Event Title

The Role of DNM1 in Mitochondrial Genome Stability in Budding Yeast

Location

Edwards Hall Lobby

Document Type

Poster Presentation (1 hour)

Description

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 respiration. In humans, mutations in the mitochondrial DNA (mtDNA) results in the loss of mitochondrial function which leads 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 protein 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 aberrant mitochondrial structures. 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. Mitochondrial genome instability can arise via spontaneous point mutations or deletion events. Assays were performed to measure the spontaneous point mutation rate between wild type and dnm1∆ mutant strains. Spontaneous point mutation rates were shown to increase in dnm1∆ mutants. Strains were constructed to determine the role of DNM1 in spontaneous direct repeat-mediated deletion (DRMD) events within the mitochondrial genome as well as the nuclear genome. The rate of DRMD events in the mitochondrial genome was increased in the dnm1∆ strain compared to that of the wild type. However, there was no change in the rate of nuclear DRMD events for the nuclear genome. Additionally, the lab is determining the effect of DNM1 on the rate of induced DRMD events. Currently, the lab is isolating mtDNA from dnm1∆ and wild type strains in order to determine whether there are any apparent structural differences between them.

Start Date

April 2014

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Apr 26th, 1:00 PM

The Role of DNM1 in Mitochondrial Genome Stability in Budding Yeast

Edwards Hall Lobby

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 respiration. In humans, mutations in the mitochondrial DNA (mtDNA) results in the loss of mitochondrial function which leads 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 protein 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 aberrant mitochondrial structures. 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. Mitochondrial genome instability can arise via spontaneous point mutations or deletion events. Assays were performed to measure the spontaneous point mutation rate between wild type and dnm1∆ mutant strains. Spontaneous point mutation rates were shown to increase in dnm1∆ mutants. Strains were constructed to determine the role of DNM1 in spontaneous direct repeat-mediated deletion (DRMD) events within the mitochondrial genome as well as the nuclear genome. The rate of DRMD events in the mitochondrial genome was increased in the dnm1∆ strain compared to that of the wild type. However, there was no change in the rate of nuclear DRMD events for the nuclear genome. Additionally, the lab is determining the effect of DNM1 on the rate of induced DRMD events. Currently, the lab is isolating mtDNA from dnm1∆ and wild type strains in order to determine whether there are any apparent structural differences between them.