bims-cebooc Biomed News
on Cell biology of oocytes
Issue of 2026–09–27
nine papers selected by
Gabriele Zaffagnini, Universität zu Köln
  1. A somatic checkpoint through NHR-49/HNF4α governs reproductive investment and longevity in C. elegans.
  2. Direct cell-to-cell transmission of retrotransposons.
  3. MATR3 is essential for oocyte growth and maturation quality through a dual molecular mechanism.
  4. NEMP1 organizes the meiotic telomere LINC interface to control chromosome movement and telomere integrity.
  5. Ovarian fibrosis as a common mechanism of infertility.
  6. Metabolic regulation of oocyte maturation and early embryo development in mammals.
  7. Cytokinesis genes regulate ring canal patterning and follicle cell differentiation in Drosophila.
  8. Divergent microtubule-organizing center strategies in mammalian gametogenesis.
  9. Maternal Huluwa regulates postfertilization microtubule array organization for asymmetrical transport of dorsal determinants in zebrafish.
  1. Nat Commun. 2026 Aug 22. pii: 10046. [Epub ahead of print]17(1):
    A somatic checkpoint through NHR-49/HNF4α governs reproductive investment and longevity in C. elegans.
    Sharada Gopal, Amaresh Chaturbedi, Tej Ramachandrula, John OuYang, Rebecca Rodell, Siu Sylvia Lee.
      The nuclear hormone receptor NHR-49, a homolog of mammalian PPARα and HNF4α, is a key transcriptional regulator of nutrition sensing and fatty acid metabolism in Caenorhabditis elegans. Here, we examine the role of NHR-49 in reproduction, including oocyte activation and ovulation. Loss of NHR-49 causes inappropriate oocyte activation and laying of unfertilized oocytes in the absence of sperm, resulting in rapid loss of yolk and stored fat, and drastic shortening of lifespan. Conversely, prevention of yolk transfer into the oocytes largely restores fat storage and partially rescues lifespan in the nhr-49 mutants. Additionally, NHR-49 couples germline proliferation to nutritional status, as evidenced by its requirement for pausing germline proliferation upon starvation. Interestingly, NHR-49 primarily acts in somatic cells, rather than the germline itself, to regulate oocyte activation and ovulation. Combined genomic analyses identify GSA-1, a G protein alpha s subunit (Gαs), as a direct transcriptional target of NHR-49 highlighting a mechanistic link between metabolic sensing, fertility and longevity maintenance.
    DOI:  https://doi.org/10.1038/s41467-026-77056-4
  2. Cell. 2026 Sep 23. pii: S0092-8674(26)01020-2. [Epub ahead of print]
    Direct cell-to-cell transmission of retrotransposons.
    Maya Voichek, Andreas Bernhard, Lea Lauterjung, Maria Novatchkova, Dominik Handler, Paul Möseneder, Liudmila Protsenko, Baptiste Rafanel, Svetlana Iarovenko, Peter Duchek, Kirsten-André Senti, Julius Brennecke.
      Transposable elements are abundant in host genomes but are generally considered to be confined to the cell in which they are expressed, with the notable exception of endogenous retroviruses. Here, we identify a group of long terminal repeat (LTR) retrotransposons that infect the germline from somatic cells within the Drosophila ovary, despite lacking the fusogenic Envelope protein typically required for retroviral entry. Instead, these elements encode a short transmembrane protein, sORF2, which bears structural features reminiscent of viral cell-cell fusogens. Through genetics, imaging, and electron microscopy, we show that sORF2 localizes to invasive somatic protrusions that contain retroviral capsids and establish physical contact with the oocyte membrane. In the absence of sORF2, protrusion formation and soma-to-germline transmission of capsids are abolished. Remarkably, sORF2-like proteins are widespread among insect retrotransposons and also occur in piscine nackednaviruses and avian picornaviruses. These findings reveal a noncanonical, Envelope-independent transmission mechanism shared by retrotransposons and non-enveloped viruses.
    Keywords:  Drosophila; FAST proteins; LTR retrotransposons; VLPs; cell-cell fusion; invasive protrusions; non-enveloped viruses; oogenesis; transposable elements
    DOI:  https://doi.org/10.1016/j.cell.2026.08.047
  3. Elife. 2026 Sep 21. pii: RP110703. [Epub ahead of print]15
    MATR3 is essential for oocyte growth and maturation quality through a dual molecular mechanism.
    Yibing Bao, Zhenzi Zuo, Tengteng Wang, Lin Lin, Meng Gao, Shaogang Qin, Qingfeng Yang, Bingying Liu, Wanyuan Sun, Jie Ma, Tianhua Zhu, Guoliang Xia, Bo Zhou, Rong Hu, Hua Zhang, Fengchao Wang, Chao Wang.
      The molecular mechanisms governing mRNA accumulation during oocyte growth, essential for developmental competence, remain poorly understood. This study investigates the role of Matrin-3 (MATR3), a highly expressed RNA-binding protein in growing oocytes (GOs), using oocyte-specific knockout mouse models and human oocyte maturation arrest (OMA) samples. The results showed that MATR3 was more abundant in GOs than fully grown oocytes (FGOs), highly expressed in the nucleus of non-surrounded nucleolus (NSN) oocytes, and exited the nucleus during the NSN-to-surrounded nucleolus (SN) transition. In OMA patients, MATR3 nuclear localization was missed, with smaller oocytes than FGOs. Further, Matr3 deletion in mouse GOs caused restricted oocyte growth, global transcription disorders, follicle development failure, blocked GO-granulosa cell communication (via reduced Gdf9 and Rdx expression), and infertility. Mechanistically, MATR3 regulated transcription by recruiting H3K9me2-demethylating lysine-specific demethylase 3B or binding target gene promoters, like Rdx. These findings reveal a critical role of MATR3 in orchestrating transcription and paracrine signaling during oogenesis and suggest its potential as a diagnostic and therapeutic target for OMA.
    Keywords:  Matrin-3; developmental biology; epigenetic modification; fertility; follicle development; growing oocyte; mouse
    DOI:  https://doi.org/10.7554/eLife.110703
  4. bioRxiv. 2026 Sep 18. pii: 2026.09.17.752236. [Epub ahead of print]
    NEMP1 organizes the meiotic telomere LINC interface to control chromosome movement and telomere integrity.
    Hui Zhang, Ling Zhang, Stephanie Pangas, Andrea Jurisicova, Helen McNeill.
      Nuclear Envelope Membrane Protein 1 (NEMP1) is highly expressed in oocytes and required for fertility, yet its meiotic function remains poorly understood. Here, we identify NEMP1 as a critical organizer of meiotic telomere-nuclear envelope coupling and chromosome dynamics. Loss of NEMP1 causes telomere aggregation, loss of shelterin protection, telomere shortening, persistent DNA damage, aberrant non-homologous end joining, and chromosome end-to-end fusion, ultimately leading to aneuploidy in mouse oocyte. NEMP1 is required during early fetal meiotic prophase I for telomere-nuclear envelope attachment, bouquet formation, homolog pairing, and synapsis. Live cell imaging revealed robust rapid prophase movements in wild-type meiocytes, which were nearly abolished by NEMP1 loss and restored by NEMP1-GFP re-expression. Mechanistically, NEMP1 associates with telomeric DNA and the SUN1-KASH5 LINC machinery, and SUN1-GFP restores chromosome movement in Nemp1-deficient meiocytes. Together, these findings establish NEMP1 as a nuclear-envelope organizer linking telomere protection, chromosome dynamics, and genome integrity during mammalian oogenesis.
    DOI:  https://doi.org/10.64898/2026.09.17.752236
  5. Biol Reprod. 2026 Sep 24. pii: ioag214. [Epub ahead of print]
    Ovarian fibrosis as a common mechanism of infertility.
    Caroline J Aitken, David A Landry.
      Female fertility has long been explained through observation of the ovarian follicle: the number of residing follicles and the quality of the oocyte. This review argues that the tissue surrounding those follicles involved in regulating cyclical ovarian remodelling is an additional contributor to female subfertility. Ovarian fibrosis, the accumulation of extracellular matrix with stromal stiffening and inflammation, was historically viewed as a passive consequence of aging or injury. Here, we present evidence that this phenomenon may be an active constraint on fertility, altering the biomechanical environment that manages follicle activation, ovulation, and oocyte quality. Although reproductive aging, premature ovarian insufficiency, polyendocrine metabolic ovarian syndrome, obesity, endometriosis, chronic psychological stress, and treatment/environment-induced ovarian injury have different underlying causes, all reach a similar fibrotic state. Strong causal evidence comes from in vitro hydrogel studies isolating stiffness from all other variables, where stiff matrices inhibit follicle growth, survival and quality. Despite this highly fibrotic morphology impacting maturation of follicles, pre-clinical and human studies have shown the efficacy of antifibrotic drugs in restoring follicular growth. Further, in early human trials, antifibrotic finerenone yields mature oocytes and embryos in women with premature ovarian insufficiency. While the current focus in standard infertility treatment aims to improve follicle and hormone health, fibrosis may be reversible and preventable, making it a candidate therapeutic target that could complement existing treatments. However, key gaps remain: no standardized measure of ovarian fibrosis, uncertain rodent-to-human translation, and no study linking fibrosis measurement to a fertility outcome in human patients.
    Keywords:  Antifibrotic treatments; Extracellular Matrix; Female Infertility; Mechanobiology; Ovarian Aging; Ovarian Fibrosis; Ovarian Stroma; Polyendocrine metabolic ovarian syndrome; Tissue Stiffness; premature ovarian insufficiency
    DOI:  https://doi.org/10.1093/biolre/ioag214
  6. Life Metab. 2026 Dec;5(6): loag024
    Metabolic regulation of oocyte maturation and early embryo development in mammals.
    Sifan Rong, Yixuan Fu, Yan Li, Yingxin Celia Jiang, Lanruo Chen, Yue Zhao, Wencheng Zhu, Liangshan Mu.
      Metabolism plays a central role in coordinating mammalian oocyte maturation and early embryonic development. The metabolic changes that occur during these stages are essential for the acquisition of developmental competence and successful reproduction. This review summarizes metabolic regulation from oocyte growth and maturation through fertilization and preimplantation development, with particular emphasis on glucose, lipid, and amino acid metabolism, as well as mitochondrial function. We also discuss how metabolic disturbances associated with maternal obesity, ovarian aging, and polyendocrine metabolic ovarian syndrome (formerly termed polycystic ovary syndrome) impair oocyte quality and embryonic developmental potential. By integrating recent insights from multi-omics, live-cell imaging, and genetic studies, we propose a framework for understanding how metabolism not only supports but also actively governs developmental decisions. We further discuss mechanism-based strategies to restore metabolic balance and improve reproductive outcomes.
    Keywords:  embryo metabolism; metabolic regulation; oocyte metabolism
    DOI:  https://doi.org/10.1093/lifemeta/loag024
  7. bioRxiv. 2026 Sep 16. pii: 2026.09.10.750734. [Epub ahead of print]
    Cytokinesis genes regulate ring canal patterning and follicle cell differentiation in Drosophila.
    Cristy P Mendoza, Andreana Gomez, Michael Baumgartner, Todd G Nystul.
      Stable intercellular bridges that form through incomplete cytokinesis are present in a wide variety of cell types but their function in somatic cell differentiation is not well understood. Using super-resolution confocal microscopy, we identified a stepwise process of ring canal development in the follicle cells of the Drosophila ovary. Using a custom-trained deep learning model to aid in 3D image segmentation and follicle cell quantification, we found that ring canals are more heterogeneous at the early prefollicle stages compared to the more differentiated later stages. In addition, we found that depletion of the septin, peanut , caused cytokinetic defects but did not disrupt ring canal formation, whereas depletion of the ESCRT III gene, shrub , increased ring canal number in prefollicle cells and caused proliferation and differentiation phenotypes. Our findings identify cytokinesis and ring canal formation as a point of regulation in the patterning of proliferation and differentiation in the Drosophila follicle stem cell lineage.
    Summary: Somatic ring canals in the Drosophila ovary develop through a stepwise series of states and are a point of regulation of proliferation and differentiation toward a postmitotic cell fate called stalk cells.
    DOI:  https://doi.org/10.64898/2026.09.10.750734
  8. Trends Open. 2026 Sep;1(3): 305-322
    Divergent microtubule-organizing center strategies in mammalian gametogenesis.
    Marnie W Skinner, Philip W Jordan.
      Meiotic chromosome segregation relies on the spindle microtubules, which are assembled by microtubule-organizing centers (MTOCs). Mammalian gametogenesis reveals starkly divergent strategies between the sexes. Spermatocytes harbor canonical centrosomes that undergo biogenesis events unique to the meiotic cycle. However, recent findings reviewed here show that these centrosomes are dispensable for chromosome segregation and that a noncentrosomal MTOC pathway can accomplish this segregation. By contrast, oocytes eliminate centrioles and assemble microtubule spindles by coalescing pericentriolar material components to form bipolar MTOCs, a process assisted by a chromosome-driven spindle assembly pathway. This review discusses the species-specific differences in MTOC regulation between mouse and human oocytes and examines how defects in these MTOC pathways are a primary cause of aneuploidy and infertility.
    DOI:  https://doi.org/10.1016/j.treopn.2025.12.002
  9. Nat Commun. 2026 Aug 24. pii: 10114. [Epub ahead of print]17(1):
    Maternal Huluwa regulates postfertilization microtubule array organization for asymmetrical transport of dorsal determinants in zebrafish.
    Xin Liu, Fangjie Cao, Yaqi Li, Tursunjan Aziz, Tong Lv, Jing Chen, Xiaotong Wu, Anming Meng.
      The dorsal organizer, essential for vertebrate embryonic axis formation, is induced by microtubule-mediated transport of maternal determinants. Maternal Huluwa (Hwa) has been identified as an essential organizer inducer in zebrafish and frogs, functioning at midblastula stages to activate β-catenin signaling in the preorganizer. It remains unknown if maternal Hwa functions at or before fertilization. Here, we report that maternal Hwa protein is critical for organizing the vegetal parallel microtubule array immediately after fertilization in zebrafish. Hwa protein and mRNA are enriched at the vegetal pole and facilitate microtubule network formation, enabling asymmetrical transport of dorsal determinants. Loss of maternal Hwa disrupts this microtubule architecture and abrogates mRNA transport, revealing a self-reinforcing mechanism where Hwa regulates its own asymmetrical distribution. Hwa may regulate the vegetal microtubule network through other signaling pathways and microtubule-associated proteins. Our findings establish a dual-phase model of dorsal specification: Hwa initially governs symmetry breaking through postfertilization microtubule organization and later on activates β-catenin signaling at blastula stages. This work provides fundamental insights into how the key maternal factor regulates the organizer and body axis formation at different developmental stages.
    DOI:  https://doi.org/10.1038/s41467-026-77005-1
This page is being maintained by Thomas Krichel. It was last updated on 2026‒09‒27 at 6:30.