论文成果
Interference with the C-terminalstructure of MARF1 causes defective oocyte meiotic division and female infertility in mice.
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发表刊物：
J Biomed Res
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刊物所在地：
CHINA
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关键字：
MARF1, meiosis, oocyte aneuploidy, female infertility, knock in, CRISPER/Cas9
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摘要：
Meiosis-arrest female 1 (MARF1) is a recently identified key oogenic regulator essential for the maintenance of female fertility and genome integrity in mice. However, the detailed functions and the underlying mechanisms of MARF1 remain elusive. Here, in an attempt to create a mouse model expressing fluorescent protein-tagged MARF1 to facilitate further exploration of the roles of MARF1 in oocytes, we produced a Marf1-eGFP knockin (KI) mouse line in which the C-terminal structure and function of MARF1 were interfered by its fusing eGFP peptide. Using these Marf1-eGFP-KI mice, we revealed, unexpectedly, the functions of MARF1 in the control of oocyte meiotic division. We found that the Marf1-eGFP-KI females ovulated mature oocytes with severe meiotic and developmental defects, and thus were infertile. Moreover, meiotic reinitiation was delayed while meiotic completion was accelerated in the KI-oocytes, which was coincident with the increased incidence of oocyte aneuploidy. Therefore, MARF1 is indispensable for maintaining the fidelity of homolog segregation during oocyte maturation, and this function relies on its C-terminal domains.
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全部作者：
Ming-Zhe Li, Hao Wang, Lan-Ying Shi
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第一作者：
Guang-Yi Cao
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论文类型：
Research Article
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通讯作者：
You-Qiang Su
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论文编号：
10.7555/JBR.32.20170108
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卷号：
32
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期号：
1
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页面范围：
58-67
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ISSN号：
1674-8301
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是否译文：
否
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CN号：
32-1810/R
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发表时间：
2018-01-18
上一条：Participation of EML6 in the regulation of oocyte meiotic progression in mice.
下一条：The RNA-binding protein MARF1 promotes cortical neurogenesis through its RNase activity domain.
