Combination of S-adenosylhomocysteine and scriptaid, a non-toxic epigenetic modifying reagent, modulates the reprogramming of bovine somatic-cell nuclear transfer embryos

Molecular Reproduction and Development
Hui ZhangSong Hua

Abstract

The goal of this study was to improve the development of bovine somatic-cell nuclear transfer (SCNT) embryos by optimizing the combination of DNA methyltransferases inhibitor S-adenosylhomocysteine (SAH) and histone deacetylase inhibitor Scriptaid (SPD). A. 4 × 4-factor design of different drug combinations (0, 0.75, 1.0, and 1.5 mM SAH and 0, 5, 250, and 500 nM SPD) was used to identify an optimal combination of 0.75 mM SAH and 250 nM SPD that improved the developmental competence of bovine SCNT embryos. Further experiments using this combination revealed that methylation levels of CpG islands near exon 1 of the pluripotent gene SOX2; the epigenetic-related gene HDAC3 and DNMT3a; imprinted genes XIST and PEG3; as well as apoptosis-related genes BCL2 and BAX were returned to levels similar to those of in vitro fertilized (IVF) embryo after treatment, which also normalized transcript levels for these genes. This combination also returned global DNA methylation to a normal level, correcting H4K12ac levels while enhancing H3K9ac levels. Thus, the combined application of 0.75 mM SAH and 250 nM SPD can significantly improve the reprogramming of bovine SCNT embryos by stabilizing how embryos utilize their genomes.

References

Jul 15, 1994·Experientia·S F De CaboJ Fernández-Piqueras
Aug 11, 2001·Science·W ReikJ Walter
Nov 22, 2001·Proceedings of the National Academy of Sciences of the United States of America·W DeanW Reik
Feb 16, 2002·Methods : a Companion to Methods in Enzymology·K J Livak, T D Schmittgen
Jan 14, 2003·Seminars in Cell & Developmental Biology·Wendy DeanWolf Reik
Jun 20, 2003·Reproduction : the Official Journal of the Society for the Study of Fertility·R AugustinB Fischer
Jul 23, 2004·Cloning and Stem Cells·D N WellsB Oback
Sep 17, 2004·Nature·Victor Ambros
Jul 19, 2005·Cancer Research·Jennifer A ChanKenneth S Kosik
Sep 17, 2005·Proceedings of the National Academy of Sciences of the United States of America·Amelia CimminoCarlo M Croce
Dec 24, 2005·The Journal of Biological Chemistry·Gabbine WeeYong-Mahn Han
Feb 28, 2007·Nature Genetics·Xiangzhong YangTeruhiko Wakayama
Jul 10, 2007·Reproduction : the Official Journal of the Society for the Study of Fertility·Yang YuWeizhi Ji
Sep 22, 2007·Molecular Reproduction and Development·Jing-He LiuQing-Yuan Sun
Feb 29, 2008·Reproduction : the Official Journal of the Society for the Study of Fertility·Byeong-Gyun JeonW Allan King
Jul 25, 2008·Reproduction in Domestic Animals = Zuchthygiene·Björn Oback
Aug 30, 2008·Proceedings of the National Academy of Sciences of the United States of America·Munekazu YamakuchiCharles J Lowenstein
Jan 21, 2009·Reproduction, Fertility, and Development·X Cindy TianRandall S Prather
Jun 3, 2011·Animal Reproduction Science·Song HuaYong Zhang
Jul 2, 2011·Molecular Reproduction and Development·Shahram JafariMohammad H Nasr-Esfahani

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Citations

Aug 8, 2014·Environmental Science & Technology·Mingzhe FuSong Hua

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