Presenter Information

Melissa Hoyer, University of Wyoming

Department

Molecular Biology Department

First Advisor

Dr. Peter Thorsness

Description

In Saccharomyces cerevisiae the Mmm1 and Fzo1 proteins play key roles in retaining mitochondrial DNA. In order to see the Mmm1 and Fzo1 proteins’ effects on mitochondrial morpholo gy, the TOM - 70 GFP fusion was transf ormed into various strains and mitochondria were examined using fluorescence microscopy. In the mmm1 deletion strain, the mitochondria lost the extended network usually seen in wild type cells. In the mmm1 deletion and fzo1 point mutant strain, the mitocho ndrial morphology lost the extended wild type network, but the difference was less dramatic. In the fzo1 point mutant control, the mitochondrial network was similar to wild type but had a more fragmented appearance. The loss of mitochondrial DNA in the mmm 1 deletion strain correlates to error in mitochondrial morphology in the mmm1 deletion strain. Revertance of wild type mitochondrial DNA retention by adding the fzo1 point mutant to the mmm1 deletion correlates to the revertance of mitochondrial morphology in the mmm1 deletion and fzo1 point mutant strain. Therefore there is a correlation between retention of mitochondrial DNA and mitochondrial morphology in these experimental strains, but further research must be done in this area to discover the exact cau se of this correlation.

Comments

Oral Presentation, Wyoming NSF EPSCoR

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The Importance of Mitochondrial Morphology in Saccharomyces cerevisiae

In Saccharomyces cerevisiae the Mmm1 and Fzo1 proteins play key roles in retaining mitochondrial DNA. In order to see the Mmm1 and Fzo1 proteins’ effects on mitochondrial morpholo gy, the TOM - 70 GFP fusion was transf ormed into various strains and mitochondria were examined using fluorescence microscopy. In the mmm1 deletion strain, the mitochondria lost the extended network usually seen in wild type cells. In the mmm1 deletion and fzo1 point mutant strain, the mitocho ndrial morphology lost the extended wild type network, but the difference was less dramatic. In the fzo1 point mutant control, the mitochondrial network was similar to wild type but had a more fragmented appearance. The loss of mitochondrial DNA in the mmm 1 deletion strain correlates to error in mitochondrial morphology in the mmm1 deletion strain. Revertance of wild type mitochondrial DNA retention by adding the fzo1 point mutant to the mmm1 deletion correlates to the revertance of mitochondrial morphology in the mmm1 deletion and fzo1 point mutant strain. Therefore there is a correlation between retention of mitochondrial DNA and mitochondrial morphology in these experimental strains, but further research must be done in this area to discover the exact cau se of this correlation.