Mitochondria contain their own genome, mtDNA (mitochondrial DNA), which codes for products necessary for metabolism and mitochondrial function. Disruption of the mtDNA sequence can lead to a decrease in organismal fitness. To further understand the effects of mtDNA mutations, the PolG mutant mouse was created, which contains a mutated mtDNA proofreading mechanism and accumulates mtDNA mutations, leading to premature aging and death. The aging mechanisms and physiology of PolG mice have been well studied, but little has been done to analyze the location, frequency, and diversity of their specific mtDNA point mutations and indels. Previous studies on the PolG mtDNA spectrum have been limited by sample size or have not covered the entire mtDNA genome. This study explores the mtDNA mutation spectrum of the PolG mouse using metrics that are specific to mtDNA. Mutation counts, which quantify mutation diversity, and frequencies, which report mutation abundance, were the lowest in the d-loop, where the mtDNA origin of replication is located. Germline mutations had a lower probability of causing missense or nonsense changes compared with somatic mutations, likely because they screened more effectively by natural selection. Cytosine to thymine mutations are the plurality of mutations in the PolG mouse and appear to primarily contribute to a change in hydrophobicity in protein products. Our results provide insight into the connection between aging and mtDNA mutations as well as how selection acts on mtDNA mutations within an organism.