Dual-Mode Modulation of Smad Signaling by Smad-Interacting Protein Sip1 Is Required for Myelination in the Central Nervous System
Myelination by oligodendrocytes in the central nervous system (CNS) is essential for proper brain function, yet the molecular determinants that control this process remain poorly understood. The basic helix-loop-helix transcription factors Olig1 and Olig2 promote myelination, whereas bone morphogene...
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| Veröffentlicht in: | Neuron (Cambridge, Mass.) Mass.), 2012-02, Vol.73 (4), p.713-728 |
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| creator | Weng, Qinjie Chen, Ying Wang, Haibo Xu, Xiaomei Yang, Bo He, Qiaojun Shou, Weinian Chen, Yan Higashi, Yujiro van den Berghe, Veronique Seuntjens, Eve Kernie, Steven G. Bukshpun, Polina Sherr, Elliott H. Huylebroeck, Danny Lu, Q. Richard |
| description | Myelination by oligodendrocytes in the central nervous system (CNS) is essential for proper brain function, yet the molecular determinants that control this process remain poorly understood. The basic helix-loop-helix transcription factors Olig1 and Olig2 promote myelination, whereas bone morphogenetic protein (BMP) and Wnt/β-catenin signaling inhibit myelination. Here we show that these opposing regulators of myelination are functionally linked by the Olig1/2 common target Smad-interacting protein-1 (Sip1). We demonstrate that Sip1 is an essential modulator of CNS myelination. Sip1 represses differentiation inhibitory signals by antagonizing BMP receptor-activated Smad activity while activating crucial oligodendrocyte-promoting factors. Importantly, a key Sip1-activated target, Smad7, is required for oligodendrocyte differentiation and partially rescues differentiation defects caused by Sip1 loss. Smad7 promotes myelination by blocking the BMP- and β-catenin-negative regulatory pathways. Thus, our findings reveal that Sip1-mediated antagonism of inhibitory signaling is critical for promoting CNS myelination and point to new mediators for myelin repair.
► Zinc finger homeobox transcription factor Sip1/Zfhx1b is required for CNS myelination ► Sip1 promotes CNS myelination by modulating BMP-Smad signaling activity ► Identification of a new oligodendrocyte-enriched gene Smad7 as a key Sip1 target ► Smad7 is both sufficient and critical for oligodendrocyte differentiation
Weng et al. find the transcription factor Sip1 governs myelination by modulating Smad signaling and reveal a key Sip1-induced target, Smad7, which promotes oligodendrocyte differentiation by blocking BMP and β-catenin negative regulatory pathways. |
| doi_str_mv | 10.1016/j.neuron.2011.12.021 |
| format | Article |
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► Zinc finger homeobox transcription factor Sip1/Zfhx1b is required for CNS myelination ► Sip1 promotes CNS myelination by modulating BMP-Smad signaling activity ► Identification of a new oligodendrocyte-enriched gene Smad7 as a key Sip1 target ► Smad7 is both sufficient and critical for oligodendrocyte differentiation
Weng et al. find the transcription factor Sip1 governs myelination by modulating Smad signaling and reveal a key Sip1-induced target, Smad7, which promotes oligodendrocyte differentiation by blocking BMP and β-catenin negative regulatory pathways.</description><identifier>ISSN: 0896-6273</identifier><identifier>EISSN: 1097-4199</identifier><identifier>DOI: 10.1016/j.neuron.2011.12.021</identifier><identifier>PMID: 22365546</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Age Factors ; Animals ; Animals, Newborn ; Antagonism ; Basic Helix-Loop-Helix Transcription Factors - genetics ; Basic Helix-Loop-Helix Transcription Factors - metabolism ; Bone Morphogenetic Proteins - metabolism ; Caspase 3 - metabolism ; Cell Differentiation - genetics ; Cells, Cultured ; Central Nervous System - cytology ; Central Nervous System - physiology ; Central Nervous System - ultrastructure ; Embryo, Mammalian ; Facies ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation, Developmental - genetics ; Genomes ; Green Fluorescent Proteins - genetics ; Hirschsprung Disease - genetics ; Hirschsprung Disease - pathology ; Homeodomain Proteins - metabolism ; Humans ; Immunoprecipitation ; Intellectual Disability - genetics ; Intellectual Disability - pathology ; Ki-67 Antigen - metabolism ; Kinases ; Mice ; Mice, Knockout ; Microcephaly - genetics ; Microcephaly - pathology ; Microscopy, Electron, Transmission ; Models, Molecular ; Multiple sclerosis ; Myelin Sheath - metabolism ; Nerve Tissue Proteins - deficiency ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Nervous system ; Oligodendrocyte Transcription Factor 2 ; Oligodendroglia - metabolism ; Oligonucleotide Array Sequence Analysis ; Optic Nerve - embryology ; Optic Nerve - growth & development ; Optic Nerve - metabolism ; Organogenesis ; Proteins ; Receptor, Platelet-Derived Growth Factor alpha - metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases - metabolism ; Repressor Proteins - metabolism ; RNA, Messenger - metabolism ; Rodents ; Signal Transduction - genetics ; Signal Transduction - physiology ; Smad Proteins - genetics ; Smad Proteins - metabolism ; Smad7 Protein - genetics ; Smad7 Protein - metabolism ; Transcription factors ; Transfection ; Zinc Finger E-box Binding Homeobox 2</subject><ispartof>Neuron (Cambridge, Mass.), 2012-02, Vol.73 (4), p.713-728</ispartof><rights>2012 Elsevier Inc.</rights><rights>Copyright © 2012 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Feb 23, 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c533t-1cd7e058b9c8b1d0617e5496c1f9efadad338f5f2b85d660c8da77d8dd96e0883</citedby><cites>FETCH-LOGICAL-c533t-1cd7e058b9c8b1d0617e5496c1f9efadad338f5f2b85d660c8da77d8dd96e0883</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0896627312000402$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22365546$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Weng, Qinjie</creatorcontrib><creatorcontrib>Chen, Ying</creatorcontrib><creatorcontrib>Wang, Haibo</creatorcontrib><creatorcontrib>Xu, Xiaomei</creatorcontrib><creatorcontrib>Yang, Bo</creatorcontrib><creatorcontrib>He, Qiaojun</creatorcontrib><creatorcontrib>Shou, Weinian</creatorcontrib><creatorcontrib>Chen, Yan</creatorcontrib><creatorcontrib>Higashi, Yujiro</creatorcontrib><creatorcontrib>van den Berghe, Veronique</creatorcontrib><creatorcontrib>Seuntjens, Eve</creatorcontrib><creatorcontrib>Kernie, Steven G.</creatorcontrib><creatorcontrib>Bukshpun, Polina</creatorcontrib><creatorcontrib>Sherr, Elliott H.</creatorcontrib><creatorcontrib>Huylebroeck, Danny</creatorcontrib><creatorcontrib>Lu, Q. Richard</creatorcontrib><title>Dual-Mode Modulation of Smad Signaling by Smad-Interacting Protein Sip1 Is Required for Myelination in the Central Nervous System</title><title>Neuron (Cambridge, Mass.)</title><addtitle>Neuron</addtitle><description>Myelination by oligodendrocytes in the central nervous system (CNS) is essential for proper brain function, yet the molecular determinants that control this process remain poorly understood. The basic helix-loop-helix transcription factors Olig1 and Olig2 promote myelination, whereas bone morphogenetic protein (BMP) and Wnt/β-catenin signaling inhibit myelination. Here we show that these opposing regulators of myelination are functionally linked by the Olig1/2 common target Smad-interacting protein-1 (Sip1). We demonstrate that Sip1 is an essential modulator of CNS myelination. Sip1 represses differentiation inhibitory signals by antagonizing BMP receptor-activated Smad activity while activating crucial oligodendrocyte-promoting factors. Importantly, a key Sip1-activated target, Smad7, is required for oligodendrocyte differentiation and partially rescues differentiation defects caused by Sip1 loss. Smad7 promotes myelination by blocking the BMP- and β-catenin-negative regulatory pathways. Thus, our findings reveal that Sip1-mediated antagonism of inhibitory signaling is critical for promoting CNS myelination and point to new mediators for myelin repair.
► Zinc finger homeobox transcription factor Sip1/Zfhx1b is required for CNS myelination ► Sip1 promotes CNS myelination by modulating BMP-Smad signaling activity ► Identification of a new oligodendrocyte-enriched gene Smad7 as a key Sip1 target ► Smad7 is both sufficient and critical for oligodendrocyte differentiation
Weng et al. find the transcription factor Sip1 governs myelination by modulating Smad signaling and reveal a key Sip1-induced target, Smad7, which promotes oligodendrocyte differentiation by blocking BMP and β-catenin negative regulatory pathways.</description><subject>Age Factors</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Antagonism</subject><subject>Basic Helix-Loop-Helix Transcription Factors - genetics</subject><subject>Basic Helix-Loop-Helix Transcription Factors - metabolism</subject><subject>Bone Morphogenetic Proteins - metabolism</subject><subject>Caspase 3 - metabolism</subject><subject>Cell Differentiation - genetics</subject><subject>Cells, Cultured</subject><subject>Central Nervous System - cytology</subject><subject>Central Nervous System - physiology</subject><subject>Central Nervous System - ultrastructure</subject><subject>Embryo, Mammalian</subject><subject>Facies</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Developmental - genetics</subject><subject>Genomes</subject><subject>Green Fluorescent Proteins - genetics</subject><subject>Hirschsprung Disease - genetics</subject><subject>Hirschsprung Disease - pathology</subject><subject>Homeodomain Proteins - metabolism</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Intellectual Disability - genetics</subject><subject>Intellectual Disability - pathology</subject><subject>Ki-67 Antigen - metabolism</subject><subject>Kinases</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Microcephaly - genetics</subject><subject>Microcephaly - pathology</subject><subject>Microscopy, Electron, Transmission</subject><subject>Models, Molecular</subject><subject>Multiple sclerosis</subject><subject>Myelin Sheath - metabolism</subject><subject>Nerve Tissue Proteins - deficiency</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Nervous system</subject><subject>Oligodendrocyte Transcription Factor 2</subject><subject>Oligodendroglia - metabolism</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Optic Nerve - embryology</subject><subject>Optic Nerve - growth & development</subject><subject>Optic Nerve - metabolism</subject><subject>Organogenesis</subject><subject>Proteins</subject><subject>Receptor, Platelet-Derived Growth Factor alpha - metabolism</subject><subject>Receptor-Interacting Protein Serine-Threonine Kinases - metabolism</subject><subject>Repressor Proteins - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Signal Transduction - genetics</subject><subject>Signal Transduction - physiology</subject><subject>Smad Proteins - genetics</subject><subject>Smad Proteins - metabolism</subject><subject>Smad7 Protein - genetics</subject><subject>Smad7 Protein - metabolism</subject><subject>Transcription factors</subject><subject>Transfection</subject><subject>Zinc Finger E-box Binding Homeobox 2</subject><issn>0896-6273</issn><issn>1097-4199</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u1DAUhSMEokPhDRCyxIJVgn9ix94goSk_I7WAGFhbjn1TPMrYUzupNEveHE9TWLCAjS1dfefYul9VPSe4IZiI17smwJxiaCgmpCG0wZQ8qFYEq65uiVIPqxWWStSCduysepLzDmPSckUeV2eUMsF5K1bVz4vZjPVVdIDKMY9m8jGgOKDt3ji09dfBjD5co_54N6k3YYJk7HSafUlxAh8KdSBok9FXuJl9AoeGmNDVEUpwqSvM9APQGsKUzIg-QbqNc0bbY55g_7R6NJgxw7P7-7z6_v7dt_XH-vLzh8367WVtOWNTTazrAHPZKyt74rAgHfBWCUsGBYNxxjEmBz7QXnInBLbSma5z0jklAEvJzqtXS-8hxZsZ8qT3PlsYRxOg_EYrIUnXMkz_T1KmOBd3nS__IndxTmVlWRPBWtlxzFSh2oWyKeacYNCH5PcmHTXB-uRS7_TiUp9cakJ1cVliL-7L534P7k_ot7wCvFkAKGu79ZB0th6CBVcs2Em76P_9wi-EULJD</recordid><startdate>20120223</startdate><enddate>20120223</enddate><creator>Weng, Qinjie</creator><creator>Chen, Ying</creator><creator>Wang, Haibo</creator><creator>Xu, Xiaomei</creator><creator>Yang, Bo</creator><creator>He, Qiaojun</creator><creator>Shou, Weinian</creator><creator>Chen, Yan</creator><creator>Higashi, Yujiro</creator><creator>van den Berghe, Veronique</creator><creator>Seuntjens, Eve</creator><creator>Kernie, Steven G.</creator><creator>Bukshpun, Polina</creator><creator>Sherr, Elliott H.</creator><creator>Huylebroeck, Danny</creator><creator>Lu, Q. Richard</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><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>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20120223</creationdate><title>Dual-Mode Modulation of Smad Signaling by Smad-Interacting Protein Sip1 Is Required for Myelination in the Central Nervous System</title><author>Weng, Qinjie ; Chen, Ying ; Wang, Haibo ; Xu, Xiaomei ; Yang, Bo ; He, Qiaojun ; Shou, Weinian ; Chen, Yan ; Higashi, Yujiro ; van den Berghe, Veronique ; Seuntjens, Eve ; Kernie, Steven G. ; Bukshpun, Polina ; Sherr, Elliott H. ; Huylebroeck, Danny ; Lu, Q. Richard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c533t-1cd7e058b9c8b1d0617e5496c1f9efadad338f5f2b85d660c8da77d8dd96e0883</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Age Factors</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Antagonism</topic><topic>Basic Helix-Loop-Helix Transcription Factors - genetics</topic><topic>Basic Helix-Loop-Helix Transcription Factors - metabolism</topic><topic>Bone Morphogenetic Proteins - metabolism</topic><topic>Caspase 3 - metabolism</topic><topic>Cell Differentiation - genetics</topic><topic>Cells, Cultured</topic><topic>Central Nervous System - cytology</topic><topic>Central Nervous System - physiology</topic><topic>Central Nervous System - ultrastructure</topic><topic>Embryo, Mammalian</topic><topic>Facies</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Developmental - genetics</topic><topic>Genomes</topic><topic>Green Fluorescent Proteins - genetics</topic><topic>Hirschsprung Disease - genetics</topic><topic>Hirschsprung Disease - pathology</topic><topic>Homeodomain Proteins - metabolism</topic><topic>Humans</topic><topic>Immunoprecipitation</topic><topic>Intellectual Disability - genetics</topic><topic>Intellectual Disability - pathology</topic><topic>Ki-67 Antigen - metabolism</topic><topic>Kinases</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Microcephaly - genetics</topic><topic>Microcephaly - pathology</topic><topic>Microscopy, Electron, Transmission</topic><topic>Models, Molecular</topic><topic>Multiple sclerosis</topic><topic>Myelin Sheath - metabolism</topic><topic>Nerve Tissue Proteins - deficiency</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Nervous system</topic><topic>Oligodendrocyte Transcription Factor 2</topic><topic>Oligodendroglia - metabolism</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Optic Nerve - embryology</topic><topic>Optic Nerve - growth & development</topic><topic>Optic Nerve - metabolism</topic><topic>Organogenesis</topic><topic>Proteins</topic><topic>Receptor, Platelet-Derived Growth Factor alpha - metabolism</topic><topic>Receptor-Interacting Protein Serine-Threonine Kinases - metabolism</topic><topic>Repressor Proteins - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><topic>Signal Transduction - genetics</topic><topic>Signal Transduction - physiology</topic><topic>Smad Proteins - genetics</topic><topic>Smad Proteins - metabolism</topic><topic>Smad7 Protein - genetics</topic><topic>Smad7 Protein - metabolism</topic><topic>Transcription factors</topic><topic>Transfection</topic><topic>Zinc Finger E-box Binding Homeobox 2</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Weng, Qinjie</creatorcontrib><creatorcontrib>Chen, Ying</creatorcontrib><creatorcontrib>Wang, Haibo</creatorcontrib><creatorcontrib>Xu, Xiaomei</creatorcontrib><creatorcontrib>Yang, Bo</creatorcontrib><creatorcontrib>He, Qiaojun</creatorcontrib><creatorcontrib>Shou, Weinian</creatorcontrib><creatorcontrib>Chen, Yan</creatorcontrib><creatorcontrib>Higashi, Yujiro</creatorcontrib><creatorcontrib>van den Berghe, Veronique</creatorcontrib><creatorcontrib>Seuntjens, Eve</creatorcontrib><creatorcontrib>Kernie, Steven G.</creatorcontrib><creatorcontrib>Bukshpun, Polina</creatorcontrib><creatorcontrib>Sherr, Elliott H.</creatorcontrib><creatorcontrib>Huylebroeck, Danny</creatorcontrib><creatorcontrib>Lu, Q. Richard</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuron (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Weng, Qinjie</au><au>Chen, Ying</au><au>Wang, Haibo</au><au>Xu, Xiaomei</au><au>Yang, Bo</au><au>He, Qiaojun</au><au>Shou, Weinian</au><au>Chen, Yan</au><au>Higashi, Yujiro</au><au>van den Berghe, Veronique</au><au>Seuntjens, Eve</au><au>Kernie, Steven G.</au><au>Bukshpun, Polina</au><au>Sherr, Elliott H.</au><au>Huylebroeck, Danny</au><au>Lu, Q. Richard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dual-Mode Modulation of Smad Signaling by Smad-Interacting Protein Sip1 Is Required for Myelination in the Central Nervous System</atitle><jtitle>Neuron (Cambridge, Mass.)</jtitle><addtitle>Neuron</addtitle><date>2012-02-23</date><risdate>2012</risdate><volume>73</volume><issue>4</issue><spage>713</spage><epage>728</epage><pages>713-728</pages><issn>0896-6273</issn><eissn>1097-4199</eissn><abstract>Myelination by oligodendrocytes in the central nervous system (CNS) is essential for proper brain function, yet the molecular determinants that control this process remain poorly understood. The basic helix-loop-helix transcription factors Olig1 and Olig2 promote myelination, whereas bone morphogenetic protein (BMP) and Wnt/β-catenin signaling inhibit myelination. Here we show that these opposing regulators of myelination are functionally linked by the Olig1/2 common target Smad-interacting protein-1 (Sip1). We demonstrate that Sip1 is an essential modulator of CNS myelination. Sip1 represses differentiation inhibitory signals by antagonizing BMP receptor-activated Smad activity while activating crucial oligodendrocyte-promoting factors. Importantly, a key Sip1-activated target, Smad7, is required for oligodendrocyte differentiation and partially rescues differentiation defects caused by Sip1 loss. Smad7 promotes myelination by blocking the BMP- and β-catenin-negative regulatory pathways. Thus, our findings reveal that Sip1-mediated antagonism of inhibitory signaling is critical for promoting CNS myelination and point to new mediators for myelin repair.
► Zinc finger homeobox transcription factor Sip1/Zfhx1b is required for CNS myelination ► Sip1 promotes CNS myelination by modulating BMP-Smad signaling activity ► Identification of a new oligodendrocyte-enriched gene Smad7 as a key Sip1 target ► Smad7 is both sufficient and critical for oligodendrocyte differentiation
Weng et al. find the transcription factor Sip1 governs myelination by modulating Smad signaling and reveal a key Sip1-induced target, Smad7, which promotes oligodendrocyte differentiation by blocking BMP and β-catenin negative regulatory pathways.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>22365546</pmid><doi>10.1016/j.neuron.2011.12.021</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0896-6273 |
| ispartof | Neuron (Cambridge, Mass.), 2012-02, Vol.73 (4), p.713-728 |
| issn | 0896-6273 1097-4199 |
| language | eng |
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| source | MEDLINE; Cell Press Free Archives; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Age Factors Animals Animals, Newborn Antagonism Basic Helix-Loop-Helix Transcription Factors - genetics Basic Helix-Loop-Helix Transcription Factors - metabolism Bone Morphogenetic Proteins - metabolism Caspase 3 - metabolism Cell Differentiation - genetics Cells, Cultured Central Nervous System - cytology Central Nervous System - physiology Central Nervous System - ultrastructure Embryo, Mammalian Facies Gene expression Gene Expression Profiling Gene Expression Regulation, Developmental - genetics Genomes Green Fluorescent Proteins - genetics Hirschsprung Disease - genetics Hirschsprung Disease - pathology Homeodomain Proteins - metabolism Humans Immunoprecipitation Intellectual Disability - genetics Intellectual Disability - pathology Ki-67 Antigen - metabolism Kinases Mice Mice, Knockout Microcephaly - genetics Microcephaly - pathology Microscopy, Electron, Transmission Models, Molecular Multiple sclerosis Myelin Sheath - metabolism Nerve Tissue Proteins - deficiency Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Nervous system Oligodendrocyte Transcription Factor 2 Oligodendroglia - metabolism Oligonucleotide Array Sequence Analysis Optic Nerve - embryology Optic Nerve - growth & development Optic Nerve - metabolism Organogenesis Proteins Receptor, Platelet-Derived Growth Factor alpha - metabolism Receptor-Interacting Protein Serine-Threonine Kinases - metabolism Repressor Proteins - metabolism RNA, Messenger - metabolism Rodents Signal Transduction - genetics Signal Transduction - physiology Smad Proteins - genetics Smad Proteins - metabolism Smad7 Protein - genetics Smad7 Protein - metabolism Transcription factors Transfection Zinc Finger E-box Binding Homeobox 2 |
| title | Dual-Mode Modulation of Smad Signaling by Smad-Interacting Protein Sip1 Is Required for Myelination in the Central Nervous System |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-11T12%3A42%3A38IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Dual-Mode%20Modulation%20of%20Smad%20Signaling%20by%20Smad-Interacting%20Protein%20Sip1%20Is%20Required%20for%20Myelination%20in%20the%20Central%20Nervous%20System&rft.jtitle=Neuron%20(Cambridge,%20Mass.)&rft.au=Weng,%20Qinjie&rft.date=2012-02-23&rft.volume=73&rft.issue=4&rft.spage=713&rft.epage=728&rft.pages=713-728&rft.issn=0896-6273&rft.eissn=1097-4199&rft_id=info:doi/10.1016/j.neuron.2011.12.021&rft_dat=%3Cproquest_cross%3E923955688%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1634875039&rft_id=info:pmid/22365546&rft_els_id=S0896627312000402&rfr_iscdi=true |