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NEDDylation modifies mitochondrial transcription to maintain oocyte quality

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE273836 | GEO | 2026/01/01

REPOSITORIES: GEO

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NEDDylation modifies mitochondrial transcription to maintain oocyte quality (Oocyte)

Project description:Aging decreases oocyte quality, leading to infertility, miscarriage, and birth defects. Major contributors to this decline include mitochondrial dysfunction and chromosome dynamics dysregulation. Here, we show that oocyte-specific deletion of Uba3, which encodes the catalytic subunit of the E1 NEDDylation activating complex (NAE), in mice causes sterility and premature depletion of the ovarian reserve. Fully grown Uba3 conditional knockout oocytes show hallmarks of mitochondrial abnormalities, including increased reactive oxygen species, decreased oxidative phosphorylation, and increased unhealthy mitochondria. These discoveries provide insight into mechanisms governing oocyte quality and a regulatory role of NEDDylation for mitochondrial transcription in gametes.

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NEDDylation modifies mitochondrial transcription to maintain oocyte quality (Ovary)

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NEDDylation modifies mitochondrial transcription to maintain oocyte quality (Oocyte)

Project description:NEDDylation modifies mitochondrial transcription to maintain oocyte quality (Oocyte)

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NEDDylation modifies mitochondrial transcription to maintain oocyte quality

Project description:NEDDylation modifies mitochondrial transcription to maintain oocyte quality

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NEDDylation modifies mitochondrial transcription to maintain oocyte quality (Ovary)

Project description:NEDDylation modifies mitochondrial transcription to maintain oocyte quality (Ovary)

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NEDDylation maintains oocyte quality by stabilizing mitochondrial transcription

Project description: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.

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