期刊
CELL RESEARCH
卷 23, 期 1, 页码 6-9出版社
INST BIOCHEMISTRY & CELL BIOLOGY
DOI: 10.1038/cr.2012.117
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- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [R01HD065812] Funding Source: NIH RePORTER
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R00HD055333] Funding Source: NIH RePORTER
- NATIONAL CANCER INSTITUTE [R01CA151535] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI044432] Funding Source: NIH RePORTER
- OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [DP2OD008646] Funding Source: NIH RePORTER
- NCI NIH HHS [R01 CA151535] Funding Source: Medline
- NIAID NIH HHS [R01 AI044432] Funding Source: Medline
- NICHD NIH HHS [R01 HD065812, R00 HD055333, R00HD055333, HD065812] Funding Source: Medline
- NIH HHS [DP2 OD008646, DP2-OD-008646] Funding Source: Medline
In zygotes, a global loss of DNA methylation occurs selectively in the paternal pronucleus before the first cell division, concomitantly with the appearance of modified forms of 5-methylcytosine. The adjacent maternal pronucleus and certain paternally-imprinted loci are protected from this process. Nakamura et al. recently clarified the molecular mechanism involved: PGC7/Stella/Dppa3 binds to dimethylated histone 3 lysine 9 (H3K9me2), thereby blocking the activity of the Tet3 methylcytosine oxidase in the maternal genome as well as at certain imprinted loci in the paternal genome.
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