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dc.contributor.advisorRiddle, Donald L.eng
dc.contributor.authorZheng, Qun, 1968-eng
dc.date.issued2005eng
dc.date.submitted2005 Springeng
dc.descriptionThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.eng
dc.descriptionTitle from title screen of research.pdf file viewed on (January 25, 2007)eng
dc.descriptionIncludes bibliographical references.eng
dc.descriptionVita.eng
dc.descriptionThesis (Ph.D.) University of Missouri-Columbia 2005.eng
dc.descriptionDissertations, Academic -- University of Missouri--Columbia -- Neuroscience.eng
dc.description.abstractIn eukaryotes, two large subunits form the core catalytic structure of RNA polymerase III (Pol III), which is conserved in other RNA polymerases, Pol I and Pol II. It has been found that Pol III activity is tightly associated to cell growth. TFIII B has been shown to be one of main mediators in this process. No regulation of the Pol III largest subunit gene has been found. In C. elegans, the rpc-1 gene encodes the largest subunit of Pol III. Here, I identified two critical structural components of RPC-1, Gly644 and Gly1055, whose mutations result in larval lethal arrestment. These two amino acid residues are universally conserved in RNA polymerases, indicating their overall involvement in gene transcription mechanism. Also, I found that maternally inherited, not embryonically expressed, rpc-1 gene products survive early development. Starvation was found to suppress rpc-1 gene expression and re-feeding treatment enhances rpc-1 gene expression rapidly. No similar regulation was detected in genes encoding largest subunits of Pol I and Pol II. This is the first time that rpc-1 gene regulation has been reported. Insulin signaling may not be involved in this regulation. Also, I found that rpc-1 promoter is not ubiquitously active in C. elegans. Using the rpc-1p::gfp transgene, the rpc-1 promoter activity is only detected in a subset of neurons in the head and the tail and the intestine. While starvation silences the rpc-1 promoter activity in most tissues and cells, ASK neurons still show GFP staining in the rpc-1p::gfp transgenic animals, indicating that rpc-1 transcription in ASK neurons is continuously active under starvation conditions. Further studies suggest that TGF-[beta] signaling is involved in mediating the rpc-1 promoter activity in ASK neurons.eng
dc.identifier.merlinb57681521eng
dc.identifier.urihttps://hdl.handle.net/10355/4129
dc.identifier.urihttps://doi.org/10-32469/10355/4129eng
dc.languageEnglisheng
dc.publisherUniversity of Missouri--Columbiaeng
dc.relation.ispartofcollectionUniversity of Missouri--Columbia. Graduate School. Theses and Dissertationseng
dc.subject.lcshEukaryotic cellseng
dc.subject.lcshCaenorhabditis eleganseng
dc.subject.lcshCells -- Growtheng
dc.subject.lcshRNA -- Metabolismeng
dc.subject.lcshGenetic regulationeng
dc.titleAnalysis of the Caenorhabditis elegans rpc-1 geneeng
dc.typeThesiseng
thesis.degree.disciplineNeuroscience (MU)eng
thesis.degree.disciplineBiological sciences (MU)eng
thesis.degree.grantorUniversity of Missouri--Columbiaeng
thesis.degree.levelDoctoraleng
thesis.degree.namePh. D.eng


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