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A more recent version of this article appeared on March 3, 2006
Papers In Press, published online ahead of print December 21, 2005
J. Biol. Chem, 10.1074/jbc.M511340200
Submitted on October 19, 2005
Revised on December 19, 2005
Accepted on December 21, 2005
Inheritable histone H4 acetylation of somatic chromatins in cloned embryos
Gabbine Wee, Deog-Bon Koo, Bong-Seok Song, Ji-Su Kim, Man-Jong Kang, Seung-Ju Moon, Yong-Kook Kang, Kyung-Kwang Lee, and Yong-Mahn Han
Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806
Corresponding Author: ymhan{at}kribb.re.kr
A viable cloned animal indicates that epigenetic status of the differentiated cell nucleus reprogrammed to an embryonic totipotent state. However, molecular events regarding epigenetic reprogramming of the somatic chromatin are poorly understood. Here we provide a new insight that somatic chromatins are refractory to reprogramming of histone acetylation during early development. A low level of acetylated histone H4-lysine 5 (AcH4K5) of the somatic chromatin was sustained at the pronuclear stage. Unlike in vitro fertilized (IVF) embryos, the AcH4K5 level remarkably reduced at the 8-cell stage in cloned bovine embryos. The AcH4K5 status of somatic chromatins transmitted to cloned and even recloned embryos. Differences of AcH4K5 signal intensity were more distinguishable in the metaphase chromosomes between IVF and cloned embryos. Two imprinted genes, Ndn and Xist, was aberrantly expressed in cloned embryos as compared with IVF embryos, which is partly associated with the AcH4K5 signal intensity. Our findings suggest that abnormal epigenetic reprogramming in cloned embryos may be due to a memory mechanism, epigenetic status itself of somatic chromatins.

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Copyright © 2005 by the American Society for Biochemistry and Molecular Biology.
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