bims-cebooc Biomed News
on Cell biology of oocytes
Issue of 2026–03–22
fourteen papers selected by
Gabriele Zaffagnini, Universität zu Köln



  1. Nature. 2026 Mar 17.
      Mammalian oocytes are filled by fibric structure called cytoplasmic lattice (CPL), essential for oocyte maturation and early embryonic development1-3. CPL comprises subcortical maternal complex (SCMC) and multiple components, including PADI62,4,5. Despite its discovery in the 1960s, the molecular architecture and assembly mechanisms of CPL have remained poorly understood. Here we present the cryo-electron microscopy (cryo-EM) structure of the CPL isolated from mouse oocytes. Our analysis identified 14 constitutive protein subunits and revealed that CPL is composed of repeating "U-shaped basket" (UB) and "adapter ring" (AR)- featured units, forming a filamentous architecture. AR adopts a two-fold symmetric conformation, containing two NLRP4f, four SCMC and two ZBED3 subunits circularized via two distinct interaction clusters. The UB is anchored by PADI6, a didecamer composed of ten homodimers assembled by two back-to-back pentamers, each forming the lateral side of UB. The underfoot base and up-down sides of the UB are formed by multiple central-symmetric assemblies (UBE2D3-UHRF1-NLRP14) and (TUBB2B-TUBB2A-FBXW24-SKP1) respectively, associating with the PADI6 pentamers to construct the intact UB structure. Two SCMC dimer within each AR connect the up and down sides of two adjacent UBs with an extensive protein-protein interaction network and thus maintain the repetitive connection between the neighboring CPL units. Our work unveils the architectural principles underlying the assembly of this large, periodic CPL filament, offering a molecular basis for understanding CPL's functions in early mammalian embryogenesis and female reproductive disorders.
    DOI:  https://doi.org/10.1038/s41586-026-10360-7
  2. Nat Commun. 2026 Mar 18.
      Maternal obesity is known to cause systemic lipid dysregulation, yet its effect on lipid reprogramming during the maternal-to-zygotic transition (MZT) remains unknown. Here we show that obesity disrupts very-long-chain fatty acids (VLCFAs) storage in oocytes and downregulates PEX13, impairing peroxisomal protein import in 2-cell embryos. Normally, peroxisomal β-oxidation converts oocyte-stored VLCFAs into medium- and long-chain fatty acids, which fuel triglyceride synthesis and drive phosphatidylethanolamine (PE) methylation to phosphatidylcholine (PC). This metabolic flux consumes methyl donors to facilitate H3K4me3 erasure and zygotic genome activation (ZGA). In obese mice, VLCFAs deficiency and PEX13 dysfunction lead to metabolic-epigenetic uncoupling, depleting lipid droplets and sustaining H3K4me3, thereby suppressing ZGA and blastocyst development. Importantly, supplying long-chain fatty acids or overexpressing PEMT restore the phospholipid-methyl cycle, rescuing epigenetic reprogramming and embryonic development. Our findings establish peroxisomal β-oxidation as a metabolic-epigenetic nexus essential for MZT and reveal a phospholipid-methyl coupling mechanism underlying obesity-associated embry development, offering novel therapeutic entry points to improve fertility in metabolic disorders.
    DOI:  https://doi.org/10.1038/s41467-026-70492-2
  3. Curr Top Dev Biol. 2026 ;pii: S0070-2153(26)00015-3. [Epub ahead of print]166 121-133
      Faithful chromosome segregation emerges from the mutual cooperation of chromosomes and spindle microtubules. Textbook models of mitosis traditionally emphasize centrosome-driven spindle formation and chromosome capture. However, early mammalian development proceeds under constraints which are incompatible which a centrosome-driven model. Here, we briefly review the non-standard mechanisms of chromosome organization operating during early mouse development. We propose that these mechanisms, despite their differences, reflect a conserved set of organizational principles adapted to distinct developmental contexts.
    Keywords:  Actin; Cell division; Cytoskeleton; Meiosis; Microtubules; Mitosis
    DOI:  https://doi.org/10.1016/bs.ctdb.2026.01.015
  4. Proc Natl Acad Sci U S A. 2026 Mar 24. 123(12): e2532671123
      Meiotic prophase is characterized by a dynamic program in which germ cells undergo a complex series of associations and dissociations of protein complexes that drive assembly, remodeling, and disassembly of meiosis-specific chromosome structures and dramatic changes in chromosome compaction. Failure to properly coordinate these processes can result in improper chromosome segregation, producing aneuploid gametes and inviable zygotes. Here, we investigate the roles of Caenorhabditis elegans DUO-1, an ortholog of mammalian ubiquitin-specific proteases USP26 and USP29, in mediating these dynamic chromosomal events during meiotic prophase. Cytological analyses of duo-1 null mutants indicate that loss of DUO-1 function leads to impaired assembly of meiotic chromosome axes and synaptonemal complexes (SCs), loss of integrity of meiotic chromosome axes, ineffective homolog pairing, premature separation of sister chromatids, and late-prophase chromosome decompaction. Further, axis/SC instability in duo-1 mutants correlates with depletion of REC-8 cohesin complexes and is accompanied by massive accumulation of early DSB repair intermediates. By using a dual-AID-tagged allele to deplete DUO-1 during meiotic development, we demonstrate that DUO-1 is continually required throughout meiotic prophase progression, to promote proper axis/SC assembly in early prophase, to maintain axis/SC stability during the late pachytene stage, and to promote/maintain chromosome compaction at the end of meiotic prophase. Together, our data emphasize the importance of mechanisms that actively maintain meiotic chromosome structure and meiosis-specific chromosome architecture throughout meiotic prophase and implicate DUO-1 as a key player in these active maintenance processes.
    Keywords:  C. elegans; chromosome structure; meiosis; synaptonemal complex
    DOI:  https://doi.org/10.1073/pnas.2532671123
  5. Nat Commun. 2026 Mar 19.
      Mouse oocytes exhibit a unique chromatin landscape characterized by broad H3K27ac and H3K27me3 domains, demarcating euchromatin and facultative heterochromatin, respectively. However, the mechanisms underlying this non-canonical landscape remain elusive. Here we report BAP1, a core component of the Polycomb Repressive-Deubiquitinase (PR-DUB) complex, as a key negative regulator of Polycomb activity during oogenesis. BAP1 restricts pervasive H2AK119ub1 accumulation and protects oocyte-specific broad H3K27ac, particularly within gene-poor regions, from ectopic H3K27me3 deposition. While PR-DUB has been linked to gene repression, in oocytes BAP1 primarily promotes transcription and contributes minimally to Polycomb-mediated silencing. BAP1-dependent transcriptional activation during oogenesis is essential for oocyte developmental competence, maternal-to-zygotic transition, and female fertility. Notably, ectopic H3K27me3 domains established in BAP1-deficient oocytes persist in preimplantation embryos but are resolved after implantation, and loss of maternal BAP1 does not impair either canonical or non-canonical genomic imprinting. Together, these findings reveal a critical role for PR-DUB in safeguarding the oocyte epigenome by protecting euchromatin from ectopic Polycomb activity, rather than enforcing transcriptional repression.
    DOI:  https://doi.org/10.1038/s41467-026-70845-x
  6. Sci Adv. 2026 Mar 20. 12(12): eaec7919
      To produce healthy offspring, an organism must pass on its genetic material with high fidelity. In many species, this is accomplished by primordial germ cells (PGCs), which give rise to sperm or eggs. PGCs are often specified far from the future gonads and must migrate through developing tissues to reach them. Failure to do so can result in infertility or germ cell tumors. While PGC migration is well characterized in some species, very little is known about their migration in mammalian embryos. Here, we performed dynamic and quantitative analyses of PGC migration from E7.5 to E9.5 in the mouse embryo, providing the first comprehensive study of the migratory characteristics of PGCs from their point of origin to the gonads. We demonstrate that migrating PGCs are influenced by the surrounding environment and, in contrast to other organisms, extend highly dynamic, actin-rich protrusions to navigate through extracellular matrix (ECM) barriers, and tight intercellular spaces. As PGCs migrate through increasingly confined spaces, they undergo significant nuclear deformation and become prone to nuclear rupture and DNA damage. Their migration under confinement may be aided in part by a depleted nuclear lamina that leads to wrinkled nuclear morphology. Our high-resolution and dynamic imaging approaches have uncovered an unexpected risk to genome integrity in migrating PGCs, with implications for DNA repair and adaptations in nuclear mechanics in PGCs.
    DOI:  https://doi.org/10.1126/sciadv.aec7919
  7. Dev Biol. 2026 Mar 13. pii: S0012-1606(26)00063-1. [Epub ahead of print]
      Germ granules are ribonucleoprotein condensates that concentrate key maternal mRNAs needed for germ cell development. In Drosophila, nanos mRNA is selectively enriched in germ granules but the specific cis-acting elements mediating this process remain poorly defined. Here, we identify discrete sequence motifs in the nanos 3' UTR that regulate nanos enrichment specifically by promoting the growth of homotypic nanos mRNA clusters within granules, without affecting the initial targeting of nanos to germ granules. These sequence motifs are binding sites for the hnRNP M homolog Rumpelstiltskin (Rump) and mutation of Rump binding sites or Rump attenuates nanos homotypic cluster growth, reducing the amount of nanos inherited by germ cells. Consequently, germ cells exhibit defective migration to the gonad. Together, our findings reveal how small repeated sequence motifs and cognate RNA-binding proteins can tune enrichment of germ granule mRNAs by driving self-assembly into large RNA clusters. This strategy ensures sufficient inheritance of mRNAs to support germ cell development and may represent a general mechanism by which RNP condensates regulate transcript dosage.
    DOI:  https://doi.org/10.1016/j.ydbio.2026.03.007
  8. EMBO J. 2026 Mar 20.
      The activation of the embryonic genome is a crucial step in development. In addition to thousands of genes, many transposable elements (TEs) are robustly transcribed during early mammalian development. However, their transcriptional regulators remain largely unexplored. Here, we set out to identify transcription factors regulating the expression of TEs from the LINE, SINE and ERVL families during mouse preimplantation development. In particular, the MaLR family are the most abundant ERVL in the mouse genome and are also the most abundant constituent of the transcriptome in early mouse embryos. We find that the general transcription factor TBP binds and activates MaLRs in mouse embryos. Loss-of-function of TBP leads to downregulation of MaLRs, specifically the ORR1A family, which is the youngest ORR subclass and contributes a significant portion of major zygotic genome activation transcripts. Our work identifies regulators of TE expression in vivo and highlights a previously unrecognised role for the general transcription factor TBP in regulating a highly specific TE transcriptional programme.
    Keywords:  ERVL; MaLR; Mouse Embryos; Retrotransposons; TBP
    DOI:  https://doi.org/10.1038/s44318-026-00736-w
  9. Proc Natl Acad Sci U S A. 2026 Mar 24. 123(12): e2526998123
      Embryonic genome activation (EGA) marks the onset of the embryonic program and enables the transition toward the first lineage specification. However, the molecular features of EGA and the transcription factors (TFs) orchestrating this process remain unclear. Here, by performing single-cell RNA-seq on bovine embryos, we reveal that major EGA is asynchronously initiated among blastomeres at the 8-cell stage. Integrative analyses reveal distinct protein accumulation compared with transcriptional and translational activation during bovine EGA. Furthermore, we investigate the role of SP1, a TF activated at the minor EGA stage, with motifs enriched in accessible chromatin during the major EGA stage in bovine and human embryos. SP1 deficiency leads to morula arrest in bovine and impairs EGA in human embryos. Multiomics analysis demonstrates that SP1 promotes early lineage gene expression by modulating nearby chromatin states in bovine and directly targets key EGA genes in human embryos. Together, our study delineates the dynamics of bovine EGA and uncovers the conserved and species-specific roles of SP1 in regulating EGA and early development in mammals.
    Keywords:  EGA; SP1; bovine embryo; human embryo; preimplantation
    DOI:  https://doi.org/10.1073/pnas.2526998123
  10. J Reprod Dev. 2026 Mar 16.
      In vitro experiments have become a powerful alternative to in vivo approaches for analyzing gene functions and molecular mechanisms. However, successful in vitro oogenesis using the C57BL/6 strain-widely used as a standard mouse model in mammalian studies-has not yet been reported. In this study, we established a 30-day culture system combining ovarian and follicular culture, and successfully produced fully competent oocytes from neonatal C57BL/6N ovaries, which contain only non-growing oocytes prior to primordial follicle formation. A key contributing factor to this success was the supplementation of dibutyryl cyclic AMP, a membrane-permeable analogue of endogenous cyclic AMP, which promoted follicular growth. This culture system provides a valuable tool for investigating the mechanisms underlying oogenesis.
    Keywords:  C57BL/6; Development; In vitro growth; In vitro maturation; Oocyte
    DOI:  https://doi.org/10.1262/jrd.2026-008
  11. Curr Top Dev Biol. 2026 ;pii: S0070-2153(25)00096-1. [Epub ahead of print]166 41-65
      The mammalian embryo establishes the first direct contact with the maternal tissues during implantation. As the blastocyst attaches to the uterine wall, it initiates transformation into a post-implantation conceptus, laying the foundations for placentation and foetal development. The peri-implantation embryogenesis relies on the coordinated growth, morphogenesis, and cell fate transitions of the embryonic and extra-embryonic tissues, entailing changes in cell shape and tissue architecture. In some species, including mice, this process is suspended in a non-receptive uterine environment, where embryonic development arrests at the blastocyst stage and the embryo enters a dormant state known as diapause. However, despite being dormant, relatively slow morphogenetic changes continue to reshape the embryonic cells. Here, we will briefly review the process of murine blastocyst formation before focusing primarily on cell shape and tissue dynamics during peri-implantation embryogenesis. Finally, we will synthesise the current knowledge on tissue morphogenesis during embryo dormancy.
    Keywords:  Blastocyst; Cavity; Cell shape; Diapause; Dormancy; Egg cylinder; Embryo; Implantation; Lumenogenesis; Morphogenesis
    DOI:  https://doi.org/10.1016/bs.ctdb.2025.10.001
  12. Dev Biol. 2026 Mar 17. pii: S0012-1606(26)00070-9. [Epub ahead of print]
      Alternative polyadenylation (APA) generates mRNA isoforms with distinct 3' UTR lengths, yet its role in mammalian preimplantation development remains largely unexplored. Here, we systematically delineated single-cell 3' UTR APA dynamics in human and mouse preimplantation embryos. The pronounced cell heterogeneity and developmental stage-specific of APA patterns were uncovered. Zygotic genome activation (ZGA) genes predominantly utilized shortened 3' UTRs, indicating a potential role for 3' UTR shortening in ZGA. Integrative analyses with APAFlow and DAPAFlow revealed that N6-methyladenosine modification and its reader proteins coordinately regulate APA via APA-associated factors during ZGA. Moreover, the occurrence and expression of 3' UTR APA events are linked to miRNAs located adjacent to polyadenylation sites. Together, these findings delineate a dynamic 3' UTR APA landscape across mammalian preimplantation stages, highlighting its contribution to cellular heterogeneity and developmental regulation. Shortened 3' UTR APA may serve as a hallmark of ZGA, providing new insight into post-transcriptional regulation during preimplantation development.
    Keywords:  Mammals; alternative polyadenylation; early embryonic development; miRNA; zygotic genome activation
    DOI:  https://doi.org/10.1016/j.ydbio.2026.03.014
  13. Trends Biochem Sci. 2026 Mar 17. pii: S0968-0004(26)00006-X. [Epub ahead of print]
      Programmed DNA double-strand breaks (DSBs) catalyzed by the conserved topoisomerase-like complex SPO11-TOP6BL, together with its accessory proteins, initiate meiotic recombination, a process central to meiosis. In mammals, DSBs are distributed nonrandomly at preferential genomic sites (called hotspots) defined largely by the meiosis-specific protein PRDM9. Precise temporal and spatial control of DSB formation is essential for generating genetic diversity while maintaining genomic stability during meiosis. Disruption of this process leads to aberrant recombination, chromosome mis-segregation, and reproductive defects. In this review, we summarize recent genetic, biochemical, and structural advances clarifying the molecular architecture and regulation of meiotic DSB formation in mammals.
    Keywords:  DNA double-strand breaks; DSB-forming machinery; PRDM9; meiosis; meiotic recombination; tethered loop-axis complex
    DOI:  https://doi.org/10.1016/j.tibs.2026.01.006
  14. Nat Commun. 2026 Mar 16.
      The germ cell fate in zebrafish is determined by germ plasm, whereas mammalian germ cell fate is induced by bone morphogenetic protein (BMP) signaling. It remains elusive whether BMP signaling is implicated in zebrafish germ cell development. Here, we demonstrate that BMP-Smad1/9 signaling plays a critical role in zebrafish primordial germ cell (PGC) maintenance rather than fate determination. BMP inhibition or smad1/9 knockdown reduces PGC numbers. Furthermore, we generated PGC-specific smad1/9 knockouts using a transgenic approach with PGC-specifically expressed Cas9 and ubiquitously expressed guide RNAs. Smad1/9 deficiency in PGCs leads to impaired PGC proliferation and increased apoptosis, consequently reducing PGC numbers. Transcriptome analysis revealed unchanged PGC-specific gene expression, but a marked upregulation of DNA damage response-related genes, which is validated by ectopic ATR-pChk1 activation in PGCs and PGC restoring by ATR inhibition. Collectively, these findings underscore conserved but functionally distinct roles of BMP signaling in vertebrate PGC development.
    DOI:  https://doi.org/10.1038/s41467-026-70624-8