysis of the novel C. elegans NMD factors showed that these proteins are conserved in human, with the exception of NOAH-2, which only has a homologue in Drosophila melanogaster, NOMPA. By performing an NMD assay in human cells, I demonstrated that GNL2 (NGP-1) and SEC13 (NPP-20) are functionally conserved NMD factors in human. Analysis of the consequences of depletion of GNL2, SEC13, UPF1 or UPF2 on the transcriptome of HeLa cells revealed that these four proteins co-regulate a subset of endogenous NMD targets, whilst also independently regulating the expression of other sets of transcripts. The findings presented in this thesis further our knowledge of the biology of NMD in both nematodes and humans. They demonstrate the existence of further regulators of this surveillance pathway, and add a layer of complexity to this fine-tuned biological process.
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Hatzold, Julia. "Identification of factors that establish asymmetry and cell-death fate in the NSM lineage in Caenorhabditis elegans." Diss., [S.l.] : [s.n.], 2006. http://edoc.ub.uni-muenchen.de/archive/00005384.
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Garroni, Michael Kenneth. "Identification of cis-acting elements and trans-acting factors responsible for her-1 regulation in Caenorhabditis elegans." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ58700.pdf.
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Krüger, Angela. "Systematic and quantitative analysis of the early embryonic development of Caenorhabditis elegans." Doctoral thesis, Universitat Pompeu Fabra, 2012. http://hdl.handle.net/10803/128514.
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The embryo of Caenorhabditis elegans is a model system in which development can be studied at single cell resolution. In this thesis I describe the use of a semi-automatic nuclear tracking algorithm to analyze cellular movements in the early embryo, as well as how embryos respond to mechanical deformation and to genetic perturbation. During gastrulation cells were observed to not only ingress into the interior of the embryo, but also to egress onto the surface. Moreover, cell lineages were identified that undergo both directional movements, i.e. first internalize and then continue to move until finally reemerging on the surface, “transgressing” or “tunnelling” through the embryo. The previously described stereotypical early rotation movements in compressed embryos were found to be highly variable in uncompressed embryos, with this variable global rotation largely determining the final embryonic axes. In addition to constraining this early rotation, compression of the embryo was found to alter the relative positions of cell groups. A compensatory mechanism was identified consisting of a global rotation of cells initiating more than an hour after the four-cell stage that realigns the relative positions of cell groups and results in a further rotation of the embryonic axes. Possible mechanisms that drive these corrective cell movements are discussed. Inhibiting the expression of 20 general regulators of chromatin and analyzing the phenotypic consequences at single cell resolution revealed functions in chromosome segregation, mitotic cell cycle progression, cellular movements and lineage-specific development, and suggested the existence of functionally diverse chromatin-modifying protein complexes in the embryo. Moreover, a global re-arrangement of nuclear architecture was observed upon the inhibition of zygotic gene expression. Taken together, these analyses illustrate the power of single cell resolution phenotyping, identify previously unrecognized cell behaviors during early development, and identify regulative cell movements as a mechanism that confers robustness to the effects of mechanical deformation.El nemátodo Caernorhabditis elegans ofrece la posibilidad de estudiar el desarrollo embrionario con una resolución celular. En esta tesis, describo el uso de un algoritmo semi-automático de seguimiento nuclear para analizar movimientos celulares en el embrión temprano, así como la manera en que el embrión responde a deformaciones mecánicas y a perturbaciones genéticas. Durante el proceso de gastrulación, observamos que ciertas células no solo ingresan al interior del embrión, pero también egresan hasta la superficie. Asimismo, identificamos linajes celulares que llevan a cabo ambos tipos de movimientos direccionales, esto es, primero internalizan y luego la continuan su movimiento hasta finalmente re-emerger en la superficie, “transgressing” o “tunneling” a través del embrión. Hemos descubierto que los movimientos estereotípicos de rotación en el embrión temprano, descritos previamente, son altamente variables en ausencia de compresión y esta variabilidad total en la rotación determina los ejes finales del embrión. Además de limitar esta rotación temprana, la compresión del embrión altera la posición relativa de grupos celulares. Hemos identificado un mecanismo compensatorio que consiste en la rotación global de células el cual tiene lugar mas de una hora después del estadio de cuatro células. Ese mecanismo re-alinea la posición relativa de los grupos celulares resultando en una rotación adicional de los ejes embrionarios. Posibles mecanismos responsables de estos movimientos correctivos son discutidos. La inhibición de la expresión de 20 reguladores generales de la cromatina y el análisis de las consecuencias fenotípicas con resolución celular ha revelado funciones en la segregación de cromosomas, la progresión mitótica del ciclo celular, movimientos celulares y desarrollo linaje-especifico, sugiriendo la existencia de diversos complejos de proteínas modificadoras de la cromatina en el embrión. Además, hemos observado una re-organización global de la arquitectura nuclear al inhibir la expresión zigótica en el embrión. En conclusión, estos análisis han permitido ilustrar el poder de la fenotipificación con resolución celular, así como la identificación de comportamientos celulares previamente desconocidos durante el desarrollo temprano y movimientos celulares regulativos como un mecanismo que confiere robustez a los efectos de deformaciones mecánicas.
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Round, June L. "Characterization of ABF-1 in C. elegans and regulation of cellular growth and ID3 by human ABF-1." Scholarly Commons, 2002. https://scholarlycommons.pacific.edu/uop_etds/568.
Full textAbstract:
ABF -1 is a human class II bHLH transcription factor that is expressed predominantly in activated B cells and EBV immortalized cell lines. A portion of this study sought to characterize the homolog of ABF- l in Caenorhabditis e/egans. The nematode gene product, ceABF -1, is capable of forming heterodimers with E2A gene products and binding E box binding sites. HeLa cells transfected with ceABF-1 reveal that it is capable of blocking E2A mediated gene transcription. In order to maintain full repression capabilities, two conserved amino acid residues within helix I ofthe HLH domain are required. These results show a conserved mechanism of gene repression between invertebrates and vertebrates. This study also sought to analyze ABF-1 mediated regulation of both ld3 and cellular growth. Using a human ABF-1 stably transfected cell line, ID3 protein levels and transcript levels were shown to increase in response to overexpression of ABF-1 via western and northern blot, respectively. Flow cytometry analysis and Real-time PCR revealed that ABF-1 programs a slow down in the cell cycle, however this growth arrest is not mediated by ID3.
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Tseng, Rong-Jeng. "Identification and characterization of factors functioning with EGL-38 PAX to regulate lin-48 in Caenorhabditis elegans." Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1213384889.
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