As women age, their oocytes decline in both quantity and quality, leading to eventual infertility. Part of this decline is associated with increased levels of reactive oxygen species and decreased mitochondrial function, which are associated with lower live birth rates. However, detailed mechanisms regulating mitochondrial function and mitochondrial decline in aged oocytes are unknown. Here we show that NEDDylation, a protein posttranslational modification, modulates mitochondrial transcription in oocytes to maintain quality over time. In this proteomic study we compared NEDDylation pathway, UBA3, knockout oocytes to control oocytes to investigate proteomic changes due to loss of NEDD8 conjugation.