UHRF1 is essential for proper cytoplasmic architecture and function of mouse oocytes and derived embryos
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- Shuhei Uemura
- Division of Epigenomics and Development, Medical Institute of Bioregulation, Kyushu University
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- Shoji Maenohara
- Division of Epigenomics and Development, Medical Institute of Bioregulation, Kyushu University
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- Kimiko Inoue
- Bioresource Engineering Division, RIKEN BioResource Research Center
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- Narumi Ogonuki
- Bioresource Engineering Division, RIKEN BioResource Research Center
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- Shogo Matoba
- Bioresource Engineering Division, RIKEN BioResource Research Center
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- Atsuo Ogura
- Bioresource Engineering Division, RIKEN BioResource Research Center
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- Mayuko Kurumizaka
- Center for Genetic Analysis of Biological Responses, Research Institute for Microbial Diseases, Osaka University
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- Kazuo Yamagata
- Center for Genetic Analysis of Biological Responses, Research Institute for Microbial Diseases, Osaka University
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- Jafar Sharif
- Laboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan
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- Haruhiko Koseki
- Laboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan
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- Koji Ueda
- Cancer Proteomics Group, Cancer Precision Medicine Center, Japanese Foundation for Cancer Research, Tokyo, Japan
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- Motoko Unoki
- Division of Epigenomics and Development, Medical Institute of Bioregulation, Kyushu University
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- Hiroyuki Sasaki
- Division of Epigenomics and Development, Medical Institute of Bioregulation, Kyushu University
説明
<jats:p>Ubiquitin-like with PHD and RING finger domains 1 (UHRF1) is a protein essential for the maintenance of DNA methylation in somatic cells. However, UHRF1 is predominantly localized in the cytoplasm of mouse oocytes and preimplantation embryos, where it may play a role unrelated to the nuclear function. We herein report that oocyte-specific<jats:italic>Uhrf1</jats:italic>KO results in impaired chromosome segregation, abnormal cleavage division, and preimplantation lethality of derived embryos. Our nuclear transfer experiment showed that the phenotype is attributable to cytoplasmic rather than nuclear defects of the zygotes. A proteomic analysis of KO oocytes revealed the down-regulation of proteins associated with microtubules including tubulins, which occurred independently of transcriptomic changes. Intriguingly, cytoplasmic lattices were disorganized, and mitochondria, endoplasmic reticulum, and components of the subcortical maternal complex were mislocalized. Thus, maternal UHRF1 regulates the proper cytoplasmic architecture and function of oocytes and preimplantation embryos, likely through a mechanism unrelated to DNA methylation.</jats:p>
収録刊行物
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- Life Science Alliance
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Life Science Alliance 6 (8), e202301904-, 2023-05-24
Life Science Alliance, LLC
