Format

Send to

Choose Destination
Sci Rep. 2016 Dec 5;6:38192. doi: 10.1038/srep38192.

ECAT1 is essential for human oocyte maturation and pre-implantation development of the resulting embryos.

Author information

1
Molecular and Cell Genetics Laboratory; The CAS Key Laboratory of Innate Immunity and Chronic Disease; Hefei National Laboratory for Physical Sciences at Microscale; School of Life Sciences, University of Science and Technology of China, Hefei 230027, China.
2
Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology and Key Laboratory of Assisted Reproduction, Ministry of Education, Center of Reproductive Medicine, Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing 100191, China.

Abstract

ECAT1 is a subunit of the subcortical maternal complex that is required for cell cycle progression during pre-implantation embryonic development; however, its exact function remains to be elucidated. Here we investigated the expression of ECAT1 in human ovarian tissue, oocytes and pre-implantation embryos and assessed its function by using RNA interference (RNAi) in oocytes. ECAT1 mRNA was highly expressed in human oocytes and zygotes, as well as in two-cell, four-cell and eight-cell embryos, but declined significantly in morulae and blastocysts. ECAT1 was expressed in the cytoplasm of oocytes and pre-implantation embryos and was localized more specifically in the cortical region than in the inner cytoplasm. RNAi experiments demonstrated that down-regulation of ECAT1 expression not only impaired spindle assembly and reduced maturation and fertilization rates of human oocytes but also decreased the cleavage rate of the resulting zygotes. In conclusion, our study indicates that ECAT1 may play a role in meiotic progression by maintaining the accuracy of spindle assembly in human oocytes, thus promoting oocyte maturation and subsequent development of the embryo.

PMID:
27917907
PMCID:
PMC5137016
DOI:
10.1038/srep38192
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center