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Chk2 Regulates Cell Cycle Progression during Mouse Oocyte Maturation and Early Embryo Development
As a tumor suppressor homologue during mitosis, Chk2 is involved in replication checkpoints, DNA repair, and cell cycle arrest, although its functions during mouse oocyte meiosis and early embryo development remain uncertain. We investigated the functions of Chk2 during mouse oocyte maturation and e...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Korea Society for Molecular and Cellular Biology
2014
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3935625/ https://www.ncbi.nlm.nih.gov/pubmed/24598997 http://dx.doi.org/10.14348/molcells.2014.2259 |
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author | Dai, Xiao-Xin Duan, Xing Liu, Hong-Lin Cui, Xiang-Shun Kim, Nam-Hyung Sun, Shao-Chen |
author_facet | Dai, Xiao-Xin Duan, Xing Liu, Hong-Lin Cui, Xiang-Shun Kim, Nam-Hyung Sun, Shao-Chen |
author_sort | Dai, Xiao-Xin |
collection | PubMed |
description | As a tumor suppressor homologue during mitosis, Chk2 is involved in replication checkpoints, DNA repair, and cell cycle arrest, although its functions during mouse oocyte meiosis and early embryo development remain uncertain. We investigated the functions of Chk2 during mouse oocyte maturation and early embryo development. Chk2 exhibited a dynamic localization pattern; Chk2 expression was restricted to germinal vesicles at the germinal vesicle (GV) stage, was associated with centromeres at pro-metaphase I (Pro-MI), and localized to spindle poles at metaphase I (MI). Disrupting Chk2 activity resulted in cell cycle progression defects. First, inhibitor-treated oocytes were arrested at the GV stage and failed to undergo germinal vesicle breakdown (GVBD); this could be rescued after Chk2 inhibition release. Second, Chk2 inhibition after oocyte GVBD caused MI arrest. Third, the first cleavage of early embryo development was disrupted by Chk2 inhibition. Additionally, in inhibitor-treated oocytes, checkpoint protein Bub3 expression was consistently localized at centromeres at the MI stage, which indicated that the spindle assembly checkpoint (SAC) was activated. Moreover, disrupting Chk2 activity in oocytes caused severe chromosome misalignments and spindle disruption. In inhibitor-treated oocytes, centrosome protein γ-tubulin and Polo-like kinase 1 (Plk1) were dissociated from spindle poles. These results indicated that Chk2 regulated cell cycle progression and spindle assembly during mouse oocyte maturation and early embryo development. |
format | Online Article Text |
id | pubmed-3935625 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Korea Society for Molecular and Cellular Biology |
record_format | MEDLINE/PubMed |
spelling | pubmed-39356252014-02-26 Chk2 Regulates Cell Cycle Progression during Mouse Oocyte Maturation and Early Embryo Development Dai, Xiao-Xin Duan, Xing Liu, Hong-Lin Cui, Xiang-Shun Kim, Nam-Hyung Sun, Shao-Chen Mol Cells As a tumor suppressor homologue during mitosis, Chk2 is involved in replication checkpoints, DNA repair, and cell cycle arrest, although its functions during mouse oocyte meiosis and early embryo development remain uncertain. We investigated the functions of Chk2 during mouse oocyte maturation and early embryo development. Chk2 exhibited a dynamic localization pattern; Chk2 expression was restricted to germinal vesicles at the germinal vesicle (GV) stage, was associated with centromeres at pro-metaphase I (Pro-MI), and localized to spindle poles at metaphase I (MI). Disrupting Chk2 activity resulted in cell cycle progression defects. First, inhibitor-treated oocytes were arrested at the GV stage and failed to undergo germinal vesicle breakdown (GVBD); this could be rescued after Chk2 inhibition release. Second, Chk2 inhibition after oocyte GVBD caused MI arrest. Third, the first cleavage of early embryo development was disrupted by Chk2 inhibition. Additionally, in inhibitor-treated oocytes, checkpoint protein Bub3 expression was consistently localized at centromeres at the MI stage, which indicated that the spindle assembly checkpoint (SAC) was activated. Moreover, disrupting Chk2 activity in oocytes caused severe chromosome misalignments and spindle disruption. In inhibitor-treated oocytes, centrosome protein γ-tubulin and Polo-like kinase 1 (Plk1) were dissociated from spindle poles. These results indicated that Chk2 regulated cell cycle progression and spindle assembly during mouse oocyte maturation and early embryo development. Korea Society for Molecular and Cellular Biology 2014-02-28 2014-02-19 /pmc/articles/PMC3935625/ /pubmed/24598997 http://dx.doi.org/10.14348/molcells.2014.2259 Text en © The Korean Society for Molecular and Cellular Biology. All rights reserved. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/. |
spellingShingle | Dai, Xiao-Xin Duan, Xing Liu, Hong-Lin Cui, Xiang-Shun Kim, Nam-Hyung Sun, Shao-Chen Chk2 Regulates Cell Cycle Progression during Mouse Oocyte Maturation and Early Embryo Development |
title | Chk2 Regulates Cell Cycle Progression during Mouse Oocyte Maturation and Early Embryo Development |
title_full | Chk2 Regulates Cell Cycle Progression during Mouse Oocyte Maturation and Early Embryo Development |
title_fullStr | Chk2 Regulates Cell Cycle Progression during Mouse Oocyte Maturation and Early Embryo Development |
title_full_unstemmed | Chk2 Regulates Cell Cycle Progression during Mouse Oocyte Maturation and Early Embryo Development |
title_short | Chk2 Regulates Cell Cycle Progression during Mouse Oocyte Maturation and Early Embryo Development |
title_sort | chk2 regulates cell cycle progression during mouse oocyte maturation and early embryo development |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3935625/ https://www.ncbi.nlm.nih.gov/pubmed/24598997 http://dx.doi.org/10.14348/molcells.2014.2259 |
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