Mitochondria are essential organelles in eukaryotes. Known as the “power house” of the cell, mitochondria manufacture ATP which is required for the successful completion of many cellular processes. Mitochondria have individual genomes, separate from the nuclear DNA, which encode for proteins required for the production of ATP. In humans, mutations in the mitochondrial DNA (mtDNA) result in the loss of mitochondrial function, leading to neuromuscular and neurodegenerative disorders. The focus of this study is to determine the role of the nuclear gene DNM1 in maintaining mtDNA stability in the budding yeast, Saccharomyces cerevisiae. Dnm1p is a dynamin-related GTPase protein localized to the outer membrane of mitochondria. Mitochondria undergo a constant state of fusion and fission within the cell which allows for mitochondrial segregation during cellular division. Dnm1p is a key regulator of mitochondrial fission. Loss of Dnm1p leads to the formation of large lattice-like structures of mitochondria. The lab is interested in determining whether loss of the dnm1 gene plays a role in mitochondrial genome stability. We observed in dnm1∆ mutants a 3-fold increase in spontaneous respiration loss which may be a result of altered mtDNA stability.
|Presenter:||Christopher Prevost (Undergraduate Student)|
|Time:||1:15 pm (Session III)
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