Determining the Significance of the MICOS Protein Complex on the Frequency of Spontaneous Cellular Respiration Loss in Saccharomyces cerevisiae

Abstract

The Mitochondria is a double-membraned organelle found in all eukaryotic cells. It is the organelle most known for taking nutrients from the cell, breaking it down, and turning it into energy; a process known as cellular respiration. The DNA of the mitochondria (mtDNA) is circular, and differs greatly from the nuclear genome. In order to prevent mutations, there are genes that present proteins involved in DNA repair mechanisms. Response to DNA damage, lack of nutrients and other stress conditions is an essential property of living systems. The coordinate response includes DNA damage repair, activation of alternate biochemical pathways, adjustment of cellular proliferation and cell cycle progression as well as drastic measures like cellular suicide which prevents proliferation of severely damaged cells (1). One gene complex, known as the MICOS Complex, is composed of six different genes. MICOS (Mitochondrial contact site and Cristae Organizing System) is a mitochondrial inner membrane complex that extends into the intermembrane space and has a role in the maintenance of crista junctions, inner membrane architecture, and formation of contact sites to the outer membrane (2). Mic60p can be described as the core component for the maintenance of the MICOS complex, controlling protein transport, mitochondrial DNA transcription, and the connection between the inner and outer mitochondrial membranes. In the lab, a set of mutant strains, each representing one of the six genes from the MICOS complex have been developed. As one experiment, the mic60Δ mutant strain is compared to the wild type strain, MIC60, in an assay determining respiration loss, overall determining the significance of the MICOS complex on cellular respiration. Rich growth medias containing dextrose as the sole carbon source were used to determine spontaneous respiration loss in both the mic60Δ and MIC60 strains initially. The mic60Δ strain has revealed a 2.05-fold increase in loss of cellular respiration compared to that of the wild type when grown on dextrose. When these strains were grown on raffinose or fructose as the sole carbon source, the mic60Δ strain revealed a 1.46-fold increase in loss of cellular respiration compared to that of the wild-type. This data shows that Mic60p plays a vital role in the functioning mitochondria.