ArticleFrontiers in cell and developmental biology2026
Blunted Lsm14b activation disrupts maternal mRNA remodeling during the GV-to-MII transition in a mouse model of polycystic ovary syndrome.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Polycystic ovary syndrome (PCOS) is the leading cause of anovulatory infertility and is consistently associated with poor oocyte developmental competence, yet the molecular basis of this qualitative defect remains poorly defined. Because the germinal vesicle (GV)-to-metaphase II (MII) transition occurs under global transcriptional silence and depends entirely on the post-transcriptional remodeling of pre-stored maternal mRNAs, we hypothesized that PCOS may selectively disrupt this regulatory program rather than impose a constitutive transcriptomic lesion. Methods: To test this, we established a DHEA-induced PCOS mouse model, validated by estrous acyclicity, hyperandrogenism, and polycystic ovarian morphology, and performed parallel Smart-seq2 profiling of oocytes at both the GV and MII stages. Integrated analyses combining differential expression, maturation trajectory modeling, weighted gene co-expression network analysis (WGCNA), and protein-protein interaction mapping, together with independent RT-qPCR validation of four hub transcripts, were used to dissect stage-specific transcriptomic dynamics. Results: Control and PCOS oocytes were largely similar at the single-gene level at the GV stage (35 differentially expressed genes), with subtle network-level perturbations detectable only by co-expression analysis, but diverged dramatically upon meiotic maturation (292 differentially expressed genes), with the majority of dynamic transcripts diverted into pathological trajectories. This maturation-coupled collapse manifested as a dual-layered post-transcriptional failure: aberrant retention of maternal mitochondrial OXPHOS transcripts ( Discussion: These findings reframe PCOS-associatedoocyte dysfunction as a stage-specific failure of post-transcriptional remodeling competence and identify the Lsm14b-P-body axis as a candidate molecular target for improving oocyte quality in assisted reproduction.
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