Fruit acidity has a significant effect on fruit quality. Previous apple studies have reported that low (<3.0 mg/ml in titratable acidity (TA)) fruit acidity was predominantly controlled by two major quantitative trait loci (QTLs) Ma and Ma3. However, genetic linkage regions for high (>10.0 mg/ml in TA) acidity apples remain unknown. Chapter two of this dissertation identifies two QTLs putatively associated with high acidity, Ma4 and Ma5 on chromosomes four and six respectively, using a pooled genome sequencing approach with an F1 population segregating for fruit acidity. To further study apple fruit acidity, the third chapter investigates the evolution of apple acidity based on the functional allele of the Ma1 gene located in the Ma region. There is still limited information how Ma1 has been affected by nature and/or human selection during evolution. To achieve this goal, targeted genome sequencing analysis of the Ma region in diverse Malus accessions was conducted. We conclude that apples have evolved to avoid homozygous high acidity alleles, not only by human selection, but also pre-domestication adaptation. The fourth and fifth chapters represent the comparative transcriptome analysis of a somatic mutation bud sport and its parent apple to identify mechanisms responsible for the delayed maturation, different ripening behavior, and better shelf life. The difference between the two was also analyzed through the characterization of apple fruit and hormone accumulation patterns. In chapter four, transcriptome and Sanger sequencing analyses reveals a loss of heterozygosity in the 2.8 Mb occurring in mutant and inferred that fruit development and maturation would be delayed due to an absence of wild Actin7 allele in the mutant. In chapter five, putative major regulators, such as ethylene and cell walls have been identified that may contribute to the superior shelf life of a mutant.