bims-cebooc Biomed News
on Cell biology of oocytes
Issue of 2026–05–31
eighteen papers selected by
Gabriele Zaffagnini, Universität zu Köln
  1. A cohesion optimum underlies chromosome segregation fidelity in oocytes.
  2. The SPARK complex forms the molecular basis of vertebrate fertilization.
  3. PIWIL3-piRNA pathway controls rabbit oogenesis and embryogenesis via broad regulation of the transcriptome and proteome.
  4. R-loop homeostasis at transposable elements safeguards transcriptional silencing in replication-quiescent oocytes.
  5. Reciprocal constraint couples architectural protein abundance and pericentromeric satellite expansion.
  6. Functional consequences of centromeric satellite array asymmetry in female meiosis.
  7. Dynamic regulation of H3K9 dimethylation drives mouse minor zygotic genome activation.
  8. Single-nucleus profiling reveals age-associated remodeling opposed by parity in the postmenopausal human ovary.
  9. Camsap3-mediated microtubules maintain transzonal projections essential for soma-germ communication during ovarian follicle maturation in mice.
  10. The Cappuccino interactome reveals an intracellular role for Semaphorin-2a in Drosophila oogenesis.
  11. Analysis of a hypomorphic mei-P26 mutation reveals coordination between developmental programming of germ cells and meiotic chromosome dynamics.
  12. Disordered protein COSA-2 maintains crossover-specific repair compartments to ensure meiotic crossover maturation.
  13. Selective cellular localization of UHRF1 safeguards mammalian zygotic genome activation and early embryonic development.
  14. Reorganization of E-cadherin into apical spot junctions mediates interlineage adhesion between epithelial and germline cells.
  15. Endometriosis disrupts oocyte metabolism and cortical granule function, impairing fertilization.
  16. From germline immortality to somatic rejuvenation: Unlocking the ovarian blueprint for longevity.
  17. Nests in an egg cell: structures of protein-storage units in oocytes.
  18. Organ formation in early human embryos captured in spatial cell atlas.
  1. bioRxiv. 2026 May 11. pii: 2026.05.08.723885. [Epub ahead of print]
    A cohesion optimum underlies chromosome segregation fidelity in oocytes.
    Yan Yun, Kanako Ikami, Duy Do, Ziyang Guo, Jiyeon Leem, Hilina Bekele, Binyam Mogessie, Neil Hunter.
      Chromosome segregation is compromised in eggs from women of both early and advanced reproductive ages. Deteriorating cohesion causes premature separation of sister-chromatids in eggs from older females. We show that the converse is true for oocytes of adolescents, with excessive cohesion impeding segregation. Oocytes from juvenile mice show severe chromosome lagging in anaphase I, leading to nondisjunction or, in extreme cases, failure of the first meiotic division. These defects are suppressed by experimentally weakening cohesion or enhancing its resolution during anaphase I. By contrast, lagging and nondisjunction are rare in the oocytes of young adults because cohesion is inherently weaker. Thus, relative cohesion strength underlies both the frequency and type of segregation errors observed in eggs throughout the female reproductive lifespan.
    One-Sentence Summary: In eggs, errors in chromosome segregation arise from age-dependent imbalances in how tightly chromosomes are held together.
    DOI:  https://doi.org/10.64898/2026.05.08.723885
  2. bioRxiv. 2026 May 15. pii: 2026.05.13.724128. [Epub ahead of print]
    The SPARK complex forms the molecular basis of vertebrate fertilization.
    Victoria E Deneke, Johannes P Suwita, Haoting Wang, Shingo Tonai, Yonggang Lu, Karin Panser, Alexander Schleiffer, Jeremy A Hollis, Maria Novatchkova, Gerhard Dürnberger, Karel Stejskal, Gabriela Krssakova, Andreas Blaha, Aleq Adrianne R Andresan, Muriel Mirus, Hana Marvanova, Hsin-Yi Chang, Taichi Noda, Alejandro Burga, Elisabeth Roitinger, Masahito Ikawa, An-Drea Pauli.
      Fertilization requires gamete recognition and membrane fusion, yet the molecular basis of this process in vertebrates remains unknown. Here we identify SPARK (sperm protein assembly and receptor-binding key), a conserved multi-protein complex that integrates all known sperm fertilization factors, including TMEM81-IZUMO1-SPACA6 and DCST1/2, together with two newly identified components, TMDD1 and FAM187A. SPARK subunits are mutually dependent for stability in mature sperm, and disruption of any single component causes male sterility in zebrafish and mice. Incubating zebrafish sperm with soluble egg receptor Bouncer partially rescues fertilization of Bouncer-deficient eggs in a SPARK-dependent manner, consistent with egg receptor binding priming the complex for fusion. Thus, we propose SPARK as a con-served molecular machine that couples gamete recognition to membrane fusion.
    DOI:  https://doi.org/10.64898/2026.05.13.724128
  3. Nat Commun. 2026 May 26.
    PIWIL3-piRNA pathway controls rabbit oogenesis and embryogenesis via broad regulation of the transcriptome and proteome.
    Yuanyuan Gong, Shuo Shi, Ling Li, Yuqiang Qian, Ting Lu, Zhaoran Zhang, Lichun Jiang, Guohui Liu, Meihua Cui, Shangang Li, Zhanjun Li, Haifan Lin.
      Female infertility often arises from oogenic defects, yet the underlying molecular mechanisms remain elusive. The Piwi-piRNA pathway is crucial for gametogenesis, but its role in mammalian female fertility remains unclear, partly due to reliance on mouse models lacking PIWIL3. PIWIL3 exits in most other placental mammals and is highly expressed in human oocytes, but its function remains largely unexplored. Here, we show that rabbit PIWIL3 closely resembles its human counterpart and is the predominant PIWI protein in oocytes. Using CRISPR-Cas9 knockout, we demonstrate that PIWIL3 is essential for female fertility in rabbits, its loss leads to severe defects in oogenesis. Embryos lacking maternal PIWIL3 arrest by the 8-cell stage. Mechanistically, PIWIL3 binds ~18-nucleotide piRNAs, supports piRNA biogenesis, and regulates transcriptomic, proteomic, and transposable element dynamics during oocyte maturation and early embryogenesis. These findings establish PIWIL3 as an essential regulator of female fertility in non-rodent mammals, potentially including humans.
    DOI:  https://doi.org/10.1038/s41467-026-73503-4
  4. Nat Commun. 2026 May 29.
    R-loop homeostasis at transposable elements safeguards transcriptional silencing in replication-quiescent oocytes.
    Shao-Yuan Liu, Xin-Yi Tian, Hong-Fen Fu, Yong Zhou, Yi-Sha Cai, Jun Wen, Ze-Lin Wang, Yun-Wen Wu, Qiong-Wen Lu, Xiu-Quan Liao, Qian-Qian Sha.
      R-loops, though implicated in genome stability, have poorly defined transcriptional roles due to confounding replication processes in proliferating cells. Here, by leveraging replication-free oocytes and RTACC-seq, a tailored high-specificity R-loop mapping approach for low-input samples, we identify dynamic R-loop enrichment at both gene promoters and distal transposable elements. We find that transposable element-associated R-loops accumulate in transcriptionally active stage oocytes and resolve in fully grown oocytes, coinciding with chromatin condensation and transcriptional silencing. R-loops exert opposing, location-dependent regulatory functions, with reduced transcription rate at promoters and enhanced rates at transposable elements, raising the possibility of enhancer-like activity at a subset of hybrid-associated transposable element loci. In mice, oocyte-specific deletion of Rnaseh1, a gene that encodes an RNA:DNA hybrid-specific endonuclease, leads to persistent R-loops, chromatin decondensation, and impaired transcriptional silencing in fully grown oocytes, culminating in premature ovarian failure and female subfertility. These findings characterize the mechanistic basis of R-loops as mediators of chromatin remodeling, transcriptional regulation, and germ cell developmental competence.
    DOI:  https://doi.org/10.1038/s41467-026-73781-y
  5. bioRxiv. 2026 May 17. pii: 2026.05.15.725447. [Epub ahead of print]
    Reciprocal constraint couples architectural protein abundance and pericentromeric satellite expansion.
    Damian Dudka, Keagan Beeravolu, Michael A Lampson.
      Long-read sequencing has enabled precise measurements of highly repetitive centromeric satellites and their rapid divergence between species 1-7 . Large satellite arrays emerge from libraries of shorter arrays via stochastic expansions 8,9 , but understanding the selective pressures constraining such expansions remains a major challenge. Here, using the mouse "major" satellite as a model, we reveal reciprocal functional constraints between increasing satellite copy number and abundance of a conserved architectural protein in female meiosis. We show that HMGA2 (high mobility group AT-hook 2) is enriched at major satellite, and its expression correlates with major satellite copy number: both are high in Mus musculus compared to the closely related Mus spretus . To test functional constraints, we modulated HMGA2 abundance by depletion or overexpression and used a musculus / spretus hybrid to generate oocytes with intermediate HMGA2 expression and major satellite copy number. We find that HMGA2 depletion disrupts major satellite packaging in major satellite-rich musculus but not hybrid oocytes, indicating that increasing copy number requires high HMGA2 expression. Conversely, HMGA2 overexpression disrupts chromosome segregation in major satellite-poor spretus but not hybrid oocytes, indicating that high HMGA2 expression requires expanded major satellite arrays. Based on these results, we propose a co-evolution model in which satellite expansion is constrained by architectural protein abundance, whereas protein abundance is constrained reciprocally by satellite array size.
    DOI:  https://doi.org/10.64898/2026.05.15.725447
  6. bioRxiv. 2026 May 17. pii: 2026.05.15.725525. [Epub ahead of print]
    Functional consequences of centromeric satellite array asymmetry in female meiosis.
    Jun Ma, Deepanshu Kumar, Advait Thaploo, Liya Ma, Michael A Lampson.
      Centromeres are epigenetically specified chromosomal sites that support kinetochore assembly and often embedded within large satellite DNA arrays. Recent telomere to telomere genome assemblies have revealed extensive variation in centromeric satellite arrays between chromosomes and between individuals, but the functional significance of this variation remains unclear. To determine how satellite array size influences centromere function, we generated hybrid mouse models in which homologous chromosomes with different array sizes are paired in meiosis I, creating array size asymmetry across each meiotic bivalent. When an extremely small array is paired with a moderate size array, we find that array size asymmetry leads to functional asymmetry in both centromere chromatin and interactions with spindle microtubules, lagging chromosomes in anaphase I, and increased aneuploidy in MII eggs. In contrast, pairing an extremely large array with a moderate array does not lead to functional centromere asymmetry. Together, these results suggest a threshold model in which centromere array size is tolerated across a broad range, but minimal arrays become functionally limiting when paired with larger arrays in meiosis.
    DOI:  https://doi.org/10.64898/2026.05.15.725525
  7. Nat Struct Mol Biol. 2026 May 26.
    Dynamic regulation of H3K9 dimethylation drives mouse minor zygotic genome activation.
    Ryo Maeda, Shunsuke Kuroki, Hiromi Shimojo, Masahiro Nagano, Masahiro Matsuwaka, Hiroshi Sasaki, Azusa Inoue, Makoto Tachibana.
      Minor zygotic genome activation (ZGA) is crucial for early development and totipotency acquisition; however, the regulatory mechanisms controlling minor ZGA gene expression remain elusive. Here, we show that mouse minor ZGA is driven by spatiotemporally dynamic regulation of H3K9 dimethylation (H3K9me2). H3K9me2 levels at the minor ZGA gene loci are reduced at the early two-cell stage and are reestablished by the morula stage. Maternal depletion of the H3K9 demethylases KDM3A and KDM3B leads to increased H3K9me2 levels and impaired minor ZGA at the early two-cell, followed by arrest at the two-cell to four-cell stage. In mouse embryonic stem cells, H3K9 at the minor ZGA loci is dimethylated. Combined loss of the H3K9 methyltransferases G9a and SETDB1 results in the synergistic derepression of minor ZGA genes. Mechanistically, SETDB1 targets the transcriptional factor Dux, while G9a broadly represses minor ZGA genes through H3K9me2 deposition linked to lamina-associated heterochromatin formation. Therefore, H3K9me2 dynamics are unveiled as an important regulator of minor ZGA, highlighting the indispensable role of epigenetic control in early embryogenesis.
    DOI:  https://doi.org/10.1038/s41594-026-01811-w
  8. bioRxiv. 2026 May 14. pii: 2026.05.11.724381. [Epub ahead of print]
    Single-nucleus profiling reveals age-associated remodeling opposed by parity in the postmenopausal human ovary.
    Josef Byrne, Nicolas Martin, Bikem Soygur, Mark A Watson, Kevin Schneider, Birgit Schilling, Simon Melov.
      The postmenopausal ovary is commonly viewed as a passive organ, and its biology and cell composition remain incompletely characterized. Here, we generated a single-nucleus atlas of the aging postmenopausal human ovary comprising 439,011 nuclei across 64 ovarian samples from 28 donors. We resolved 37 fine cell states, revealing extensive stromal, vascular, and immune heterogeneity in the postmenopausal ovary. Aging was associated with stromal stress-state expansion, vascular and immune depletion, and enrichment of steroidogenic programs consistent with ovarian androgenization. Several major age-associated compositional shifts were supported in an independent GTEx ovary bulk RNA-seq cohort. Notably, the number of live births broadly opposed age-associated transcriptional and compositional remodeling. Together, our findings show that the postmenopausal ovary remains an actively remodeled aging tissue and that reproductive history leaves durable molecular and cellular imprints on ovarian aging.
    DOI:  https://doi.org/10.64898/2026.05.11.724381
  9. iScience. 2026 Jun 19. 29(6): 115911
    Camsap3-mediated microtubules maintain transzonal projections essential for soma-germ communication during ovarian follicle maturation in mice.
    Akihiro Aikawa, Takao Tsurumaki, Erina Kuranaga, Junya Ito, Mika Toya, Masamitsu Sato.
      Oocytes are surrounded by layers of maternal somatic granulosa cells (GCs) in ovarian follicles. GCs extend actin-containing transzonal projections (TZPs) to oocytes across the zona pellucida to establish communication. Microtubules have rarely been observed in TZPs, and their significance in TZP organization and follicular maturation remains unknown. Here, using super-resolution microscopy, we visualized microtubules alongside F-actin in most TZPs. Knockout (KO) mice of the microtubule minus-end binding protein Camsap3 (calmodulin-regulated spectrin-associated protein 3) exhibited infertility without ovulation despite normal estrous cycles. Ovaries of Camsap3-KO mice contained fewer developing follicles, particularly of antral and Graafian stages. In earlier stages of Camsap3-KO follicles, TZP numbers were reduced compared to wild-type follicles, and microtubules in TZPs were disorganized, leading to decreased contact between GCs and oocytes. TZP morphology in wild-type transforms during follicle development, and Camsap3-mediated microtubules govern the number and morphology of TZPs, contributing to successful follicle development for fertile oocyte production.
    Keywords:  cell biology; reproductive medicine
    DOI:  https://doi.org/10.1016/j.isci.2026.115911
  10. bioRxiv. 2026 May 13. pii: 2026.05.11.724452. [Epub ahead of print]
    The Cappuccino interactome reveals an intracellular role for Semaphorin-2a in Drosophila oogenesis.
    Carolyn Wu, Sudeepa Rajan, Merin Rixen, James Wohlschlegel, Margot E Quinlan.
      The spatiotemporal regulation of an actin mesh during Drosophila oogenesis is essential for proper localization of cell polarity determinants that establish the future patterning of the embryo. Here, we reveal an unexpected role for Semaphorin-2a (Sema2a) in actin mesh regulation and oogenesis. Sema2a classically functions as a secreted guidance cue that binds its cognate Plexin-B (PlexB) receptor to establish neural circuits. In contrast, we find that Sema2a is expressed inside the germarium, germline, and follicle cells of the developing ovary. Sema2a mutants possess small ovaries that fail to develop past mid-oogenesis. We demonstrate that Sema2a interacts with Cappuccino (Capu), a key actin nucleator crucial for building the actin mesh in Drosophila oocytes. Sema2a inhibits the actin assembly activity of Capu in vitro. Furthermore, genetic interaction between Sema2a and Capu influences mesh density and disrupts oskar mRNA localization. PlexB mutants, however, exhibit wild-type size ovaries with oskar mRNA localization distinct from Sema2a mutants, confirming the non-canonical role of Sema2a in oogenesis.
    DOI:  https://doi.org/10.64898/2026.05.11.724452
  11. bioRxiv. 2026 May 15. pii: 2024.11.22.624911. [Epub ahead of print]
    Analysis of a hypomorphic mei-P26 mutation reveals coordination between developmental programming of germ cells and meiotic chromosome dynamics.
    Joseph Terry, Ally Solomon, Amanda M Powell, Patrick Terry, Oscar Bautista, Marty Landes, Erica Berent, Elizabeth T Ables, Nicole Crown.
      Female gametogenesis in Drosophila requires differentiation and mitotic division of germ cells, acquisition of oocyte fate, and entry into meiosis. Each of these processes is well understood individually; however, little is known about the mechanisms that ensure proper temporal integration of germ cell differentiation and meiotic chromosome dynamics. Here, we take advantage of a hypomorphic mutation in mei-P26 , a well-characterized gene with multiple diverse functions in germ cell development, to determine the consequences of disrupting the coordination between development and meiosis. While null mutations in mei-P26 lead to tumorous ovaries, the hypomorphic allele mei-P26 1 allows sufficient germ cell differentiation and fertility to support analysis of meiotic chromosome dynamics. Unlike wildtype germaria, 60% of cysts in mei-P26 1 germaria co-express the differentiation factor Bag of marbles (Bam) and the oocyte specification factor Orb, suggesting that mitotic division is delayed. In this context, the synaptonemal complex rarely assembles into full length continuous tracks and instead is missing or present only as foci. Despite these phenotypes, meiotic double-strand breaks still form and are repaired as crossovers, but the crossovers are mis-patterned and form in centromere proximal regions rather than chromosome arms. The strength of crossover interference is significantly reduced and the centromere effect is lost, but crossover assurance is intact and the meiosis-specific machinery is used to form crossovers. We suggest a model where the failure to exit mitosis in a timely fashion causes cells to enter meiosis while still receiving mitotic signals, resulting in abnormal meiotic chromosome dynamics and impaired crossover formation.
    Article summary: Female gametogenesis in Drosophila requires the precise temporal integration of germ cell differentiation and meiotic entry. Using a hypomorphic mutation in mei-P26 , we investigated how disrupting this coordination affects meiotic chromosome dynamics. In mei-P26 1 mutants, delayed mitotic exit causes cells to enter meiosis while still receiving mitotic signals. This results in fragmented synaptonemal complex and the loss of some but not all CO patterning mechanisms. These results suggest that timely mitotic exit is critical for establishing the proper regulatory landscape required for meiotic recombination.
    DOI:  https://doi.org/10.1101/2024.11.22.624911
  12. bioRxiv. 2026 May 16. pii: 2026.05.13.725012. [Epub ahead of print]
    Disordered protein COSA-2 maintains crossover-specific repair compartments to ensure meiotic crossover maturation.
    Celja J Uebel, Dahlia Y Deng, Yumi Kim, Anne M Villeneuve.
      Faithful genome inheritance during meiosis relies on crossover repair of double-strand DNA breaks (DSBs) to connect homologous chromosomes and direct their proper segregation. The formation of crossover-specific recombination intermediates and accumulation of pro-crossover factors occurs at an extremely limited subset of DSB sites, necessitating that the subset of recombination sites designated to become crossovers reliably mature into crossovers. Here we identify C. elegans disordered protein COSA-2 as crucial for meiotic crossover maturation. COSA-2 abruptly concentrates at crossover intermediates in late pachytene nuclei, where it colocalizes and associates with other pro-crossover factors. COSA-2 is dispensable for early loading of crossover factors and for crossover designation, but is required for maintenance of pro-crossover factors at crossover-designated sites and for focal enrichment of factors initially distributed throughout the synaptonemal complex. We define a COSA-2 execution point during late pachytene wherein crossover intermediates transition from a vulnerable state (in which they require COSA-2 to avoid being dismantled) to a state where COSA-2 and local crossover-factor enrichment are no longer required to connect homologs. We propose that COSA-2 scaffolds privileged DNA repair compartments that promote crossover-factor accumulation and protect crossover intermediates until completion of repair, thereby ensuring that crossover-designated sites reliably mature into crossovers.
    DOI:  https://doi.org/10.64898/2026.05.13.725012
  13. Cell Discov. 2026 May 26. pii: 38. [Epub ahead of print]12(1):
    Selective cellular localization of UHRF1 safeguards mammalian zygotic genome activation and early embryonic development.
    Rui Yan, Xin Cheng, Xin Long, Yating Zhu, Qiancheng Zhang, Fengyuan Sun, Fan Zhang, Mengyue Wang, Ruifeng Zhang, Tianzi Guo, Xinling Hou, Dongmei Ji, Yunxia Cao, Fei Gao, Dan Liang, Fan Guo.
      Zygotic genome activation (ZGA) is essential for initiating the developmental gene expression program in early embryos. However, whether a gating mechanism orchestrated by a limited number of factors exists in mammals remains debated. In this study, by utilizing an Nlrp14-deficient model that intriguingly disrupts the zygotic localization of UHRF1 and DNMT1, and in combination with comprehensive genetic approaches, we demonstrated that the nuclear exclusion of UHRF1 is essential for mouse ZGA and subsequent developmental progression. Mechanistically, the failure to exclude UHRF1 and DNMT1 from the nucleus in zygotes would impede DNA demethylation in LINE1 elements, promote UHRF1 binding to silence their expression, thereby reducing global chromatin accessibility and inhibiting ZGA. This effect was rescued in Uhrf1/Nlrp14 double knockout (DKO) embryos, which still exhibited heavy DNA methylation, highlighting a dispensable role of UHRF1 in the maintenance of genome-wide DNA methylation after fertilization. Furthermore, reducing DNA methylation through Dnmt1/Nlrp14 DKO or inhibiting the DNA methylation-binding domains of UHRF1 mitigated the adverse effects of nuclear-localized UHRF1 and reactivated the ZGA genes. Finally, we demonstrated that the residual nuclear UHRF1 in normal embryos binds to and facilitates the transcriptional inactivation of specific LTR subtypes that evade DNA demethylation during the genome-wide epigenetic reprogramming. Our findings not only highlight the biological significance of UHRF1 and DNMT1 nuclear exclusion but also elucidate the potentially conserved mechanism that regulates ZGA during mammalian preimplantation development.
    DOI:  https://doi.org/10.1038/s41421-026-00896-3
  14. Front Cell Dev Biol. 2026 ;14 1807574
    Reorganization of E-cadherin into apical spot junctions mediates interlineage adhesion between epithelial and germline cells.
    Vanessa Weichselberger, Ramya Balaji, Marta Rodriguez-Franco, Anne-Kathrin Classen.
      During development, epithelia must coordinate morphogenesis with neighboring cell lineages to drive structural remodeling of organ systems. How adhesion between epithelial and other cell types is established and maintained remains poorly understood. Using the Drosophila ovary as an in vivo model, we show that anterior follicle cells (AFCs) undergo epithelial plasticity to establish and maintain adhesion with germline nurse cells during late oogenesis. As AFCs spread over the nurse-cell compartment, adherens junctions disassemble, and E-cadherin, together with junctional partners, reorganizes into apical "spot junctions." Formation of these junctions requires E-cadherin in both follicle and germline cells and is promoted by the expansion of the AFC apical surface. Quantitative imaging reveals that spot junctions form a uniformly spaced lattice that remains stable as the AFC-nurse cell interface enlarges. Functionally, these E-cadherin-based junctions are essential to maintain soma-germline adhesion, enabling full envelopment and clearance of nurse cell remnants by AFCs during late oogenesis. Our findings uncover a mechanism by which an epithelium repurposes its apical membrane into a specialized adhesive surface, providing a paradigm for the emergence of interlineage adhesion in developing tissues.
    Keywords:  Drosophila; E-cadherin; egg chamber development; follicle cell; nurse cell
    DOI:  https://doi.org/10.3389/fcell.2026.1807574
  15. Reprod Biol Endocrinol. 2026 May 25.
    Endometriosis disrupts oocyte metabolism and cortical granule function, impairing fertilization.
    Omar G Klinsky, Paula A Wetten, Julio E Romani, Emilia C Abraham, Marcela A Michaut.
       BACKGROUND: Endometriosis is a chronic inflammatory disease strongly associated with reduced oocyte quality and subfertility, yet the underlying cytoplasmic defects remain poorly understood.
    METHODS: Using a surgically induced autologous mouse model, we examined whether endometriosis alters oocyte metabolism, cortical granule (CG) biology, actin architecture, SNARE-regulated exocytosis, fertilization, and early embryonic activation.
    RESULTS: Endometriosis markedly increased intracellular reactive oxygen species and altered quinacrine-positive acidic vesicular compartments in ovulated oocytes. Although CG localization was preserved, endometriotic oocytes failed to undergo strontium chloride-induced CG exocytosis. These defects correlated with a significantly thickened cortical F-actin cytoskeleton and a substantial reduction in α-SNAP and NSF levels-two essential regulators of SNARE complex disassembly and membrane fusion. Functionally, endometriotic oocytes exhibited decreased fertilization rates without evidence of polyspermy, while their ability to undergo TPEN-induced parthenogenetic activation and second polar body extrusion remained unchanged.
    CONCLUSIONS: These findings demonstrate that endometriosis impairs multiple aspects of cytoplasmic maturation-metabolic homeostasis, actin remodeling, and CG exocytotic machinery-ultimately reducing sperm-oocyte fusion efficiency while preserving early embryonic activation capacity. This mechanistic insight provides a foundation for understanding how endometriosis compromises oocyte competence.
    Keywords:  Cortical granule exocytosis; Endometriosis; F-actin cytoskeleton; Fertilization competence; NSF; Oocyte metabolism; Oocyte quality; Oxidative stress; SNARE complex; α-SNAP
    DOI:  https://doi.org/10.1186/s12958-026-01571-8
  16. PLoS Biol. 2026 May;24(5): e3003804
    From germline immortality to somatic rejuvenation: Unlocking the ovarian blueprint for longevity.
    Priscila Chiavellini, Vittorio Sebastiano.
      Aging is typically framed as a one-way, irreversible accumulation of molecular damage in cells and tissues, leading to progressive functional decline. Yet mammalian reproduction, and particularly female reproduction, reveals a striking exception to this rule. Despite residing within an aging organism and within a fast-aging ovarian tissue environment, oocytes give rise to embryos that begin life with restored developmental potential and youthful molecular organization. By reframing ovarian biology as a model for rejuvenation rather than solely as a site of reproductive decline, this Essay proposes that the ovary offers a powerful blueprint for advancing the biology of aging and longevity.
    DOI:  https://doi.org/10.1371/journal.pbio.3003804
  17. Nature. 2026 May 27.
    Nests in an egg cell: structures of protein-storage units in oocytes.
    Matthias Geyer, Gregor Hagelueken.
      
    Keywords:  Cell biology; Microscopy; Structural biology
    DOI:  https://doi.org/10.1038/d41586-026-01414-x
  18. Nature. 2026 May 27.
    Organ formation in early human embryos captured in spatial cell atlas.
    Varun K A Sreenivasan, Malte Spielmann.
      
    Keywords:  Developmental biology; Transcriptomics
    DOI:  https://doi.org/10.1038/d41586-026-01416-9
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