HSPC117 deficiency in cloned embryos causes placental abnormality and fetal death

Autor: Yuyu Niu, Tang Hai, Xun Zhang, Shuya Zhou, Liu Wang, Xiaoyang Zhao, Alice Jouneau, Chenhui Ding, Zichuan Liu, Zhuo Lv, Yingying Wang, Lei Liu, Man Tong, Weizhi Ji, Qi Zhou
Přispěvatelé: Chinese Academy of Sciences (CAS), State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences [Beijing], Biologie du développement et reproduction (BDR), Centre National de la Recherche Scientifique (CNRS)-École nationale vétérinaire d'Alfort (ENVA)-Institut National de la Recherche Agronomique (INRA), Massachusetts General Hospital, Massachusetts General Hospital [Boston]
Rok vydání: 2010
Předmět:
Nuclear Transfer Techniques
Transcription
Genetic
Somatic cell
[SDV]Life Sciences [q-bio]
medicine.medical_treatment
Biochemistry
Intracytoplasmic sperm injection
Mice
0302 clinical medicine
Pregnancy
implantation
RNA
Small Interfering
reproductive and urinary physiology
hspc117
Genetics
0303 health sciences
Embryo
medicine.anatomical_structure
Gene Knockdown Techniques
embryonic structures
Somatic cell nuclear transfer
Female
RNA Interference
nuclear transfer
animal structures
placenta
Cloning
Organism
développment de l'embryon
Biophysics
Embryonic Development
Biology
Andrology
03 medical and health sciences
Placenta
medicine
Animals
BIOLOGIE DU DEVELOPPEMENT
[INFO]Computer Science [cs]
Sperm Injections
Intracytoplasmic
Blastocyst
Fetal Death
Molecular Biology
030304 developmental biology
mouse embryo
Fetus
Embryogenesis
Cell Biology
Mice
Mutant Strains
030217 neurology & neurosurgery
Zdroj: Biochemical and Biophysical Research Communications
Biochemical and Biophysical Research Communications, Elsevier, 2010, 397 (3), pp.407-412. ⟨10.1016/j.bbrc.2010.05.105⟩
ISSN: 0006-291X
1090-2104
Popis: International audience; 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.
Databáze: OpenAIRE
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