The Significance of the MICOS Protein Complex on Maintaining the Function of Cellular Respiration is Saccharomyces cerevisiae

Abstract

The mitochondria are essential organelles to the survival of cells due to their important role in cellular respiration. Mitochondria have their own set of DNA (mtDNA), which encodes proteins needed for the execution of successful oxidative phosphorylation. One of these gene complexes, known as the MICOS complex, contains six genes and is responsible for encoding proteins needed for the maintenance of the inner architecture of the organelle (1). Oxidative phosphorylation is only possible due to the proton gradient that is produced across the inner mitochondrial membrane. The MICOS gene complex encodes proteins that facilitate the building of the inner membrane of the mitochondria, as well as the cristae junctions, which are required for a sufficient rate of cellular respiration. While it has been shown that other mitochondrial genes contribute to the integrity of the mtDNA, there is little research about the contribution of the MICOS complex to the integrity of the mtDNA. The lab has developed a set of mutant strains that each represent a single gene knockout from the MICOS complex. Specifically, the mic19Δ mutant strain will be compared against the wild type strain, MIC19, in a respiration loss assay to develop an understanding of the significance of the MICOS complex on cellular respiration. Rich growth media containing dextrose and raffinose as the carbon sources were used to monitor spontaneous respiration loss in both the MIC19 and mic19Δ strains. When plated using dextrose as the sole carbon source after growth on glycerol media, the mic19Δ strain demonstrated an increase in cellular respiration loss compared to that of the wild type. When plated using raffinose as the sole carbon source after growth on glycerol media, the mic19Δ strain again demonstrated an increase in cellular respiration loss compared to that of the wild type. This shows that Mic19p plays a significant role in maintaining a functional mitochondrion.