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...
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| 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. |
| doi_str_mv | 10.1371/journal.pone.0074749 |
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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.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0074749</identifier><identifier>PMID: 24066152</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acetyltransferase ; Actin ; Analysis ; Animals ; Apoptosis ; Asymmetric Cell Division - genetics ; Asymmetric Cell Division - physiology ; Asymmetry ; Biology ; Caspase ; Caspase-8 ; Cdc42 protein ; Cell cycle ; Cell division ; Cells, Cultured ; Cortex ; Cytoplasm ; Female ; Gene expression ; Gene regulation ; Genes ; Germ cells ; Histone H3 ; Homeobox ; Homeodomain Proteins - genetics ; Homeodomain Proteins - metabolism ; Infertility ; Laboratory animals ; Lysine ; Mammals ; Maturation ; Melanoma ; Mice ; Mice, Inbred ICR ; Microinjection ; Muscle proteins ; Oocytes ; Oocytes - cytology ; Oocytes - metabolism ; p53 Protein ; Polymerization ; Rac1 protein ; RhoA protein ; RNA ; siRNA ; Tissues ; TOR Serine-Threonine Kinases - genetics ; TOR Serine-Threonine Kinases - metabolism ; Transcription ; Tumor proteins</subject><ispartof>PloS one, 2013-09, Vol.8 (9), p.e74749-e74749</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Suzuki et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Suzuki et al 2013 Suzuki et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c736t-c8101f4efe80729406b15660f094ea8f187134f576860fd63625d202ce14ba973</citedby><cites>FETCH-LOGICAL-c736t-c8101f4efe80729406b15660f094ea8f187134f576860fd63625d202ce14ba973</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3774679/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3774679/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24066152$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Suzuki, Shinnosuke</creatorcontrib><creatorcontrib>Nozawa, Yusuke</creatorcontrib><creatorcontrib>Tsukamoto, Satoshi</creatorcontrib><creatorcontrib>Kaneko, Takehito</creatorcontrib><creatorcontrib>Imai, Hiroshi</creatorcontrib><creatorcontrib>Minami, Naojiro</creatorcontrib><title>ING3 is essential for asymmetric cell division during mouse oocyte maturation</title><title>PloS one</title><addtitle>PLoS One</addtitle><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. 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Therefore, ING3 may regulate asymmetric cell division through the mTOR pathway during mouse oocyte maturation.</description><subject>Acetyltransferase</subject><subject>Actin</subject><subject>Analysis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Asymmetric Cell Division - genetics</subject><subject>Asymmetric Cell Division - physiology</subject><subject>Asymmetry</subject><subject>Biology</subject><subject>Caspase</subject><subject>Caspase-8</subject><subject>Cdc42 protein</subject><subject>Cell cycle</subject><subject>Cell division</subject><subject>Cells, Cultured</subject><subject>Cortex</subject><subject>Cytoplasm</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene regulation</subject><subject>Genes</subject><subject>Germ cells</subject><subject>Histone H3</subject><subject>Homeobox</subject><subject>Homeodomain Proteins - genetics</subject><subject>Homeodomain Proteins - metabolism</subject><subject>Infertility</subject><subject>Laboratory animals</subject><subject>Lysine</subject><subject>Mammals</subject><subject>Maturation</subject><subject>Melanoma</subject><subject>Mice</subject><subject>Mice, Inbred ICR</subject><subject>Microinjection</subject><subject>Muscle proteins</subject><subject>Oocytes</subject><subject>Oocytes - cytology</subject><subject>Oocytes - metabolism</subject><subject>p53 Protein</subject><subject>Polymerization</subject><subject>Rac1 protein</subject><subject>RhoA protein</subject><subject>RNA</subject><subject>siRNA</subject><subject>Tissues</subject><subject>TOR Serine-Threonine Kinases - genetics</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><subject>Transcription</subject><subject>Tumor proteins</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl2L1DAUhoso7rr6D0QLgujFjPlq0t4Iy6LrwOqCX7fhNE1mMrTNmKSL8-9Nne4ylb2QXqScPOc9yZs3y55jtMRU4HdbN_ge2uXO9XqJkGCCVQ-yU1xRsuAE0YdH_yfZkxC2CBW05PxxdkIY4hwX5DT7vPpySXMbch2C7qOFNjfO5xD2XaejtypXum3zxt7YYF2fN4O3_Trv3BB07pzaR513EAcPMW0_zR4ZaIN-Nq1n2Y-PH75ffFpcXV-uLs6vFkpQHheqxAgbpo0ukSBVOkyNC86RQRXTUBpcCkyZKQQvU7HhlJOiIYgojVkNlaBn2cuD7q51QU5OBIkZpYhVuECJWB2IxsFW7rztwO-lAyv_FpxfS_DRqlZLWmtDaoxrTkpGCYGGNqgSqABAYJpx2vtp2lB3ulHJJw_tTHS-09uNXLsbSYVgXFRJ4M0k4N2vQYcoOxtGX6HXycjx3AJjUQiS0Ff_oPffbqLWkC5ge-PSXDWKynMmSsI4LYpELe-h0tfozqoUG2NTfdbwdtaQmKh_xzUMIcjVt6__z17_nLOvj9iNhjZugmuHMTJhDrIDqLwLwWtzZzJGckz9rRtyTL2cUp_aXhw_0F3TbczpH8Lh-vc</recordid><startdate>20130916</startdate><enddate>20130916</enddate><creator>Suzuki, Shinnosuke</creator><creator>Nozawa, Yusuke</creator><creator>Tsukamoto, Satoshi</creator><creator>Kaneko, Takehito</creator><creator>Imai, Hiroshi</creator><creator>Minami, Naojiro</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130916</creationdate><title>ING3 is essential for asymmetric cell division during mouse oocyte maturation</title><author>Suzuki, Shinnosuke ; Nozawa, Yusuke ; Tsukamoto, Satoshi ; Kaneko, Takehito ; Imai, Hiroshi ; Minami, Naojiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c736t-c8101f4efe80729406b15660f094ea8f187134f576860fd63625d202ce14ba973</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Acetyltransferase</topic><topic>Actin</topic><topic>Analysis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Asymmetric Cell Division - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Suzuki, Shinnosuke</au><au>Nozawa, Yusuke</au><au>Tsukamoto, Satoshi</au><au>Kaneko, Takehito</au><au>Imai, Hiroshi</au><au>Minami, Naojiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ING3 is essential for asymmetric cell division during mouse oocyte maturation</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-09-16</date><risdate>2013</risdate><volume>8</volume><issue>9</issue><spage>e74749</spage><epage>e74749</epage><pages>e74749-e74749</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>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.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24066152</pmid><doi>10.1371/journal.pone.0074749</doi><tpages>e74749</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 1932-6203 1932-6203 |
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| subjects | Acetyltransferase Actin Analysis Animals Apoptosis Asymmetric Cell Division - genetics Asymmetric Cell Division - physiology Asymmetry Biology Caspase Caspase-8 Cdc42 protein Cell cycle Cell division Cells, Cultured Cortex Cytoplasm Female Gene expression Gene regulation Genes Germ cells Histone H3 Homeobox Homeodomain Proteins - genetics Homeodomain Proteins - metabolism Infertility Laboratory animals Lysine Mammals Maturation Melanoma Mice Mice, Inbred ICR Microinjection Muscle proteins Oocytes Oocytes - cytology Oocytes - metabolism p53 Protein Polymerization Rac1 protein RhoA protein RNA siRNA Tissues TOR Serine-Threonine Kinases - genetics TOR Serine-Threonine Kinases - metabolism Transcription Tumor proteins |
| title | ING3 is essential for asymmetric cell division during mouse oocyte maturation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-01T20%3A23%3A13IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=ING3%20is%20essential%20for%20asymmetric%20cell%20division%20during%20mouse%20oocyte%20maturation&rft.jtitle=PloS%20one&rft.au=Suzuki,%20Shinnosuke&rft.date=2013-09-16&rft.volume=8&rft.issue=9&rft.spage=e74749&rft.epage=e74749&rft.pages=e74749-e74749&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0074749&rft_dat=%3Cgale_plos_%3EA478246355%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1433049150&rft_id=info:pmid/24066152&rft_galeid=A478246355&rft_doaj_id=oai_doaj_org_article_3bef2b11b6284322ad3d09705aa0afd7&rfr_iscdi=true |