Summary: | More than 30% of all human malignancies are brought about by mutations in RAS proto-oncogenes (HRAS, KRAS, and NRAS) that are greatly conserved in yeast <i>RAS1</i> and <i>RAS2</i>. This makes yeast (<i>Saccharomyces cerevisiae</i>) an efficient single-celled eukaryotic model organism to study their functions. In the current investigation, the null mutation of the <i>RAS2</i> gene was analyzed to find out its deleterious consequences in yeast cells based on their ability to utilize glycerol as a respiratory substrate, mtDNA mutation rate, mtDNA abundance, and distribution pattern. Mutant cells grown in YPEG plates demonstrated slight respiratory deficiency compared to the wild type. An erythromycin-resistant assay was carried out to analyze the spontaneous mitochondrial DNA mutation rate in the Δ<i>ras2</i> mutant and it was found to be greater than that of wild type. In addition, the mitochondrial DNAs of both strains were also visualized under a fluorescence microscope using DAPI fluorescent stain. It was observed that mtDNA abundance was much lower compared to wild type cells. Thus, the present investigation revealed that deletion of the <i>RAS2</i> gene resulted in mtDNA mutation and depletion.
|