Involvement of G9A-like protein (GLP) in the development of mouse preimplantation embryos in vitro
Xian-Ju Huang A , Xueshan Ma B , Xuguang Wang C , Xiaolong Zhou A , Juan Li A , Shao-Chen Sun A and Honglin Liu A DA College of Animal Science and Technology, Nanjing Agricultural University, Weigang No. 1, Nanjing 210095, China.
B State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Peking University People’s Hospital, Beichen West Road No. 1, Chaoyang District, Beijing 100101, China.
C Animal Science College, Xinjiang Agricultural University, Nongda Road No. 311, Wulumuqi, Xinjiang 830052, China.
D Corresponding author. Email: liuhonglin@njau.edu.cn
Reproduction, Fertility and Development 28(11) 1733-1740 https://doi.org/10.1071/RD14341
Submitted: 12 September 2014 Accepted: 3 April 2015 Published: 18 May 2015
Abstract
G9A-like protein (GLP) plays an important role in mouse early embryonic development. Glp-deficient embryos exhibit severe growth retardation and defects that lead to lethality at approximately Embryonic Day 9.5. In the present study we investigated the effect of microinjection of Glp-specific short interference (si) RNA into mouse zygotes on in vitro embryonic development. Knockdown of Glp induced abnormal embryonic development and reduced blastocyst formation. Expression of the pluripotency markers octamer-binding transcription factor 4 (Oct4), SRY (sex determining region Y)-box 2 (Sox2) and Nanog was also significantly decreased in Glp-deficient embryos. The apoptotic index and expression of two pro-apoptotic genes, namely Caspase 3 and Caspase 9, were increased in Glp-deficient embryos. Moreover, methylation levels of dimethylated H3K9 (H3K9me2) were decreased in Glp-knockdown embryos. In conclusion, the results of the present study suggest that Glp deficiency suppresses H3K9me2 modification and hinders mouse embryo development in vitro.
Additional keywords: abnormal development, apoptosis, Glp deficiency.
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