ArticleiScience2025
Origin and development of uniparental and polyploid blastomeres.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Underrecognized triploidy and genome-wide uniparental disomy in human blastocysts revealed by a concurrent preimplantation genetic testing approach.Human reproduction open · 2026Article
- Coupling and decoupling of the cell cycle from cell differentiation in development.Development (Cambridge, England) · 2025Review
- A mitochondrial redox switch licenses the onset of morphogenesis in animals.bioRxiv : the preprint server for biology · 2024Article
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Whole-genome (WG) abnormalities, such as uniparental diploidy and triploidy, cause fetal death. Occasionally, they coexist with biparental diploid cells in live births. Understanding the origin and early development of WG abnormal blastomeres is crucial for explaining the formation of androgenotes, gynogenotes, triploidy, chimerism, and mixoploidy. By haplotyping 118 bovine blastomeres from the first cleavages, we identified that heterogoneic division occurs in both multipolar and bipolar cleaving zygotes. During heterogoneic division, parental genomes segregate into distinct blastomeres, resulting in the coexistence of uniparental and biparental diploid or polyploid cells. After culturing the totipotent blastomeres to three preimplantation stages and exploring transcriptomes of 446 cells, we discovered that stress responses contribute to developmental impairment in WG abnormal cells, resulting in either cell arrest or blastocyst formation. Their dominance in preimplantation embryos represents an overlooked cause of abnormal development. Haplotype-based screening could improve
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