CHK1 controls zygote pronuclear envelope breakdown by regulating F-actin through interacting with MICAL3

CHK1 mutations could cause human zygote arrest at the pronuclei stage, a phenomenon that is not well understood at the molecular level. In this study, we conducted experiments where pre-pronuclei from zygotes with CHK1 mutation were transferred into the cytoplasm of normal enucleated fertilized eggs. This approach rescued the zygote arrest caused by the mutation, resulting in the production of a high-quality blastocyst. This suggests that CHK1 dysfunction primarily disrupts crucial biological processes occurring in the cytoplasm. Further investigation reveals that CHK1 mutants have an impact on the F-actin meshwork, leading to disturbances in pronuclear envelope breakdown. Through co-immunoprecipitation and mass spectrometry analysis of around 6000 mouse zygotes, we identified an interaction between CHK1 and MICAL3, a key regulator of F-actin disassembly. The gain-of-function mutants of CHK1 enhance their interaction with MICAL3 and increase MICAL3 enzymatic activity, resulting in excessive depolymerization of F-actin. These findings shed light on the regulatory mechanism behind pronuclear envelope breakdown during the transition from meiosis to the first mitosis in mammals.

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Publication Details

Journal
EMBO Reports
Published
2024-10-02
DOI
https://doi.org/10.1038/s44319-024-00267-7
Citations
1
Primary Topic
Microtubule and mitosis dynamics
Type
article
Field-Weighted Citation Impact
0.33

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article

CHK1 controls zygote pronuclear envelope breakdown by regulating F-actin through interacting with MICAL3

H. W. Zhang, Shigang Zhao, Zhenzhen Hou, Keliang Wu et al.
1 citations
EMBO Reports
Microtubule and mitosis dynamics
0.33
article

CHK1 controls zygote pronuclear envelope breakdown by regulating F-actin through interacting with MICAL3

H. W. Zhang, Shigang Zhao, Zhenzhen Hou, Keliang Wu, Mengge Zhang, Yuehong Bian, Tailai Chen, Mei Li, Han Zhao, Zi‐Jiang Chen, Bohan Yang, Ying Cui, Wei Su
article en
1 citations

Abstract

CHK1 mutations could cause human zygote arrest at the pronuclei stage, a phenomenon that is not well understood at the molecular level. In this study, we conducted experiments where pre-pronuclei from zygotes with CHK1 mutation were transferred into the cytoplasm of normal enucleated fertilized eggs. This approach rescued the zygote arrest caused by the mutation, resulting in the production of a high-quality blastocyst. This suggests that CHK1 dysfunction primarily disrupts crucial biological processes occurring in the cytoplasm. Further investigation reveals that CHK1 mutants have an impact on the F-actin meshwork, leading to disturbances in pronuclear envelope breakdown. Through co-immunoprecipitation and mass spectrometry analysis of around 6000 mouse zygotes, we identified an interaction between CHK1 and MICAL3, a key regulator of F-actin disassembly. The gain-of-function mutants of CHK1 enhance their interaction with MICAL3 and increase MICAL3 enzymatic activity, resulting in excessive depolymerization of F-actin. These findings shed light on the regulatory mechanism behind pronuclear envelope breakdown during the transition from meiosis to the first mitosis in mammals.

EMBO ReportsVol. 25(11)
Shandong University (CN), Shanghai Jiao Tong University (CN), Chinese Academy of Medical Sciences & Peking Union Medical College (CN), Renji Hospital (CN), Shandong Mental Health Center (CN), Suzhou Municipal Hospital (CN), Shandong Provincial Hospital (CN), Shandong Women’s University (CN), Shandong First Medical University (CN), Shandong Academy of Chinese Medicine (CN), Nanjing Medical University (CN)
Shandong University, National Natural Science Foundation of China, Nanjing Medical University, National Outstanding Youth Science Fund Project of National Natural Science Foundation of China, National Key Research and Development Program of China
Openalex Percentile: Top 41%
Microtubule and mitosis dynamics
0.33
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