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dc.contributor.authorColes, Garry L.
dc.date.accessioned2021-09-07T21:02:39Z
dc.date.available2021-09-07T21:02:39Z
dc.date.issued8/1/2009
dc.identifier.urihttp://hdl.handle.net/20.500.12648/4482
dc.description.abstractMitochondria are required for cellular respiration, which is essential in the production of ATP. Mitochondrial genome maintenance is necessary for the continued function of the mitochondrion. Deletions within the mitochondrial DNA (mtDNA) have been shown to be associated with a variety of human neuromuscular and age-related diseases. In this study we investigated the role of the MRX complex and the non-homologous end joining (NHEJ) DNA repair pathway in mitochondrial genome stability and repair. Specifically, we investigated the role of the MRX complex and the NHEJ pathway in the occurrence of spontaneous mitochondrial direct repeat-mediated deletions, nuclear direct repeat-mediated deletions, mitochondrial point mutations, nuclear point mutations, and spontaneous respiration loss using fluctuation analysis in the budding yeast, Saccharomyces cerevisiae. In this study, we have demonstrated that spontaneous mitochondrial direct repeat-mediated deletions are reduced 75 fold (p
dc.subjectMitochondrial DNA
dc.subjectAdenosine Triphosphate
dc.subjectATP
dc.subjectKu70p
dc.subjectGenome Stability
dc.titleThe Role of the MRX Complex and the Non-homologous End Joining DNA Repair Pathway in Mitochondrial Genome Stability and Repair
dc.typethesis
refterms.dateFOA2021-09-07T21:02:39Z
dc.description.institutionSUNY Brockport
dc.description.departmentBiology
dc.description.degreelevelMaster of Science (MS)
dc.source.statuspublished
dc.description.publicationtitleBiology Master’s Theses
dc.contributor.organizationThe College at Brockport
dc.languate.isoen_US


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