Genomic imprinting is the parent-specific epigenetic marking of certain loci — essentially methylation patterns — determining which of a gene’s two alleles is read, according to whether it comes from the mother or from the father. In humans some one hundred loci are affected.
Ontological classification
- is established during gametogenesis: maternal imprints over months in the maturing follicle, paternal imprints before birth
- is a precondition of normal embryonic development
- its disturbance produces uniparental disomies
The common misrepresentation
It is often said that a body cell does not carry the imprinting pattern of an oocyte. The opposite is true, and it is the less favourable case.
A body cell is not free of imprints. It carries a complete and correct pattern at every imprinted locus: the allele inherited from the mother bears the maternal mark, the one inherited from the father the paternal mark. This is precisely why classical cloning works at all — the clone inherits a balanced configuration.
Why halving creates the problem
A procedure such as mitomeiosis destroys this symmetry. It retains only one allele per locus, at random with respect to grandparental origin. If at a maternally imprinted locus the grandpaternal allele is retained, it meets the paternal mark of the sperm: two paternally imprinted alleles, none maternal.
Functionally this corresponds to a uniparental disomy — the same constellation underlying Angelman, Prader-Willi, Beckwith-Wiedemann, and Silver-Russell syndromes in humans. The oocyte cannot correct this: maternal imprints are set during the months of oocyte growth, and the cytoplasm of a mature oocyte is cytoplasm after that programme, not during it.
What the research shows
Imprinting has not been investigated in nuclear-transfer-derived oocytes. The relevant state of research comes from the neighbouring field of artificial gametes in mice, and there imprinting has for years been identified as the barrier. The route that worked is surgical: the imprinting control regions are removed or overwritten. Three deletions sufficed for bimaternal animals with normal growth and normal fertility; bipaternal ones required seven but at first did not reach adulthood. Only in 2025 did that succeed, following interventions at considerably more imprinted loci — and those animals remained infertile and shorter-lived. A study of the same year produced fertile animals by epigenetic editing without any intervention in the DNA sequence.
Two conclusions follow. First, the problem is more tractable than long assumed: the burden is not spread across all imprinted genes but concentrated in a few regions. Second, this only shifts where the obstacle lies — the successful route is heritable germline manipulation, prohibited in humans virtually everywhere.
The coming point of contention
The shift from deletion to methylation writing is recognizably also an evasion of the objection from germline manipulation: where nothing is cut, nothing is altered in the letter. Whether this distinction holds is open — it is the same pattern as with the prohibition of cloning, whose wording does not catch mitomeiosis. A heritable, deliberately placed methylation mark is by the letter no alteration of the genome and in substance an alteration of what the genome does.
See also
- Meiosis, Germline, Gamete
- Mitomeiosis, In Vitro Gametogenesis
- Somatic Cell Nuclear Transfer (SCNT)
- Genetic Technology
- Oocyte
Sources: Generated by querying the Personhood ontology. Research as of 27 July 2026.
Further sources:
- Li, Z.-K. et al. (2018): Generation of Bimaternal and Bipaternal Mice from Hypomethylated Haploid ESCs with Imprinting Region Deletions. Cell Stem Cell 23(5): 665–676.e4.
- Li, Z.-K. et al. (2025): Adult bi-paternal offspring generated through direct modification of imprinted genes in mammals. Cell Stem Cell 32(3): 361–374.e6.
- Wei, Y., Yue, T., Wang, Y. & Yang, Y. (2025): Fertile androgenetic mice generated by targeted epigenetic editing of imprinting control regions. PNAS 122(27): e2425307122.