ArticleThe EMBO journal2023
Cell fragmentation in mouse preimplantation embryos induced by ectopic activation of the polar body extrusion pathway.
Article in The EMBO journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- An Updated Understanding of Human Embryonic Fragmentation.Reproductive sciences (Thousand Oaks, Calif.) · 2026Pooled it
- Fertilization with Protamine-2 deficient sperm triggers abnormal pronucleus development and zygotic cleavage†.Biology of reproduction · 2026Article
- Stem cell-based embryo models as a tool for reproductive biology.Molecular human reproduction · 2026Review
- The Rac pathway prevents cell fragmentation in a nonprotrusively migrating leader cell during C. elegans gonad organogenesis.Current biology : CB · 2024Article
- Measuring the forces that shape early human embryos.Nature · 2024Article
- Getting there in one piece: The Rac pathway prevents cell fragmentation in a nonprotrusively migrating leader cell during organogenesis.bioRxiv : the preprint server for biology · 2023Article
- MRCK activates mouse oocyte myosin II for spindle rotation and male pronucleus centration.The Journal of cell biology · 2023Article
- Cell fragmentation in mouse preimplantation embryos induced by ectopic activation of the polar body extrusion pathway.The EMBO journal · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell fragmentation is commonly observed in human preimplantation embryos and is associated with poor prognosis during assisted reproductive technology (ART) procedures. However, the mechanisms leading to cell fragmentation remain largely unknown. Here, light sheet microscopy imaging of mouse embryos reveals that inefficient chromosome separation due to spindle defects, caused by dysfunctional molecular motors Myo1c or dynein, leads to fragmentation during mitosis. Extended exposure of the cell cortex to chromosomes locally triggers actomyosin contractility and pinches off cell fragments. This process is reminiscent of meiosis, during which small GTPase-mediated signals from chromosomes coordinate polar body extrusion (PBE) by actomyosin contraction. By interfering with the signals driving PBE, we find that this meiotic signaling pathway remains active during cleavage stages and is both required and sufficient to trigger fragmentation. Together, we find that fragmentation happens in mitosis after ectopic activation of actomyosin contractility by signals emanating from DNA, similar to those observed during meiosis. Our study uncovers the mechanisms underlying fragmentation in preimplantation embryos and, more generally, offers insight into the regulation of mitosis during the maternal-zygotic transition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.