HSPC117 deficiency in cloned embryos causes placental abnormality and fetal death
文献类型：期刊论文
| 作者 | Wang YY1,2,3; Hai T2,3; Liu CZ2,3; Zhou SY2,3; Lv Z2,3; Ding CH2; Liu L2; Niu YY1; Zhao XY2,3; Tong M2,3 |
| 刊名 | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
 |
| 出版日期 | 2010 |
| 卷号 | 397期号:3页码:407-412 |
| 关键词 | Nuclear transfer Mouse embryo HSPC117 Placenta Implantation |
| 通讯作者 | wji@mail.kiz.ac.cn ; qzhou@ioz.ac.cn |
| 合作状况 | 其它 |
| 英文摘要 | Somatic cell nuclear transfer (SCNT) has been successfully used in many species to produce live cloned offspring, albeit with low efficiency. The low frequency of successful development has usually been ascribed to incomplete or inappropriate reprogramming of the transferred nuclear genome. Elucidating the genetic differences between normal fertilized and cloned embryos is key to understand the low efficiency of SCNT. Here, we show that expression of HSPC117, which encodes a hypothetical protein of unknown function, was absent or very low in cloned mouse blastocysts. To investigate the role of HSPC117 in embryo development, we knocked-down this gene in normal fertilized embryos using RNA interference. We assessed the post-implantation survival of HSPC117 knock-down embryos at 3 stages: E9 (prior to placenta formation); E12 (after the placenta was fully functional) and E19 (post-natal). Our results show that, although siRNA-treated in vivo fertilized/produced (IVP) embryos could develop to the blastocyst stage and implanted without any difference from control embryos, the knock-down embryos showed substantial fetal death, accompanied by placental blood clotting, at E12. Furthermore, comparison of HSPC117 expression in placentas of nuclear transfer (NT), intracytoplasmic sperm injection (ICSI) and IVP embryos confirmed that HSPC117 deficiency correlates well with failures in embryo development: all NT embryos with a fetus, as well as IVP and ICSI embryos, had normal placental HSPC117 expression while those NT embryos showing reduced or no expression of HSPC117 failed to form a fetus. In conclusion, we show that HSPC117 is an important gene for post-implantation development of embryos, and that HSPC117 deficiency leads to fetal abnormalities after implantation, especially following placental formation. We suggest that defects in HSPC117 expression may be an important contributing factor to loss of cloned NT embryos in vivo. |
| 收录类别 | SCI |
| 资助信息 | This study was supported in part by grants from the China National Basic Research Program 2006CB701501 and grants from The Na- tional Key Scientific Program 2006CB944003. |
| 语种 | 英语 |
| 源URL | [http://159.226.149.26:8080/handle/152453/10454]  |
| 专题 | 昆明动物研究所_生殖与发育生物学 昆明动物研究所_中国科学院昆明灵长类研究中心 |
| 作者单位 | 1.Department of Reproduction and Development, Kunming Institute of Zoology & Kunming Primate Research Center, Chinese Academy of Sciences, Kunming 650223, China 2.State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100080, China 3.Graduate University of Chinese Academy of Sciences, Beijing 100049, China 4.INRA, UMR 1198, ENVA, CNRS, FRE 2857, Biologie du Développement et Reproduction, Jouy en Josas F-78350, France 5.Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA |
| 推荐引用方式 GB/T 7714 | Wang YY,Hai T,Liu CZ,et al. HSPC117 deficiency in cloned embryos causes placental abnormality and fetal death[J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,2010,397(3):407-412. |
| APA | Wang YY.,Hai T.,Liu CZ.,Zhou SY.,Lv Z.,...&Ji WZ[*].(2010).HSPC117 deficiency in cloned embryos causes placental abnormality and fetal death.BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,397(3),407-412. |
| MLA | Wang YY,et al."HSPC117 deficiency in cloned embryos causes placental abnormality and fetal death".BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 397.3(2010):407-412. |
入库方式： OAI收割
来源：昆明动物研究所
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