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ING3 Is Essential for Asymmetric Cell Division during Mouse Oocyte Maturation
ING3 (inhibitor of growth family, member 3) is a subunit of the nucleosome acetyltransferase of histone 4 (NuA4) complex, which activates gene expression. ING3, which contains a plant homeodomain (PHD) motif that can bind to trimethylated lysine 4 on histone H3 (H3K4me3), is ubiquitously expressed i...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3774679/ https://www.ncbi.nlm.nih.gov/pubmed/24066152 http://dx.doi.org/10.1371/journal.pone.0074749 |
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author | Suzuki, Shinnosuke Nozawa, Yusuke Tsukamoto, Satoshi Kaneko, Takehito Imai, Hiroshi Minami, Naojiro |
author_facet | Suzuki, Shinnosuke Nozawa, Yusuke Tsukamoto, Satoshi Kaneko, Takehito Imai, Hiroshi Minami, Naojiro |
author_sort | Suzuki, Shinnosuke |
collection | PubMed |
description | ING3 (inhibitor of growth family, member 3) is a subunit of the nucleosome acetyltransferase of histone 4 (NuA4) complex, which activates gene expression. ING3, which contains a plant homeodomain (PHD) motif that can bind to trimethylated lysine 4 on histone H3 (H3K4me3), is ubiquitously expressed in mammalian tissues and governs transcriptional regulation, cell cycle control, and apoptosis via p53-mediated transcription or the Fas/caspase-8 pathway. Thus, ING3 plays a number of important roles in various somatic cells. However, the role(s) of ING3 in germ cells remains unknown. Here, we show that loss of ING3 function led to the failure of asymmetric cell division and cortical reorganization in the mouse oocyte. Immunostaining showed that in fully grown germinal vesicle (GV) oocytes, ING3 localized predominantly in the GV. After germinal vesicle breakdown (GVBD), ING3 homogeneously localized in the cytoplasm. In oocytes where Ing3 was targeted by siRNA microinjection, we observed symmetric cell division during mouse oocyte maturation. In those oocytes, oocyte polarization was not established due to the failure to form an actin cap or a cortical granule-free domain (CGFD), the lack of which inhibited spindle migration. These features were among the main causes of abnormal symmetric cell division. Interestingly, an analysis of the mRNA expression levels of genes related to asymmetric cell division revealed that only mTOR was downregulated, and, furthermore, that genes downstream of mTOR (e.g., Cdc42, Rac1, and RhoA) were also downregulated in siIng3-injected oocytes. Therefore, ING3 may regulate asymmetric cell division through the mTOR pathway during mouse oocyte maturation. |
format | Online Article Text |
id | pubmed-3774679 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-37746792013-09-24 ING3 Is Essential for Asymmetric Cell Division during Mouse Oocyte Maturation Suzuki, Shinnosuke Nozawa, Yusuke Tsukamoto, Satoshi Kaneko, Takehito Imai, Hiroshi Minami, Naojiro PLoS One Research Article ING3 (inhibitor of growth family, member 3) is a subunit of the nucleosome acetyltransferase of histone 4 (NuA4) complex, which activates gene expression. ING3, which contains a plant homeodomain (PHD) motif that can bind to trimethylated lysine 4 on histone H3 (H3K4me3), is ubiquitously expressed in mammalian tissues and governs transcriptional regulation, cell cycle control, and apoptosis via p53-mediated transcription or the Fas/caspase-8 pathway. Thus, ING3 plays a number of important roles in various somatic cells. However, the role(s) of ING3 in germ cells remains unknown. Here, we show that loss of ING3 function led to the failure of asymmetric cell division and cortical reorganization in the mouse oocyte. Immunostaining showed that in fully grown germinal vesicle (GV) oocytes, ING3 localized predominantly in the GV. After germinal vesicle breakdown (GVBD), ING3 homogeneously localized in the cytoplasm. In oocytes where Ing3 was targeted by siRNA microinjection, we observed symmetric cell division during mouse oocyte maturation. In those oocytes, oocyte polarization was not established due to the failure to form an actin cap or a cortical granule-free domain (CGFD), the lack of which inhibited spindle migration. These features were among the main causes of abnormal symmetric cell division. Interestingly, an analysis of the mRNA expression levels of genes related to asymmetric cell division revealed that only mTOR was downregulated, and, furthermore, that genes downstream of mTOR (e.g., Cdc42, Rac1, and RhoA) were also downregulated in siIng3-injected oocytes. Therefore, ING3 may regulate asymmetric cell division through the mTOR pathway during mouse oocyte maturation. Public Library of Science 2013-09-16 /pmc/articles/PMC3774679/ /pubmed/24066152 http://dx.doi.org/10.1371/journal.pone.0074749 Text en © 2013 Suzuki et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Suzuki, Shinnosuke Nozawa, Yusuke Tsukamoto, Satoshi Kaneko, Takehito Imai, Hiroshi Minami, Naojiro ING3 Is Essential for Asymmetric Cell Division during Mouse Oocyte Maturation |
title | ING3 Is Essential for Asymmetric Cell Division during Mouse Oocyte Maturation |
title_full | ING3 Is Essential for Asymmetric Cell Division during Mouse Oocyte Maturation |
title_fullStr | ING3 Is Essential for Asymmetric Cell Division during Mouse Oocyte Maturation |
title_full_unstemmed | ING3 Is Essential for Asymmetric Cell Division during Mouse Oocyte Maturation |
title_short | ING3 Is Essential for Asymmetric Cell Division during Mouse Oocyte Maturation |
title_sort | ing3 is essential for asymmetric cell division during mouse oocyte maturation |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3774679/ https://www.ncbi.nlm.nih.gov/pubmed/24066152 http://dx.doi.org/10.1371/journal.pone.0074749 |
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