SOX2 Regulates Neuronal Differentiation of the Suprachiasmatic Nucleus
In mammals, the hypothalamic suprachiasmatic nucleus (SCN) functions as the central circadian pacemaker, orchestrating behavioral and physiological rhythms in alignment to the environmental light/dark cycle. The neurons that comprise the SCN are anatomically and functionally heterogeneous, but despi...
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| Veröffentlicht in: | International journal of molecular sciences 2021-12, Vol.23 (1), p.229 |
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| creator | Cheng, Arthur H Fung, Samuel W Hegazi, Sara Abdalla, Osama Hasan Mustafa Hasan Cheng, Hai-Ying Mary |
| description | In mammals, the hypothalamic suprachiasmatic nucleus (SCN) functions as the central circadian pacemaker, orchestrating behavioral and physiological rhythms in alignment to the environmental light/dark cycle. The neurons that comprise the SCN are anatomically and functionally heterogeneous, but despite their physiological importance, little is known about the pathways that guide their specification and differentiation. Here, we report that the stem/progenitor cell transcription factor,
(
), is required in the embryonic SCN to control the expression of SCN-enriched neuropeptides and transcription factors. Ablation of
in the developing SCN leads to downregulation of circadian neuropeptides as early as embryonic day (E) 15.5, followed by a decrease in the expression of two transcription factors involved in SCN development,
and
, in neonates. Thymidine analog-retention assays revealed that
deficiency contributed to reduced survival of SCN neurons during the postnatal period of cell clearance, but did not affect progenitor cell proliferation or SCN specification. Our results identify SOX2 as an essential transcription factor for the proper differentiation and survival of neurons within the developing SCN. |
| doi_str_mv | 10.3390/ijms23010229 |
| format | Article |
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(
), is required in the embryonic SCN to control the expression of SCN-enriched neuropeptides and transcription factors. Ablation of
in the developing SCN leads to downregulation of circadian neuropeptides as early as embryonic day (E) 15.5, followed by a decrease in the expression of two transcription factors involved in SCN development,
and
, in neonates. Thymidine analog-retention assays revealed that
deficiency contributed to reduced survival of SCN neurons during the postnatal period of cell clearance, but did not affect progenitor cell proliferation or SCN specification. Our results identify SOX2 as an essential transcription factor for the proper differentiation and survival of neurons within the developing SCN.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms23010229</identifier><identifier>PMID: 35008655</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Ablation ; Animals ; Brain ; Cell Differentiation ; Cell proliferation ; Cells (biology) ; Circadian Rhythm ; Circadian rhythms ; Differentiation ; Embryonic Development ; Embryos ; Gene expression ; Hypothalamus ; Mice ; Neonates ; Neural stem cells ; Neurogenesis ; Neurons ; Neurons - metabolism ; Neurons - physiology ; Neuropeptides ; Pacemakers ; Progenitor cells ; SIX gene family ; SOXB1 Transcription Factors - metabolism ; SOXB1 Transcription Factors - physiology ; Specifications ; Suprachiasmatic nucleus ; Suprachiasmatic Nucleus - growth & development ; Suprachiasmatic Nucleus - metabolism ; Suprachiasmatic Nucleus - physiology ; Survival ; Thymidine ; Transcription factors</subject><ispartof>International journal of molecular sciences, 2021-12, Vol.23 (1), p.229</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-cd5aeec39945d0bcf2f7e9be24dedc340fbecb6bc0f51e3184c17f745f1b9f883</citedby><cites>FETCH-LOGICAL-c412t-cd5aeec39945d0bcf2f7e9be24dedc340fbecb6bc0f51e3184c17f745f1b9f883</cites><orcidid>0000-0002-9292-7406 ; 0000-0003-3230-2639 ; 0000-0001-8214-1437</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8745319/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8745319/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27922,27923,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35008655$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cheng, Arthur H</creatorcontrib><creatorcontrib>Fung, Samuel W</creatorcontrib><creatorcontrib>Hegazi, Sara</creatorcontrib><creatorcontrib>Abdalla, Osama Hasan Mustafa Hasan</creatorcontrib><creatorcontrib>Cheng, Hai-Ying Mary</creatorcontrib><title>SOX2 Regulates Neuronal Differentiation of the Suprachiasmatic Nucleus</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>In mammals, the hypothalamic suprachiasmatic nucleus (SCN) functions as the central circadian pacemaker, orchestrating behavioral and physiological rhythms in alignment to the environmental light/dark cycle. The neurons that comprise the SCN are anatomically and functionally heterogeneous, but despite their physiological importance, little is known about the pathways that guide their specification and differentiation. Here, we report that the stem/progenitor cell transcription factor,
(
), is required in the embryonic SCN to control the expression of SCN-enriched neuropeptides and transcription factors. Ablation of
in the developing SCN leads to downregulation of circadian neuropeptides as early as embryonic day (E) 15.5, followed by a decrease in the expression of two transcription factors involved in SCN development,
and
, in neonates. Thymidine analog-retention assays revealed that
deficiency contributed to reduced survival of SCN neurons during the postnatal period of cell clearance, but did not affect progenitor cell proliferation or SCN specification. Our results identify SOX2 as an essential transcription factor for the proper differentiation and survival of neurons within the developing SCN.</description><subject>Ablation</subject><subject>Animals</subject><subject>Brain</subject><subject>Cell Differentiation</subject><subject>Cell proliferation</subject><subject>Cells (biology)</subject><subject>Circadian Rhythm</subject><subject>Circadian rhythms</subject><subject>Differentiation</subject><subject>Embryonic Development</subject><subject>Embryos</subject><subject>Gene expression</subject><subject>Hypothalamus</subject><subject>Mice</subject><subject>Neonates</subject><subject>Neural stem cells</subject><subject>Neurogenesis</subject><subject>Neurons</subject><subject>Neurons - metabolism</subject><subject>Neurons - physiology</subject><subject>Neuropeptides</subject><subject>Pacemakers</subject><subject>Progenitor cells</subject><subject>SIX gene family</subject><subject>SOXB1 Transcription Factors - metabolism</subject><subject>SOXB1 Transcription Factors - physiology</subject><subject>Specifications</subject><subject>Suprachiasmatic nucleus</subject><subject>Suprachiasmatic Nucleus - growth & development</subject><subject>Suprachiasmatic Nucleus - metabolism</subject><subject>Suprachiasmatic Nucleus - physiology</subject><subject>Survival</subject><subject>Thymidine</subject><subject>Transcription factors</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkctLAzEQxoMo1tfNsyx48WA1j812cxGkWhWkBR_gLWTTSZuyu6nJRvC_N9Iq1dMMM7_5mJkPoWOCLxgT-NIumkAZJphSsYX2SE5pH-NisL2R99B-CAuMKaNc7KIe4xiXBed7aPQ8eaPZE8xirToI2Riid62qsxtrDHhoO6s669rMmaybQ_Ycl17puVWhSXWdjaOuIYZDtGNUHeBoHQ_Q6-j2ZXjff5zcPQyvH_s6J7Tr6ylXAJoJkfMprrShZgCiAppPYapZjk0FuioqjQ0nwEiZazIwg5wbUglTluwAXa10l7Fq0kjaz6taLr1tlP-UTln5t9PauZy5D1kmEUZEEjhbC3j3HiF0srFBQ12rFlwMkhakFLgoBE7o6T904aJPv1lRlJWcsUSdryjtXQgezO8yBMtvg-SmQQk_2TzgF_5xhH0BV2ONpA</recordid><startdate>20211226</startdate><enddate>20211226</enddate><creator>Cheng, Arthur H</creator><creator>Fung, Samuel W</creator><creator>Hegazi, Sara</creator><creator>Abdalla, Osama Hasan Mustafa Hasan</creator><creator>Cheng, Hai-Ying Mary</creator><general>MDPI AG</general><general>MDPI</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-9292-7406</orcidid><orcidid>https://orcid.org/0000-0003-3230-2639</orcidid><orcidid>https://orcid.org/0000-0001-8214-1437</orcidid></search><sort><creationdate>20211226</creationdate><title>SOX2 Regulates Neuronal Differentiation of the Suprachiasmatic Nucleus</title><author>Cheng, Arthur H ; Fung, Samuel W ; Hegazi, Sara ; Abdalla, Osama Hasan Mustafa Hasan ; Cheng, Hai-Ying Mary</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-cd5aeec39945d0bcf2f7e9be24dedc340fbecb6bc0f51e3184c17f745f1b9f883</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Ablation</topic><topic>Animals</topic><topic>Brain</topic><topic>Cell Differentiation</topic><topic>Cell proliferation</topic><topic>Cells (biology)</topic><topic>Circadian Rhythm</topic><topic>Circadian rhythms</topic><topic>Differentiation</topic><topic>Embryonic Development</topic><topic>Embryos</topic><topic>Gene expression</topic><topic>Hypothalamus</topic><topic>Mice</topic><topic>Neonates</topic><topic>Neural stem cells</topic><topic>Neurogenesis</topic><topic>Neurons</topic><topic>Neurons - metabolism</topic><topic>Neurons - physiology</topic><topic>Neuropeptides</topic><topic>Pacemakers</topic><topic>Progenitor cells</topic><topic>SIX gene family</topic><topic>SOXB1 Transcription Factors - metabolism</topic><topic>SOXB1 Transcription Factors - physiology</topic><topic>Specifications</topic><topic>Suprachiasmatic nucleus</topic><topic>Suprachiasmatic Nucleus - growth & development</topic><topic>Suprachiasmatic Nucleus - metabolism</topic><topic>Suprachiasmatic Nucleus - physiology</topic><topic>Survival</topic><topic>Thymidine</topic><topic>Transcription factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cheng, Arthur H</creatorcontrib><creatorcontrib>Fung, Samuel W</creatorcontrib><creatorcontrib>Hegazi, Sara</creatorcontrib><creatorcontrib>Abdalla, Osama Hasan Mustafa Hasan</creatorcontrib><creatorcontrib>Cheng, Hai-Ying Mary</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cheng, Arthur H</au><au>Fung, Samuel W</au><au>Hegazi, Sara</au><au>Abdalla, Osama Hasan Mustafa Hasan</au><au>Cheng, Hai-Ying Mary</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SOX2 Regulates Neuronal Differentiation of the Suprachiasmatic Nucleus</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2021-12-26</date><risdate>2021</risdate><volume>23</volume><issue>1</issue><spage>229</spage><pages>229-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>In mammals, the hypothalamic suprachiasmatic nucleus (SCN) functions as the central circadian pacemaker, orchestrating behavioral and physiological rhythms in alignment to the environmental light/dark cycle. The neurons that comprise the SCN are anatomically and functionally heterogeneous, but despite their physiological importance, little is known about the pathways that guide their specification and differentiation. Here, we report that the stem/progenitor cell transcription factor,
(
), is required in the embryonic SCN to control the expression of SCN-enriched neuropeptides and transcription factors. Ablation of
in the developing SCN leads to downregulation of circadian neuropeptides as early as embryonic day (E) 15.5, followed by a decrease in the expression of two transcription factors involved in SCN development,
and
, in neonates. Thymidine analog-retention assays revealed that
deficiency contributed to reduced survival of SCN neurons during the postnatal period of cell clearance, but did not affect progenitor cell proliferation or SCN specification. Our results identify SOX2 as an essential transcription factor for the proper differentiation and survival of neurons within the developing SCN.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>35008655</pmid><doi>10.3390/ijms23010229</doi><orcidid>https://orcid.org/0000-0002-9292-7406</orcidid><orcidid>https://orcid.org/0000-0003-3230-2639</orcidid><orcidid>https://orcid.org/0000-0001-8214-1437</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Ablation Animals Brain Cell Differentiation Cell proliferation Cells (biology) Circadian Rhythm Circadian rhythms Differentiation Embryonic Development Embryos Gene expression Hypothalamus Mice Neonates Neural stem cells Neurogenesis Neurons Neurons - metabolism Neurons - physiology Neuropeptides Pacemakers Progenitor cells SIX gene family SOXB1 Transcription Factors - metabolism SOXB1 Transcription Factors - physiology Specifications Suprachiasmatic nucleus Suprachiasmatic Nucleus - growth & development Suprachiasmatic Nucleus - metabolism Suprachiasmatic Nucleus - physiology Survival Thymidine Transcription factors |
| title | SOX2 Regulates Neuronal Differentiation of the Suprachiasmatic Nucleus |
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