bims-cebooc Biomed News
on Cell biology of oocytes
Issue of 2026–05–10
fifteen papers selected by
Gabriele Zaffagnini, Universität zu Köln
  1. Germ granule components regulate endosomal switching during the oocyte-to-embryo transition in Caenorhabditis elegans.
  2. Caenorhabditis elegans form sexually dimorphic and dynamic germ granules throughout meiotic prophase I progression.
  3. Cyst-ained connections in the mammalian germline.
  4. Polycomb shapes active chromatin and promoter bivalency during ovarian reserve formation and activation.
  5. A human CEP120 gene variant impairs meiotic spindle building causing aneuploidy†.
  6. Ypel5 preserves female fertility by regulating folliculogenesis and oocyte maturation.
  7. Role of zygotic arrest genes in female meiosis and early embryonic development.
  8. MCM8-9 helicase activity protects primordial germ cell development to prevent premature ovarian insufficiency.
  9. High-resolution global recombination mapping in C. elegans reveals sexual dimorphisms shaped by meiotic chromosomal features and structures.
  10. Znhit1 mediated H2A.Z deposition governs transcriptional programs essential for oocyte meiotic progression.
  11. Age-related upregulation of p16 expression in mouse ovarian somatic cells correlated with reproductive function decline p16 expression and ovarian aging in mice.
  12. Gut microbiota-modulated glutamic acid rejuvenates the quality of oocytes deteriorated by advanced reproductive age.
  13. Transmembrane ROOM proteins ensure rooms for germ cells by maintaining intercellular bridges.
  14. Synaptonemal complex: The structural basis for meiosis I.
  15. Egg activation.
  1. Commun Biol. 2026 May 07.
    Germ granule components regulate endosomal switching during the oocyte-to-embryo transition in Caenorhabditis elegans.
    Shun-Ichi Suto, Koh-Ichi Teraoka, Ichiro Kawasaki, Kenta Sugiura, Taeko Sasaki, Ikuko Maejima, Hidetaka Kosako, Miyuki Sato, Ken Sato.
      The egg cytoplasm undergoes large-scale remodeling after fertilization. Here, we reveal that the germ granule component, HERD-1, is involved in selective degradation of maternal plasma membrane proteins after fertilization in Caenorhabditis elegans. HERD-1 is specifically expressed in the germline and mainly localized in a subtype of germ granules, Z granules. HERD-1 loss caused maternal plasma membrane protein accumulation in ubiquitin-positive early and late endosomal assemblies in the early embryos. The proteomic analysis showed that HERD-1 loss substantially reduced the protein levels of a subset of endolysosomal regulators such as ESCRT-0 components regulating the multivesicular body pathway. Defects in maternal membrane protein degradation in herd-1-deficient embryos were suppressed with the loss of DEPS-1 or PRG-1, which are required for germ granule organization and small-RNA biogenesis. These results suggest that several germ granule components maintain appropriate endolysosomal component levels via small RNA-mediated regulation during the oocyte-to-embryo transition, promoting endosomal switching toward embryogenesis.
    DOI:  https://doi.org/10.1038/s42003-026-10193-0
  2. bioRxiv. 2026 Apr 30. pii: 2026.04.27.721164. [Epub ahead of print]
    Caenorhabditis elegans form sexually dimorphic and dynamic germ granules throughout meiotic prophase I progression.
    Acadia L DiNardo, Diana E Libuda.
      In sexually reproducing organisms, germ cells faithfully transmit both the genome and epigenetic information across generations through the formation of haploid gametes, such as eggs and sperm. Small RNA pathways tune gene expression in a sex-specific manner during germ cell development to facilitate both proper germ cell formation and transgenerational inheritance of epigenetic information. In Caenorhabditis elegans , components of small RNA pathways localize to germ granules, liquid-like membraneless organelles within the cytoplasm of developing germ cells. During oogenesis, germ granules form hierarchal sub-compartments that may be required for proper germ cell development and epigenetic inheritance. However, germ granule structure during spermatogenesis remains largely undescribed. Here we determine that the germ granule structural components PGL-1 and ZNFX-1 display sexually dimorphic foci morphology and size during meiotic prophase I progression. Further, we quantitate the sexually dimorphic sub-compartmentalization of these two proteins within the germ granule, determining that while PGL-1 and ZNFX-1 do associate during germ cell development, the extent of overlap varies between sexes and throughout meiotic progression. Additionally, we identify WAGO-4, a Argonaute protein central to gene regulation by small RNA pathways, as a sexually dimorphic component of the germ granule during germ cell development. Together, our studies reveal that the overall structure of the germ granule, as well as an Argonaute protein housed inside, are sexually dimorphic, which may underpin sex-specific regulation by small RNA pathways during germ cell development.
    Author Summary: Small RNA pathways are critical for the regulation and passage of genomic and epigenetic information to the next generation. Components of these pathways are housed in germ granules during egg and sperm development. Previous work examining germ granule structure in Caenorhabditis elegans focused on oocytes and the late stages of meiosis I. Here, we comprehensively characterize the localization of two structural and one functional component of the germ granule throughout meiotic progression of both developing egg and sperm cells. We identify that both biophysical properties and germ granule configurations are dependent upon meiotic stage and sex.
    DOI:  https://doi.org/10.64898/2026.04.27.721164
  3. Curr Top Dev Biol. 2026 ;pii: S0070-2153(26)00032-3. [Epub ahead of print]168 81-135
    Cyst-ained connections in the mammalian germline.
    Isabella Leite, Tiffany V Roach, Katherine W Boer, Francesca T deFaria, Georgia Post, Eszter Posfai.
      The germline cyst is a highly conserved structure that supports the proliferation and differentiation of gametes across many species. Germline cysts form when germ cells divide with incomplete cytokinesis, resulting in stable intercellular bridges that act as cytoplasmic channels between sister cells. In mammals, both male and female germ cells develop and enter meiosis within cysts, and disruption of intercellular bridges leads to defects in meiotic progression and gamete formation. However, we are only beginning to understand the biological mechanisms uniquely needed in the germline that are enabled by this structure. In this review, we provide an overview of germ cell development in cysts, from cyst formation through gamete individualization, culminating in the production of mature spermatozoa and oocytes. We highlight studies that examine the functional roles of intercellular bridges and discuss the potential advantages of gamete development within a syncytium, including intercellular communication, resource sharing, and coordinated cell fate decisions. Understanding the formation and breakdown of the cyst as well as the functions it supports will be essential for advancing our understanding of mammalian gametogenesis and for leveraging this knowledge to improve in vitro approaches for gamete generation.
    Keywords:  Cytoplasmic sharing; Germline cyst; Intercellular bridge; Oogenesis; Spermatogenesis
    DOI:  https://doi.org/10.1016/bs.ctdb.2026.03.004
  4. bioRxiv. 2026 Apr 25. pii: 2026.04.22.720278. [Epub ahead of print]
    Polycomb shapes active chromatin and promoter bivalency during ovarian reserve formation and activation.
    Mengwen Hu, Yasuhisa Munakata, Yu-Han Yeh, Neil Hunter, Richard M Schultz, Satoshi H Namekawa.
      The ovarian reserve, a finite pool of long-lived non-growing oocytes established at birth, determines female reproductive lifespan, yet how these oocytes establish long-term quiescence while retaining the capacity for future growth and embryogenesis remains poorly understood. Here, we define a regulatory logic by which Polycomb repressive complexes shape stage-specific active chromatin remodeling during ovarian reserve formation and early oocyte growth. During ovarian reserve formation, H3K27ac, an active promoter- and enhancer-associated mark, undergoes extensive genome-wide redistribution. A key feature of this transition is CpG island promoter remodeling, in which many loci lose H3K27ac while gaining PRC1-dependent H2AK119ub, a repressive mark. This early reprogramming is followed during oocyte growth by acquisition of PRC2-dependent H3K27me3, de novo establishment of bivalent promoters, and protection of promoter regions from de novo DNA methylation. Oocyte growth is also accompanied by broad gains in both H3K27ac and H3K4me3, an active promoter-associated mark. Analyses of PRC1- and PRC2-deficient oocytes reveal unequal Polycomb contributions: PRC2 broadly constrains H3K27ac, whereas PRC1 more selectively shapes genome-wide H3K27ac redistribution and restricts H3K4me3 accumulation at bivalent promoters. Together, these findings identify staged active chromatin remodeling as an integral feature of perinatal oocyte development and reveal that Polycomb shapes chromatin state transitions as oocytes enter quiescence and become poised for future growth.
    One-Sentence Summary: Polycomb repressive complexes shape stage-specific active chromatin remodeling to establish quiescence and future promoter states during ovarian reserve formation and early oocyte growth.
    DOI:  https://doi.org/10.64898/2026.04.22.720278
  5. Biol Reprod. 2026 May 07. pii: ioag094. [Epub ahead of print]
    A human CEP120 gene variant impairs meiotic spindle building causing aneuploidy†.
    Marlena Duke, Cecilia S Blengini, Sophia Maddocks, Mansour Aboelenain, Christine Prorock-Rogers, Karen Schindler.
      Infertility is increasing, leading more women to seek assisted reproduction treatments than ever before. One of the main causes of infertility and pregnancy loss is aneuploidy, an incorrect number of chromosomes in the embryo or developing fetus, which hinders normal development. Aneuploidy overwhelmingly arises from the missegregation of chromosomes during the maternal meiotic divisions that produce haploid oocytes (or eggs). Variants of genes involved in spindle building are of primary interest when searching for genetic causes of aneuploidy because the oocyte meiotic spindle is responsible for faithful chromosome segregation. We previously identified a genetic variant in a human centrosome gene, CEP120, as associated with high embryonic aneuploidy. To evaluate the functional significance of this genetic variant, we generated a knock-in mouse model and found that female mice had reduced fertility and increased egg aneuploidy. By assessing microtubule re-establishment after cold temperature exposure and warming after vitrification, we found that oocytes from mice harboring the genetic variant had reduced microtubule nucleation efficiency. Because mouse and human oocytes present differences in spindle building mechanism, we modified mouse oocyte spindle building assembly by pericentrin depletion to better mimic human oocytes and found that aneuploidy levels significantly increase in CEP120 variant eggs. Although PGT-A allows the deselection of aneuploid embryos, the development of biomarkers for predisposition to aneuploidy could be used to identify subfertile patients and model their aneuploid risk. Therefore, our data indicate that patients harboring common genetic variants in CEP120 may require additional counseling when considering egg cryopreservation procedures.
    Keywords:  CEP120; IVF; MTOC; aneuploidy; gene variants; meiosis; oocyte; spindle; vitrification
    DOI:  https://doi.org/10.1093/biolre/ioag094
  6. Cell Death Differ. 2026 May 05.
    Ypel5 preserves female fertility by regulating folliculogenesis and oocyte maturation.
    Ling Ding, Qianying Guo, Yao Li, Fanqing Xu, Qiang Liu, Shaogang Qin, Ying Kuo, Jie Qiao, Peng Yuan, Liying Yan.
      Maintaining the primordial follicle pool and precisely regulating folliculogenesis are critical for female fertility. Despite advances in understanding ovarian development, the molecular mechanisms safeguarding follicle survival and oocyte maturation remain incompletely defined. Here, we identify YPEL5 as an essential regulator of folliculogenesis and oocyte development. Using an oocyte-specific conditional knockout (cKO) mouse model, we demonstrate that Ypel5 deletion causes complete female infertility, characterized by accelerated depletion of the primordial follicle pool, defective antral follicle formation, and impaired oocyte maturation. Loss of Ypel5 results in increased DNA damage, disrupted mitochondrial homeostasis, elevated oxidative stress, and ultimately triggers apoptotic depletion of primordial follicle oocytes. Moreover, Ypel5-deficient oocytes exhibit severe abnormalities in spindle organization and mitochondrial distribution, culminating in defective oocyte maturation. Collectively, these findings establish YPEL5 as a critical regulator of follicle development and oocyte maturation, and provide mechanistic insights into the molecular basis of female infertility.
    DOI:  https://doi.org/10.1038/s41418-026-01744-3
  7. Dev Biol. 2026 May 01. pii: S0012-1606(26)00100-4. [Epub ahead of print]536 32-40
    Role of zygotic arrest genes in female meiosis and early embryonic development.
    Srija Sadhukhan, Kousik Pramanick.
      Zygotic arrest genes play an indispensable role in regulating the critical transition from maternal to zygotic control during early embryonic development, commonly referred to as zygotic genome activation (ZGA). These genes orchestrate fundamental processes such as maternal mRNA clearance, chromatin remodelling, epigenetic reprogramming, and transcriptional activation, ensuring the developmental competence of embryos. Key genes, including ZAR1, ZAR2, BTG4, NPM2, PADI6, and KHDC3, have been identified as essential regulators of oocyte maturation, meiotic progression, and cleavage-stage development. Dysregulation or mutations in these genes often result in embryonic arrest at the 1-cell, 2-cell, or 4-cell stage, with profound implications for fertility and reproductive success in both humans and animal models. Recent advances in experimental approaches, including gene knockout/knockdown studies, RNA sequencing, transcriptomic profiling, and CRISPR-Cas9 genome editing, have significantly enhanced our understanding of zygotic arrest gene function. Clinical studies have further linked specific mutations to recurrent infertility and poor outcomes in assisted reproductive technologies (ART), such as in vitro fertilisation (IVF) and intracytoplasmic sperm injection (ICSI). These findings underscore the translational potential of zygotic arrest gene research, with prospects for genetic screening, personalized treatment strategies, and novel therapeutic targets. Future directions emphasize integrative omics approaches, cross-species comparative studies, and ethical considerations in embryo manipulation, aiming to bridge fundamental developmental biology with clinical reproductive medicine. Collectively, zygotic arrest genes represent a vital nexus between basic science and translational applications, holding promise for improving fertility outcomes and advancing reproductive health.
    Keywords:  Assisted reproductive technologies (ART); Chromatin remodelling; Embryo development; Infertility; Maternal mRNA clearance; Oocyte maturation; Zygotic arrest genes; Zygotic genome activation (ZGA)
    DOI:  https://doi.org/10.1016/j.ydbio.2026.04.019
  8. Proc Natl Acad Sci U S A. 2026 May 12. 123(19): e2535910123
    MCM8-9 helicase activity protects primordial germ cell development to prevent premature ovarian insufficiency.
    Xiaofei Jiao, Zhifang Li, Zhenghui Tang, Jun Xu, Lin-Yu Lu, Yidan Liu.
      MCM8 and MCM9 form a hexameric helicase critical for homologous recombination (HR). While their variants are strongly associated with premature ovarian insufficiency (POI), with many clustering within their AAA+ ATPase domains, the requirement for their helicase activity remains unknown. Here, we show that MCM8-9's helicase activity is essential for ovarian reserve preservation and POI prevention. Using a series of helicase-deficient mouse models, we demonstrate that this activity is dispensable for meiotic recombination but critically required for mitotic HR and primordial germ cell (PGC) development. The two distinct ATPase active sites of MCM8-9 exhibit marked functional asymmetry, a property regulated by residues within their Walker B motifs. Despite this asymmetry, both ATPase active sites are equally essential for MCM8-9's function in HR, PGC development, ovarian reserve preservation, and POI prevention. Our findings establish a direct mechanistic link between compromised MCM8-9 helicase activity and POI pathogenesis through its essential role in PGC development.
    Keywords:  helicase; homologous recombination; premature ovarian insufficiency; primordial germ cell
    DOI:  https://doi.org/10.1073/pnas.2535910123
  9. bioRxiv. 2026 Apr 28. pii: 2026.04.25.720830. [Epub ahead of print]
    High-resolution global recombination mapping in C. elegans reveals sexual dimorphisms shaped by meiotic chromosomal features and structures.
    Zachary D Bush, John S Conery, Hannah R Wilson, Alice F S Naftaly, Devin Dinwiddie, Kenneth J Hillers, Diana E Libuda.
      Crossover recombination events during meiosis repair double-strand DNA breaks and ensure accurate chromosome segregation in most organisms. For many species, the genomic distribution of crossovers is nonrandom and sexually dimorphic. While many species evolved kilobase-scale "hotspots" for crossover formation, the Caenorhabditis elegans genome lacks hotspots, and crossovers are enriched across megabase-scale domains. Further, genetic and cytological studies indicate the crossover frequency in C. elegans spermatogenesis is higher relative to oogenesis in many but not all genetic intervals. To determine the genomic features that contribute to the sexually dimorphic recombination landscape in the absence of hot spots, we defined and analyzed the recombination landscape across the whole genome in C. elegans using whole-genome sequencing and high-resolution recombination mapping in single worms bearing recombinant chromosomes from individual sperm and oocytes. We find that the spatial distribution of crossovers is sexually dimorphic on chromosomes I, II , and III , and that the global rate of double-crossover events is 4.7-fold higher in spermatocytes. Additionally, we find that pairing and synapsis may contribute to the sexually dimorphic crossover landscape. In comparison to the spermatocyte crossover landscape, a higher proportion of oocyte crossovers are formed in the domains directly adjacent to the pairing centers of each chromosome. Further, reducing the genetic dosage of the synaptonemal complex central region protein SYP-2, which is a meiotic chromosome structural protein required for homologous chromosome synapsis, reshapes the oocyte crossover landscape to resemble observations in wild-type spermatocytes. Finally, we found that spermatocyte crossovers are partially enriched in H3K36me3-marked euchromatic regions, while many oocyte crossovers are enriched in H3K27me3-marked heterochromatic regions. Taken together, our studies reveal how synaptonemal complex component dosage and local chromatin states influence crossover placement and the sex-specific regulation of meiotic recombination.
    Author Summary: Production of viable eggs and sperm depends on accurate chromosome segregation during meiosis. Segregation of parental copies of homologous chromosomes requires the reciprocal exchange and physical linkage of DNA that arises through crossover recombination. Increasing evidence indicates the existence of sexual dimorphisms during meiotic recombination. In this study, we generated and analyzed high-resolution recombination maps specific to spermatogenesis and oogenesis in the nematode C. elegans , which reveals sex-specific crossover distributions and a higher rate of crossing over in sperm cells. Further, we indicate how specific chromosomal features and structures differentially affect the crossover landscape in eggs versus sperm. Our work highlights how, in a system absent of pre-defined "hotspots" for recombination, local chromatin structures, chromosomal pairing domains, and the abundance of synaptonemal complex proteins are potential drivers for establishing the observable sex differences in crossover recombination.
    DOI:  https://doi.org/10.64898/2026.04.25.720830
  10. Development. 2026 May 05. pii: dev.205554. [Epub ahead of print]
    Znhit1 mediated H2A.Z deposition governs transcriptional programs essential for oocyte meiotic progression.
    Na Fan, Hongyu Gong, Peijun Wang, Xue Bai, Xige He, Na Chen, Jiaying Gao, Haoran Li, Lu Wang, Gerile Naren, Fei Gao, Jiaojiao Guo, Tiemin Liu, Ning Jiang, Xinhua Lin, Xihe Li, Buhe Nashun.
      Mammalian oogenesis is a precisely orchestrated developmental process, which depends on accurate chromatin remodeling and transcriptional regulation in the absence of DNA replication. The histone variant H2A.Z is required for oogenesis and embryogenesis, yet the chaperone directing its deposition has not been well characterized in mammalian oocytes. Here, we identify Znhit1, a core subunit of the SRCAP chromatin remodeling complex, as the essential factor mediating H2A.Z deposition in oocytes. Oocyte specific depletion of Znhit1 impairs H2A.Z incorporation and leads to severe ovarian phenotype, characterized by follicle loss, homologous chromosome segregation defects and meiotic arrest, which ultimately leads to female infertility. On molecular level, integrated Smart-seq2 and H2A.Z CUT&Tag analyses demonstrate that Znhit1 depletion severely reduces genome-wide H2A.Z deposition, particularly at promoter regions of key meiotic genes such as Aurkb, Tpm3, and Zar1, resulting in transcriptional dysregulation and aberrant meiotic gene expression. Our findings pinpoint Znhit1 as the histone chaperone essential for accurate deposition of histone variant H2A.Z ensuring meiotic progression and oocyte development in mice.
    Keywords:  H2A.Z; Meiosis; Oocytes; Transcriptional regulation; Znhit1
    DOI:  https://doi.org/10.1242/dev.205554
  11. PLoS One. 2026 ;21(5): e0348870
    Age-related upregulation of p16 expression in mouse ovarian somatic cells correlated with reproductive function decline p16 expression and ovarian aging in mice.
    Yorino Sato, Yuta Kawagoe, Kazuhiro Kawamura.
      Female reproductive aging is a major clinical challenge associated with declining fertility and increased pregnancy complications. The urgent clinical need for developing reliable biomarkers to evaluate ovarian aging has become increasingly evident. Cellular senescence, marked by p16, contributes to age-related tissue dysfunction. However, the relationship between p16 levels and ovarian aging remains poorly understood. Age-related changes in p16 levels across multiple tissues in ICR mice were examined in ICR mice at 4, 30, 45, and 60 weeks of age using qRT-PCR, ELISA, and immunohistochemistry. Cell-type specific p16 levels were analyzed in isolated ovarian cells. Reproductive function was assessed through superovulation, in vitro fertilization, and embryo transfer experiments. p16 mRNA levels increased progressively with age in ovarian tissue (6.8-fold increase at 60 weeks vs. 4 weeks, P < 0.05), with corresponding increases in p16 protein levels. Among tissues examined, ovaries, kidneys, liver, uterus, spleen, and pancreas showed significant age-related p16 upregulation, while brain, heart, and lung did not. Cell-type analysis revealed that somatic cells exhibited pronounced p16 upregulation with age (cumulus cells: 3.2-fold, granulosa cells: 4.6-fold, theca cells: 2.8-fold increase), whereas oocytes and blastocysts showed no significant changes. Ovulation numbers decreased significantly with age (42.3 ± 3.1 vs. 15.6 ± 1.9 oocytes in young vs. aging mice), but fertilization rates and early embryo development remained unaffected. However, post-implantation outcomes deteriorated substantially, with implantation rates declining from 78.4% to 38.1% and live birth rates from 82.3% to 43.2% in aging mice at 60 weeks of age. Age-related upregulation of p16 in ovarian somatic cells, but not in oocytes, correlated with declining reproductive function, particularly affecting post-implantation development. These findings suggest that somatic cell senescence may contribute to age-related declines in oocyte competence, leading to fertility decline with aging.
    DOI:  https://doi.org/10.1371/journal.pone.0348870
  12. EMBO Mol Med. 2026 May 08.
    Gut microbiota-modulated glutamic acid rejuvenates the quality of oocytes deteriorated by advanced reproductive age.
    Feixue Wang, Wenjun Zeng, Zihao Zhang, Na Li, Zhaokang Cui, Jie Bai, Jiner Yan, Yu Zhang, Yilong Miao, Ling Gu, Bo Xiong.
      The gut microbiota plays a vital role in maintaining the physiological function of host health and the pathogenesis of various diseases. However, its relationship with maternal age-associated decline in oocyte quality remains elusive. Here, we report that establishment of gut microbiota from young donors in aged mice by fecal microbiota transplantation (FMT) is an effective method to rejuvenate the quality of maternally aged oocytes. Specifically, young gut microbiota promoted the ovulation and maturation of aged oocytes, and inhibited occurrence of cytoplasm fragmentation and spindle/chromosome abnormalities, hence enhancing the oocyte quality and female fertility. By integrating metagenome and untargeted metabolome of intestinal digesta, as well as targeted metabolome of ovaries and micro-transcriptome of oocytes, we identified that Bacteroides_caecimuris-modulated glutamic acid levels mediated the restorative effects of young gut microbiota on the aged oocytes through strengthening the mitochondria function. In addition, we demonstrated that in vivo supplementation of glutamic acid also enhanced the quality of aged oocytes, and the improvement of oocyte quality by glutamic acid was conserved across species. Altogether, our findings highlight the importance of gut microbiota in the oocyte aging and provide potential improvement strategies for age-related decline in oocyte quality and female fertility.
    DOI:  https://doi.org/10.1038/s44321-026-00443-3
  13. Proc Natl Acad Sci U S A. 2026 May 12. 123(19): e2522264123
    Transmembrane ROOM proteins ensure rooms for germ cells by maintaining intercellular bridges.
    Kenta Sugiura, Ichiro Kawasaki, Hidetaka Kosako, Ken Sato.
      Germ cells of diverse species form a syncytium, which is a multinucleated cell complex, and share cytoplasmic components via intercellular bridges. Here, we demonstrate that the paralogous transmembrane proteins ROOM-1 and ROOM-2, identified through the proteomic analysis of maternal membrane proteins, are essential for the maintenance of germ cell compartments from the rachis of Caenorhabditis elegans gonads. Although animals lacking each protein are fertile, the loss of both proteins resulted in complete sterility due to compartmentalization failure of individual germ cells in the late larval and adult gonads. Additionally, the ROOM proteins colocalize specifically to the intercellular bridge with F-actin and ANI-2, a protein organizing the intercellular bridge of germ cells. The localizations of ANI-2 and ROOM-1/2 on the rachis bridge were interdependent. Thus, the transmembrane ROOM proteins redundantly function to ensure "rooms" for germ cells by maintaining the intercellular bridges.
    Keywords:  C. elegans; actomyosin complex; germ cells; intercellular bridge; syncytium
    DOI:  https://doi.org/10.1073/pnas.2522264123
  14. Curr Top Dev Biol. 2026 ;pii: S0070-2153(26)00014-1. [Epub ahead of print]168 245-279
    Synaptonemal complex: The structural basis for meiosis I.
    Hanwei Jiang, Suixing Fan, Qinghua Shi.
      As a specialized form of cell division for the generation of haploid gametes, meiosis is characterized by the separation of homologous chromosomes in meiosis I. Two key events take place in meiotic prophase I to ensure the proper segregation of homologous chromosomes, including the formation of the synaptonemal complex (SC) and the initiation and repair of programmed DNA double-strand breaks (DSBs). Both of these events are essential for the generation of crossovers. The SC serves as the structural basis of all the chromosome behaviors in meiotic prophase I. It not only reorganizes the chromosomes into a highly ordered stem-loop structure and holds the homologous chromosomes together when DSBs are being repaired, but also works as a platform for the recruitment of proteins playing essential roles in the formation and repair of DSBs, as well as the checkpoint monitoring the proper meiosis progression. Given the critical role of the SC in meiosis, questions concerning its structure and function are well studied in the field of meiosis research. Here, we not only reviewed the studies concerning the assembly of the SC, the function of the SC during male meiosis, and how mutations related to the SC coding genes affect male fertility, but also summarized the critical questions to be solved in future research.
    Keywords:  Cohesin; Male fertility; Meiosis; Synaptonemal complex
    DOI:  https://doi.org/10.1016/bs.ctdb.2026.01.014
  15. Curr Biol. 2026 May 04. pii: S0960-9822(26)00329-5. [Epub ahead of print]36(9): R367-R369
    Egg activation.
    Jonathon M Thomalla, Emily L Rivard, Anyerys Diaz, Mariana F Wolfner.
      Thomalla et al. provide an overview of the conserved and divergent mechanisms of egg activation across animals.
    DOI:  https://doi.org/10.1016/j.cub.2026.03.040
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