Primordial follicle activation is affected by the absence of Sohlh1 in mice
Previous studies have reported that only primordial follicles and empty follicles can be found in 7.5 days postparturition (dpp) Sohlh1−/− mouse ovaries and females are infertility. There appears to be a defect in follicle development during the primordial‐to‐primary follicle transition in Sohlh1−/−...
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| Veröffentlicht in: | Molecular reproduction and development 2019-01, Vol.86 (1), p.20-31 |
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| creator | Liu, Gongqing Li, Yuan Du, Bing Sun, Qi Qi, Wanjing Liu, Yuan Zhang, Xue Jin, Meiyu Zheng, Zhihong |
| description | Previous studies have reported that only primordial follicles and empty follicles can be found in 7.5 days postparturition (dpp) Sohlh1−/− mouse ovaries and females are infertility. There appears to be a defect in follicle development during the primordial‐to‐primary follicle transition in Sohlh1−/− mouse ovaries. However, detailed analyses of these phenomena have not been performed. In this study, we used Sohlh1−/− transgenic mice to explore the role of Sohlh1 in folliculogenesis. The results showed that only primordial follicles and empty follicles can be observed in Sohlh1−/− ovaries from 0.5 to 23.5 dpp. The expression of Foxo3 and FOXO3 was downregulated; nucleocytoplasmic shuttling of FOXO3 was normal in 7.5‐dpp Sohlh1+/+ but not Sohlh1−/− ovaries; and primordial follicle activation (PFA) was not observed in 7.5‐dpp Sohlh1−/− mice. The expression levels of KIT, AKT, and P308‐AKT were downregulated (p 0.05). The KIT/PI3K/AKT pathway was inhibited. Furthermore, we conducted a dual luciferase assay and chromatin immunoprecipitation. The results showed that SOHLH1 can upregulate the Kit gene by binding to the −3698 bp E‐box motif. The absence of Sohlh1 may affect PFA in mouse ovaries via downregulation of Kit and inhibition of the KIT/PI3K/AKT pathway.
The absence of spermatogenesis‐ and oogenesis‐specific basic helix‐loop‐helix 1 (SOHLH1) can influence folliculogenesis by affecting primordial follicle activation in the ovaries, and can lead to disruption of the KIT/PI3K/AKT/FOXO3 pathway. SOHLH1 can control Kit by binding to −3698 E‐box site. |
| doi_str_mv | 10.1002/mrd.23078 |
| format | Article |
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The absence of spermatogenesis‐ and oogenesis‐specific basic helix‐loop‐helix 1 (SOHLH1) can influence folliculogenesis by affecting primordial follicle activation in the ovaries, and can lead to disruption of the KIT/PI3K/AKT/FOXO3 pathway. SOHLH1 can control Kit by binding to −3698 E‐box site.</description><identifier>ISSN: 1040-452X</identifier><identifier>EISSN: 1098-2795</identifier><identifier>DOI: 10.1002/mrd.23078</identifier><identifier>PMID: 30358927</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT ; AKT protein ; Animals ; Basic Helix-Loop-Helix Transcription Factors - genetics ; Basic Helix-Loop-Helix Transcription Factors - metabolism ; Chromatin ; Female ; Females ; Follicles ; Folliculogenesis ; Forkhead Box Protein O3 - genetics ; Forkhead Box Protein O3 - metabolism ; FOXO3 protein ; Gene Expression Regulation ; HEK293 Cells ; Humans ; Immunoprecipitation ; Infertility ; KIT protein ; Mice ; Mice, Knockout ; Ovarian Follicle - growth & development ; Ovaries ; PI3K ; primordial follicle activation ; Proto-Oncogene Proteins c-kit - biosynthesis ; Proto-Oncogene Proteins c-kit - genetics ; Response Elements ; Signal Transduction ; Sohlh1 ; Transgenic mice</subject><ispartof>Molecular reproduction and development, 2019-01, Vol.86 (1), p.20-31</ispartof><rights>2018 Wiley Periodicals, Inc.</rights><rights>2019 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3538-e38b8adcb7c80d35a0e178fb2f13759890cac6d8fd030b407cb6994ee465d4ea3</citedby><cites>FETCH-LOGICAL-c3538-e38b8adcb7c80d35a0e178fb2f13759890cac6d8fd030b407cb6994ee465d4ea3</cites><orcidid>0000-0002-6814-150X ; 0000-0001-7595-6849</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fmrd.23078$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmrd.23078$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30358927$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Gongqing</creatorcontrib><creatorcontrib>Li, Yuan</creatorcontrib><creatorcontrib>Du, Bing</creatorcontrib><creatorcontrib>Sun, Qi</creatorcontrib><creatorcontrib>Qi, Wanjing</creatorcontrib><creatorcontrib>Liu, Yuan</creatorcontrib><creatorcontrib>Zhang, Xue</creatorcontrib><creatorcontrib>Jin, Meiyu</creatorcontrib><creatorcontrib>Zheng, Zhihong</creatorcontrib><title>Primordial follicle activation is affected by the absence of Sohlh1 in mice</title><title>Molecular reproduction and development</title><addtitle>Mol Reprod Dev</addtitle><description>Previous studies have reported that only primordial follicles and empty follicles can be found in 7.5 days postparturition (dpp) Sohlh1−/− mouse ovaries and females are infertility. There appears to be a defect in follicle development during the primordial‐to‐primary follicle transition in Sohlh1−/− mouse ovaries. However, detailed analyses of these phenomena have not been performed. In this study, we used Sohlh1−/− transgenic mice to explore the role of Sohlh1 in folliculogenesis. The results showed that only primordial follicles and empty follicles can be observed in Sohlh1−/− ovaries from 0.5 to 23.5 dpp. The expression of Foxo3 and FOXO3 was downregulated; nucleocytoplasmic shuttling of FOXO3 was normal in 7.5‐dpp Sohlh1+/+ but not Sohlh1−/− ovaries; and primordial follicle activation (PFA) was not observed in 7.5‐dpp Sohlh1−/− mice. The expression levels of KIT, AKT, and P308‐AKT were downregulated (p < 0.05), whereas that of P473‐AKT was not significantly changed (p > 0.05). The KIT/PI3K/AKT pathway was inhibited. Furthermore, we conducted a dual luciferase assay and chromatin immunoprecipitation. The results showed that SOHLH1 can upregulate the Kit gene by binding to the −3698 bp E‐box motif. The absence of Sohlh1 may affect PFA in mouse ovaries via downregulation of Kit and inhibition of the KIT/PI3K/AKT pathway.
The absence of spermatogenesis‐ and oogenesis‐specific basic helix‐loop‐helix 1 (SOHLH1) can influence folliculogenesis by affecting primordial follicle activation in the ovaries, and can lead to disruption of the KIT/PI3K/AKT/FOXO3 pathway. SOHLH1 can control Kit by binding to −3698 E‐box site.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Basic Helix-Loop-Helix Transcription Factors - genetics</subject><subject>Basic Helix-Loop-Helix Transcription Factors - metabolism</subject><subject>Chromatin</subject><subject>Female</subject><subject>Females</subject><subject>Follicles</subject><subject>Folliculogenesis</subject><subject>Forkhead Box Protein O3 - genetics</subject><subject>Forkhead Box Protein O3 - metabolism</subject><subject>FOXO3 protein</subject><subject>Gene Expression Regulation</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Infertility</subject><subject>KIT protein</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Ovarian Follicle - growth & development</subject><subject>Ovaries</subject><subject>PI3K</subject><subject>primordial follicle activation</subject><subject>Proto-Oncogene Proteins c-kit - biosynthesis</subject><subject>Proto-Oncogene Proteins c-kit - genetics</subject><subject>Response Elements</subject><subject>Signal Transduction</subject><subject>Sohlh1</subject><subject>Transgenic mice</subject><issn>1040-452X</issn><issn>1098-2795</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10M1LHDEYx_FQlPrSHvoPlIAXPYw-SSY7ybH4jpaWvkBvQyZ5wkYyE53MKvvfm3VXDwVPCeTDj_Al5AuDYwbAT_rRHXMBjfpAdhloVfFGy63VvYaqlvzfDtnL-Q4AtFbwkewIEFJp3uySm59j6NPogonUpxiDjUiNncKjmUIaaMjUeI92Qke7JZ3m5bXLOFikydPfaR7njIaB9sHiJ7LtTcz4eXPuk78X539Or6rbH5fXp99uKyukUBUK1SnjbNdYBU5IA8ga5TvumWikVhqssTOnvAMBXQ2N7WZa14j1TLoajdgnh-vd-zE9LDBPbR-yxRjNgGmRW864FFAzkIUe_Efv0mIcyu-KmtWMgxaiqKO1smPKeUTf3pcqZly2DNpV4bYUbl8KF_t1s7joenRv8jVpASdr8BQiLt9far__OltPPgNVTYOw</recordid><startdate>201901</startdate><enddate>201901</enddate><creator>Liu, Gongqing</creator><creator>Li, Yuan</creator><creator>Du, Bing</creator><creator>Sun, Qi</creator><creator>Qi, Wanjing</creator><creator>Liu, Yuan</creator><creator>Zhang, Xue</creator><creator>Jin, Meiyu</creator><creator>Zheng, Zhihong</creator><general>Wiley Subscription Services, Inc</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>7QP</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-6814-150X</orcidid><orcidid>https://orcid.org/0000-0001-7595-6849</orcidid></search><sort><creationdate>201901</creationdate><title>Primordial follicle activation is affected by the absence of Sohlh1 in mice</title><author>Liu, Gongqing ; Li, Yuan ; Du, Bing ; Sun, Qi ; Qi, Wanjing ; Liu, Yuan ; Zhang, Xue ; Jin, Meiyu ; Zheng, Zhihong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3538-e38b8adcb7c80d35a0e178fb2f13759890cac6d8fd030b407cb6994ee465d4ea3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT</topic><topic>AKT protein</topic><topic>Animals</topic><topic>Basic Helix-Loop-Helix Transcription Factors - genetics</topic><topic>Basic Helix-Loop-Helix Transcription Factors - metabolism</topic><topic>Chromatin</topic><topic>Female</topic><topic>Females</topic><topic>Follicles</topic><topic>Folliculogenesis</topic><topic>Forkhead Box Protein O3 - genetics</topic><topic>Forkhead Box Protein O3 - metabolism</topic><topic>FOXO3 protein</topic><topic>Gene Expression Regulation</topic><topic>HEK293 Cells</topic><topic>Humans</topic><topic>Immunoprecipitation</topic><topic>Infertility</topic><topic>KIT protein</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Ovarian Follicle - growth & development</topic><topic>Ovaries</topic><topic>PI3K</topic><topic>primordial follicle activation</topic><topic>Proto-Oncogene Proteins c-kit - biosynthesis</topic><topic>Proto-Oncogene Proteins c-kit - genetics</topic><topic>Response Elements</topic><topic>Signal Transduction</topic><topic>Sohlh1</topic><topic>Transgenic mice</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Gongqing</creatorcontrib><creatorcontrib>Li, Yuan</creatorcontrib><creatorcontrib>Du, Bing</creatorcontrib><creatorcontrib>Sun, Qi</creatorcontrib><creatorcontrib>Qi, Wanjing</creatorcontrib><creatorcontrib>Liu, Yuan</creatorcontrib><creatorcontrib>Zhang, Xue</creatorcontrib><creatorcontrib>Jin, Meiyu</creatorcontrib><creatorcontrib>Zheng, Zhihong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular reproduction and development</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Gongqing</au><au>Li, Yuan</au><au>Du, Bing</au><au>Sun, Qi</au><au>Qi, Wanjing</au><au>Liu, Yuan</au><au>Zhang, Xue</au><au>Jin, Meiyu</au><au>Zheng, Zhihong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Primordial follicle activation is affected by the absence of Sohlh1 in mice</atitle><jtitle>Molecular reproduction and development</jtitle><addtitle>Mol Reprod Dev</addtitle><date>2019-01</date><risdate>2019</risdate><volume>86</volume><issue>1</issue><spage>20</spage><epage>31</epage><pages>20-31</pages><issn>1040-452X</issn><eissn>1098-2795</eissn><abstract>Previous studies have reported that only primordial follicles and empty follicles can be found in 7.5 days postparturition (dpp) Sohlh1−/− mouse ovaries and females are infertility. There appears to be a defect in follicle development during the primordial‐to‐primary follicle transition in Sohlh1−/− mouse ovaries. However, detailed analyses of these phenomena have not been performed. In this study, we used Sohlh1−/− transgenic mice to explore the role of Sohlh1 in folliculogenesis. The results showed that only primordial follicles and empty follicles can be observed in Sohlh1−/− ovaries from 0.5 to 23.5 dpp. The expression of Foxo3 and FOXO3 was downregulated; nucleocytoplasmic shuttling of FOXO3 was normal in 7.5‐dpp Sohlh1+/+ but not Sohlh1−/− ovaries; and primordial follicle activation (PFA) was not observed in 7.5‐dpp Sohlh1−/− mice. The expression levels of KIT, AKT, and P308‐AKT were downregulated (p < 0.05), whereas that of P473‐AKT was not significantly changed (p > 0.05). The KIT/PI3K/AKT pathway was inhibited. Furthermore, we conducted a dual luciferase assay and chromatin immunoprecipitation. The results showed that SOHLH1 can upregulate the Kit gene by binding to the −3698 bp E‐box motif. The absence of Sohlh1 may affect PFA in mouse ovaries via downregulation of Kit and inhibition of the KIT/PI3K/AKT pathway.
The absence of spermatogenesis‐ and oogenesis‐specific basic helix‐loop‐helix 1 (SOHLH1) can influence folliculogenesis by affecting primordial follicle activation in the ovaries, and can lead to disruption of the KIT/PI3K/AKT/FOXO3 pathway. SOHLH1 can control Kit by binding to −3698 E‐box site.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30358927</pmid><doi>10.1002/mrd.23078</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-6814-150X</orcidid><orcidid>https://orcid.org/0000-0001-7595-6849</orcidid></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase AKT AKT protein Animals Basic Helix-Loop-Helix Transcription Factors - genetics Basic Helix-Loop-Helix Transcription Factors - metabolism Chromatin Female Females Follicles Folliculogenesis Forkhead Box Protein O3 - genetics Forkhead Box Protein O3 - metabolism FOXO3 protein Gene Expression Regulation HEK293 Cells Humans Immunoprecipitation Infertility KIT protein Mice Mice, Knockout Ovarian Follicle - growth & development Ovaries PI3K primordial follicle activation Proto-Oncogene Proteins c-kit - biosynthesis Proto-Oncogene Proteins c-kit - genetics Response Elements Signal Transduction Sohlh1 Transgenic mice |
| title | Primordial follicle activation is affected by the absence of Sohlh1 in mice |
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