bims-cebooc Biomed News
on Cell biology of oocytes
Issue of 2024–12–29
five papers selected by
Gabriele Zaffagnini, Universität zu Köln
  1. Age-associated aberrations of the cumulus-oocyte interaction and in the zona pellucida structure reduce fertility in female mice.
  2. Chromosome architecture and low cohesion bias acrocentric chromosomes towards aneuploidy during mammalian meiosis.
  3. Mitochondrial DNA mutations in human oocytes undergo frequency-dependent selection but do not increase with age.
  4. An interkinetic envelope surrounds chromosomes between meiosis I and II in C. elegans oocytes.
  5. HFM1 is essential for the germ cell intercellular bridge transport in primordial follicle formation in mice.
  1. Commun Biol. 2024 Dec 24. 7(1): 1692
    Age-associated aberrations of the cumulus-oocyte interaction and in the zona pellucida structure reduce fertility in female mice.
    Yu Ishikawa-Yamauchi, Chihiro Emori, Hideto Mori, Tsutomu Endo, Kiyonori Kobayashi, Yuji Watanabe, Hiroshi Sagara, Takeshi Nagata, Daisuke Motooka, Akinori Ninomiya, Manabu Ozawa, Masahito Ikawa.
      One of the major age-related declines in female reproductive function is the reduced quantity and quality of oocytes. Here we demonstrate that structural changes in the zona pellucida (ZP) were associated with decreased fertilization rates from 34- to 38-week-old female mice, equivalent to the mid-reproductive of human females. In middle-aged mouse ovaries, the decline in the number of transzonal projections was accompanied by a decrease in cumulus cell-oocyte interactions, resulting in a deterioration of the oocyte quality. Scanning electron microscopy showed the ZP surface microfilament structure transitioning from rugged to smooth with aging, leading to decreased fertilization rates due to impaired sperm binding to the ZP. Moreover, the fertilization rate of middle-aged mice was restored to a comparable level to that of young mice by destabilizing the ZP in the presence of glutathione. These results suggest that the age-related structural changes in the ZP are key for successful fertilization at reproductive age.
    DOI:  https://doi.org/10.1038/s42003-024-07305-z
  2. Nat Commun. 2024 Dec 23. 15(1): 10713
    Chromosome architecture and low cohesion bias acrocentric chromosomes towards aneuploidy during mammalian meiosis.
    Eirini Bellou, Agata P Zielinska, Eike Urs Mönnich, Nina Schweizer, Antonio Z Politi, Antonina Wellecke, Claus Sibold, Andreas Tandler-Schneider, Melina Schuh.
      Aneuploidy in eggs is a leading cause of miscarriages or viable developmental syndromes. Aneuploidy rates differ between individual chromosomes. For instance, chromosome 21 frequently missegregates, resulting in Down Syndrome. What causes chromosome-specific aneuploidy in meiosis is unclear. Chromosome 21 belongs to the class of acrocentric chromosomes, whose centromeres are located close to the chromosome end, resulting in one long and one short chromosome arm. We demonstrate that acrocentric chromosomes are generally more often aneuploid than metacentric chromosomes in porcine eggs. Kinetochores of acrocentric chromosomes are often partially covered by the short chromosome arm during meiosis I in human and porcine oocytes and orient less efficiently toward the spindle poles. These partially covered kinetochores are more likely to be incorrectly attached to the spindle. Additionally, sister chromatids of acrocentric chromosomes are held together by lower levels of cohesin, making them more vulnerable to age-dependent cohesin loss. Chromosome architecture and low cohesion therefore bias acrocentric chromosomes toward aneuploidy during mammalian meiosis.
    DOI:  https://doi.org/10.1038/s41467-024-54659-3
  3. bioRxiv. 2024 Dec 12. pii: 2024.12.09.627454. [Epub ahead of print]
    Mitochondrial DNA mutations in human oocytes undergo frequency-dependent selection but do not increase with age.
    Barbara Arbeithuber, Kate Anthony, Bonnie Higgins, Peter Oppelt, Omar Shebl, Irene Tiemann-Boege, Francesca Chiaromonte, Thomas Ebner, Kateryna D Makova.
      Mitochondria, cellular powerhouses, harbor DNA (mtDNA) inherited from the mothers. MtDNA mutations can cause diseases, yet whether they increase with age in human germline cells-oocytes-remains understudied. Here, using highly accurate duplex sequencing of full-length mtDNA, we detected de novo mutations in single oocytes, blood, and saliva in women between 20 and 42 years of age. We found that, with age, mutations increased in blood and saliva but not in oocytes. In oocytes, mutations with high allele frequencies (≥1%) were less prevalent in coding than non-coding regions, whereas mutations with low allele frequencies (<1%) were more uniformly distributed along mtDNA, suggesting frequency-dependent purifying selection. In somatic tissues, mutations caused elevated amino acid changes in protein-coding regions, suggesting positive or destructive selection. Thus, mtDNA in human oocytes is protected against accumulation of mutations having functional consequences and with aging. These findings are particularly timely as humans tend to reproduce later in life.
    DOI:  https://doi.org/10.1101/2024.12.09.627454
  4. J Cell Biol. 2025 Mar 03. pii: e202403125. [Epub ahead of print]224(3):
    An interkinetic envelope surrounds chromosomes between meiosis I and II in C. elegans oocytes.
    Layla El Mossadeq, Laura Bellutti, Rémi Le Borgne, Julie C Canman, Lionel Pintard, Jean-Marc Verbavatz, Peter Askjaer, Julien Dumont.
      At the end of cell division, the nuclear envelope reassembles around the decondensing chromosomes. Female meiosis culminates in two consecutive cell divisions of the oocyte, meiosis I and II, which are separated by a brief transition phase known as interkinesis. Due to the absence of chromosome decondensation and the suppression of genome replication during interkinesis, it has been widely assumed that the nuclear envelope does not reassemble between meiosis I and II. By analyzing interkinesis in C. elegans oocytes, we instead show that an atypical structure made of two lipid bilayers, which we termed the interkinetic envelope, surrounds the surface of the segregating chromosomes. The interkinetic envelope shares common features with the nuclear envelope but also exhibits specific characteristics that distinguish it, including its lack of continuity with the endoplasmic reticulum, unique protein composition, assembly mechanism, and function in chromosome segregation. These distinct attributes collectively define the interkinetic envelope as a unique and specialized structure that has been previously overlooked.
    DOI:  https://doi.org/10.1083/jcb.202403125
  5. Cell Mol Life Sci. 2024 Dec 27. 82(1): 28
    HFM1 is essential for the germ cell intercellular bridge transport in primordial follicle formation in mice.
    Yuheng He, Huiyuan Wang, Tongtong Hong, Luanqian Hu, Chao Gao, Li Gao, Yugui Cui, Rongrong Tan, Danhua Pu, Jie Wu.
      The reproductive lifespan of female mammals is determined by the size of the primordial follicle pool, which comprises oocytes enclosed by a layer of flattened pre-granulosa cells. Oocyte differentiation needs acquiring organelles and cytoplasm from sister germ cells in cysts, but the mechanisms regulating this process remain unknown. Previously helicase for meiosis 1 (HFM1) is reported to be related to the development of premature ovarian insufficiency. Here, it is found that HFM1 is involved in oocyte differentiation through organelle enrichment from sister germ cells. Further study indicates that HFM1 is involved in intercellular directional transport through intercellular bridges via the RAC1/ANLN/E-cad signaling pathway, which is indispensable for oocyte differentiation and primordial follicle formation. These findings shed light on the critical role of HFM1 in intercellular bridge transport, which is essential for the establishment of the primordial follicle pool and presenting new horizons for female fertility protection.
    Keywords:  HFM1; Intercellular bridge; Oocyte differentiation; POI; Primordial follicle formation
    DOI:  https://doi.org/10.1007/s00018-024-05541-4
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