Superovulation induces defective methylation in line-1 retrotransposon elements in blastocyst

Reproductive Biology and Endocrinology

Research

Shao-Chen Sun¹  Yong-Xun Jin²  Suk Namgoong²  Nam-Hyung Kim²  Xing-Wei Liang²  Xiang-Shun Cui²  Young Tae Heo² 

[1] College of Animal Science and Technology, Nanjing Agricultural University, 210095, Nanjing, China;Department of Animal Sciences, Chungbuk National University, 361-763, Cheongju, South Korea;

关键词: Superovulation;    Oocyte;    Pre-implantation development;    DNA methylation;    Dnmt;   

DOI  :  10.1186/1477-7827-11-69

 received in 2013-05-10, accepted in 2013-07-15,  发布年份 2013

来源: Springer

【 摘 要 】

BackgroundSeries of epigenetic events happen during preimplantation development. Therefore assistant reproduction techniques (ART) have the potential to disrupt epigenetic regulation during embryo development. The purpose of this study was to investigate whether defects in methylation patterns in blastocyst due to superovulation originate from abnormal expression of Dnmts.MethodsLow- (6 IU) and high- (10 IU) dosage of PMSG was used to stimulate the female mice. The metaphase II(MII) oocytes, zygotes and blastocyst stage embryos were collected. Global methylation and methylation at H3K9 in zygote, and methylation at repeated sequence Line 1 and IAP in blastocysts were assayed. In addition, expression of Dnmts was examined in oocytes and zygotes.ResultsGlobal DNA methylation and methylation at H3K9 in zygotes derived from females after low- or high-dosage hormone treatment were unaltered compared to that in controls. Moreover, DNA methylation at IAP in blastocysts was also unaffected, regardless of hormone dosage. In contrast, methylation at Line1 decreased when high-dose hormone was administered. Unexpectedly, expression of Dnmt3a, Dnmt3b, Dnmt3L as well as maintenance Dnmt1o in oocytes and zygotes was not disrupted.ConclusionsThe results suggest that defects in embryonic methylation patterns do not originate from the disruption of Dnmt expression.

【 授权许可】

Unknown   
© Liang et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.