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Updated: May 1, 2026

Cell-Specific Paired Interrogation of the Mouse Ovarian Epigenome and Transcriptome
Published on: February 24, 2023
Maternal age effect on mouse oocytes: new biological insight from proteomic analysis
Caroline Schwarzer1, Marcin Siatkowski2, Martin J Pfeiffer1
1Max Planck Institute for Molecular BiomedicineRöntgenstraße 20, D-48149 Münster, GermanyDZNEGerman Centre for Neurodegenerative Disorders, Gehlsheimer Straße 20, D-18147 Rostock, GermanyInstitute for Biostatistics and Informatics in Medicine and Ageing ResearchRostock University Medical Center, Ernst Heydemann-Str. 8, D-18057 Rostock, GermanyArrows Biomedical GmbHGievenbecker Weg 11, D-48149 Münster, GermanyMax Planck Institute for Molecular BiomedicineBioanalytical Mass Spectrometry Facility, Röntgenstraße 20, D-48149 Münster, Germany.
Abstract:
The long-standing view of 'immortal germline vs mortal soma' poses a fundamental question in biology concerning how oocytes age in molecular terms. A mainstream hypothesis is that maternal ageing of oocytes has its roots in gene transcription. Investigating the proteins resulting from mRNA translation would reveal how far the levels of functionally available proteins correlate with mRNAs and would offer novel insights into the changes oocytes undergo during maternal ageing. Gene ontology (GO) semantic analysis revealed a high similarity of the detected proteome (2324 proteins) to the transcriptome (22 334 mRNAs), although not all proteins had a cognate mRNA. Concerning their dynamics, fourfold changes of abundance were more frequent in the proteome (3%) than the transcriptome (0.05%), with no correlation. Whereas proteins associated with the nucleus (e.g. structural maintenance of chromosomes and spindle-assembly checkpoints) were largely represented among those that change in oocytes during maternal ageing; proteins associated with oxidative stress/damage (e.g. superoxide dismutase) were infrequent. These quantitative alterations are either impoverishing or enriching. Using GO analysis, these alterations do not relate in any simple way to the classic signature of ageing known from somatic tissues. Given the lack of correlation, we conclude that proteome analysis of mouse oocytes may not be surrogated with transcriptome analysis. Furthermore, we conclude that the classic features of ageing may not be transposed from somatic tissues to oocytes in a one-to-one fashion. Overall, there is more to the maternal ageing of oocytes than mere cellular deterioration exemplified by the notorious increase of meiotic aneuploidy.
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