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Mitochondrial DNA quantity Counteracts ROS damage in oocytes during female reproductive aging

GSE251734 Mus musculus Expression profiling by high throughput sequencing 8 samples Submitted 2024/09/09 Platform GPL30215
Summary
We investigated the contentious role of mitochondrial reactive oxygen species (ROS) on mitochondrial DNA (mtDNA) quality and quantity in female reproductive aging. By conditionally knocking out the Sod2 gene in female mouse germline, we observed increased mitochondrial ROS and decreased oocyte quality, primarily due to impacts on OXPHOS complex II and mtDNA encoded mRNA levels. Interestingly, we found no increased mtDNA mutations, but alterations in mtDNA quantity, indicating the susceptibility of mtDNA to the mitochondrial ROS during reproductive aging. Notably, when we further decreased the basal level of mtDNA quantity by deactivating the mtSSB protein in Sod2 conditional knockout females, we observed an exacerbation of reproductive aging effects. This highlights the crucial role of mtDNA quantity in mitigating the impact of oxidative stress on fertility.
Published in
Maintaining mitochondrial DNA copy number mitigates ROS-induced oocyte decline and female reproductive aging
Long S, Zheng Y, Deng X et al. · Communications biology 2024 · PMID 39354016 · doi:10.1038/s42003-024-06888-x
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Also filed as BioProject PRJNA1055145 and SRA study SRP479323. Searching any of these in the dataset finder brings you back here.

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