Olig1 function is required for oligodendrocyte differentiation in the mouse brain
Oligodendrocyte differentiation and myelination are tightly regulated processes orchestrated by a complex transcriptional network. Two bHLH transcription factors in this network, Olig1 and Olig2, are expressed exclusively by oligodendrocytes after late embryonic development. Although the role of Oli...
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Veröffentlicht in: | The Journal of neuroscience 2015-03, Vol.35 (10), p.4386-4402 |
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description | Oligodendrocyte differentiation and myelination are tightly regulated processes orchestrated by a complex transcriptional network. Two bHLH transcription factors in this network, Olig1 and Olig2, are expressed exclusively by oligodendrocytes after late embryonic development. Although the role of Olig2 in the lineage is well established, the role of Olig1 is still unclear. The current studies analyzed the function of Olig1 in oligodendrocyte differentiation and developmental myelination in brain. Both oligodendrocyte progenitor cell commitment and oligodendrocyte differentiation were impaired in the corpus callosum of Olig1-null mice, resulting in hypomyelination throughout adulthood in the brain. As seen in previous studies with this mouse line, although there was an early myelination deficit in the spinal cord, essentially full recovery with normal spinal cord myelination was seen. Intriguingly, this regional difference may be partially attributed to compensatory upregulation of Olig2 protein expression in the spinal cord after Olig1 deletion, which is not seen in brain. The current study demonstrates a unique role for Olig1 in promoting oligodendrocyte progenitor cell commitment, differentiation, and subsequent myelination primarily in brain, but not spinal cord. |
doi_str_mv | 10.1523/JNEUROSCI.4962-14.2015 |
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Two bHLH transcription factors in this network, Olig1 and Olig2, are expressed exclusively by oligodendrocytes after late embryonic development. Although the role of Olig2 in the lineage is well established, the role of Olig1 is still unclear. The current studies analyzed the function of Olig1 in oligodendrocyte differentiation and developmental myelination in brain. Both oligodendrocyte progenitor cell commitment and oligodendrocyte differentiation were impaired in the corpus callosum of Olig1-null mice, resulting in hypomyelination throughout adulthood in the brain. As seen in previous studies with this mouse line, although there was an early myelination deficit in the spinal cord, essentially full recovery with normal spinal cord myelination was seen. Intriguingly, this regional difference may be partially attributed to compensatory upregulation of Olig2 protein expression in the spinal cord after Olig1 deletion, which is not seen in brain. The current study demonstrates a unique role for Olig1 in promoting oligodendrocyte progenitor cell commitment, differentiation, and subsequent myelination primarily in brain, but not spinal cord.</description><identifier>ISSN: 0270-6474</identifier><identifier>EISSN: 1529-2401</identifier><identifier>DOI: 10.1523/JNEUROSCI.4962-14.2015</identifier><identifier>PMID: 25762682</identifier><language>eng</language><publisher>United States: Society for Neuroscience</publisher><subject>2',3'-Cyclic-Nucleotide Phosphodiesterases - metabolism ; Age Factors ; Animals ; Animals, Newborn ; Basic Helix-Loop-Helix Transcription Factors - genetics ; Basic Helix-Loop-Helix Transcription Factors - metabolism ; Brain - cytology ; Brain - ultrastructure ; Cell Death - genetics ; Cell Differentiation - genetics ; Cell Differentiation - physiology ; Cells, Cultured ; Gene Expression Regulation, Developmental - genetics ; In Vitro Techniques ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation - genetics ; Myelin Basic Protein - metabolism ; Myelin Proteolipid Protein - metabolism ; Myelin-Oligodendrocyte Glycoprotein - metabolism ; Oligodendroglia - physiology ; Oligodendroglia - ultrastructure ; SOXB1 Transcription Factors - metabolism ; Spinal Cord - cytology ; Stem Cells - physiology</subject><ispartof>The Journal of neuroscience, 2015-03, Vol.35 (10), p.4386-4402</ispartof><rights>Copyright © 2015 the authors 0270-6474/15/354386-17$15.00/0.</rights><rights>Copyright © 2015 the authors 0270-6474/15/354386-17$15.00/0 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c513t-24bdb2de4f48db64ac87aa2789e30eb830c0722f0d3167836a165aea4f59337d3</citedby><cites>FETCH-LOGICAL-c513t-24bdb2de4f48db64ac87aa2789e30eb830c0722f0d3167836a165aea4f59337d3</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/PMC4461695/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4461695/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25762682$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dai, Jinxiang</creatorcontrib><creatorcontrib>Bercury, Kathryn K</creatorcontrib><creatorcontrib>Ahrendsen, Jared T</creatorcontrib><creatorcontrib>Macklin, Wendy B</creatorcontrib><title>Olig1 function is required for oligodendrocyte differentiation in the mouse brain</title><title>The Journal of neuroscience</title><addtitle>J Neurosci</addtitle><description>Oligodendrocyte differentiation and myelination are tightly regulated processes orchestrated by a complex transcriptional network. Two bHLH transcription factors in this network, Olig1 and Olig2, are expressed exclusively by oligodendrocytes after late embryonic development. Although the role of Olig2 in the lineage is well established, the role of Olig1 is still unclear. The current studies analyzed the function of Olig1 in oligodendrocyte differentiation and developmental myelination in brain. Both oligodendrocyte progenitor cell commitment and oligodendrocyte differentiation were impaired in the corpus callosum of Olig1-null mice, resulting in hypomyelination throughout adulthood in the brain. As seen in previous studies with this mouse line, although there was an early myelination deficit in the spinal cord, essentially full recovery with normal spinal cord myelination was seen. Intriguingly, this regional difference may be partially attributed to compensatory upregulation of Olig2 protein expression in the spinal cord after Olig1 deletion, which is not seen in brain. The current study demonstrates a unique role for Olig1 in promoting oligodendrocyte progenitor cell commitment, differentiation, and subsequent myelination primarily in brain, but not spinal cord.</description><subject>2',3'-Cyclic-Nucleotide Phosphodiesterases - metabolism</subject><subject>Age Factors</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Basic Helix-Loop-Helix Transcription Factors - genetics</subject><subject>Basic Helix-Loop-Helix Transcription Factors - metabolism</subject><subject>Brain - cytology</subject><subject>Brain - ultrastructure</subject><subject>Cell Death - genetics</subject><subject>Cell Differentiation - genetics</subject><subject>Cell Differentiation - physiology</subject><subject>Cells, Cultured</subject><subject>Gene Expression Regulation, Developmental - genetics</subject><subject>In Vitro Techniques</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Mutation - genetics</subject><subject>Myelin Basic Protein - metabolism</subject><subject>Myelin Proteolipid Protein - metabolism</subject><subject>Myelin-Oligodendrocyte Glycoprotein - metabolism</subject><subject>Oligodendroglia - physiology</subject><subject>Oligodendroglia - ultrastructure</subject><subject>SOXB1 Transcription Factors - metabolism</subject><subject>Spinal Cord - cytology</subject><subject>Stem Cells - physiology</subject><issn>0270-6474</issn><issn>1529-2401</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctKxDAUhoMoOl5eQbJ00zH3tBtBBq-Ig7d1SJsTjXQaTVrBt7fD6KArV2fxX_gPH0KHlEypZPz4-vbs6X7-MLuaikqxgoopI1RuoMmoVgUThG6iCWGaFEposYN2c34lhGhC9TbaYVIrpko2QXfzNjxT7Ieu6UPscMg4wfsQEjjsY8JxlKODzqXYfPaAXfAeEnR9sCt_h_sXwIs4ZMB1sqHbR1vethkOvu8eejo_e5xdFjfzi6vZ6U3RSMr7cWLtauZAeFG6WgnblNpapssKOIG65KQhmjFPHKdKl1xZqqQFK7ysONeO76GTVe_bUC_ANeOmZFvzlsLCpk8TbTB_lS68mOf4YYRQVFVyLDj6LkjxfYDcm0XIDbSt7WB8x1CtZKUZr9j_VqW4kpLLpVWtrE2KOSfw60WUmCU6s0ZnlugMFWaJbgwe_v5nHfthxb8AaeOXWQ</recordid><startdate>20150311</startdate><enddate>20150311</enddate><creator>Dai, Jinxiang</creator><creator>Bercury, Kathryn K</creator><creator>Ahrendsen, Jared T</creator><creator>Macklin, Wendy B</creator><general>Society for Neuroscience</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>7X8</scope><scope>7TK</scope><scope>5PM</scope></search><sort><creationdate>20150311</creationdate><title>Olig1 function is required for oligodendrocyte differentiation in the mouse brain</title><author>Dai, Jinxiang ; Bercury, Kathryn K ; Ahrendsen, Jared T ; Macklin, Wendy B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c513t-24bdb2de4f48db64ac87aa2789e30eb830c0722f0d3167836a165aea4f59337d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>2',3'-Cyclic-Nucleotide Phosphodiesterases - metabolism</topic><topic>Age Factors</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Basic Helix-Loop-Helix Transcription Factors - genetics</topic><topic>Basic Helix-Loop-Helix Transcription Factors - metabolism</topic><topic>Brain - cytology</topic><topic>Brain - ultrastructure</topic><topic>Cell Death - genetics</topic><topic>Cell Differentiation - genetics</topic><topic>Cell Differentiation - physiology</topic><topic>Cells, Cultured</topic><topic>Gene Expression Regulation, Developmental - genetics</topic><topic>In Vitro Techniques</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Mutation - genetics</topic><topic>Myelin Basic Protein - metabolism</topic><topic>Myelin Proteolipid Protein - metabolism</topic><topic>Myelin-Oligodendrocyte Glycoprotein - metabolism</topic><topic>Oligodendroglia - physiology</topic><topic>Oligodendroglia - ultrastructure</topic><topic>SOXB1 Transcription Factors - metabolism</topic><topic>Spinal Cord - cytology</topic><topic>Stem Cells - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dai, Jinxiang</creatorcontrib><creatorcontrib>Bercury, Kathryn K</creatorcontrib><creatorcontrib>Ahrendsen, Jared T</creatorcontrib><creatorcontrib>Macklin, Wendy B</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dai, Jinxiang</au><au>Bercury, Kathryn K</au><au>Ahrendsen, Jared T</au><au>Macklin, Wendy B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Olig1 function is required for oligodendrocyte differentiation in the mouse brain</atitle><jtitle>The Journal of neuroscience</jtitle><addtitle>J Neurosci</addtitle><date>2015-03-11</date><risdate>2015</risdate><volume>35</volume><issue>10</issue><spage>4386</spage><epage>4402</epage><pages>4386-4402</pages><issn>0270-6474</issn><eissn>1529-2401</eissn><abstract>Oligodendrocyte differentiation and myelination are tightly regulated processes orchestrated by a complex transcriptional network. Two bHLH transcription factors in this network, Olig1 and Olig2, are expressed exclusively by oligodendrocytes after late embryonic development. Although the role of Olig2 in the lineage is well established, the role of Olig1 is still unclear. The current studies analyzed the function of Olig1 in oligodendrocyte differentiation and developmental myelination in brain. Both oligodendrocyte progenitor cell commitment and oligodendrocyte differentiation were impaired in the corpus callosum of Olig1-null mice, resulting in hypomyelination throughout adulthood in the brain. As seen in previous studies with this mouse line, although there was an early myelination deficit in the spinal cord, essentially full recovery with normal spinal cord myelination was seen. Intriguingly, this regional difference may be partially attributed to compensatory upregulation of Olig2 protein expression in the spinal cord after Olig1 deletion, which is not seen in brain. The current study demonstrates a unique role for Olig1 in promoting oligodendrocyte progenitor cell commitment, differentiation, and subsequent myelination primarily in brain, but not spinal cord.</abstract><cop>United States</cop><pub>Society for Neuroscience</pub><pmid>25762682</pmid><doi>10.1523/JNEUROSCI.4962-14.2015</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 2',3'-Cyclic-Nucleotide Phosphodiesterases - metabolism Age Factors Animals Animals, Newborn Basic Helix-Loop-Helix Transcription Factors - genetics Basic Helix-Loop-Helix Transcription Factors - metabolism Brain - cytology Brain - ultrastructure Cell Death - genetics Cell Differentiation - genetics Cell Differentiation - physiology Cells, Cultured Gene Expression Regulation, Developmental - genetics In Vitro Techniques Mice Mice, Inbred C57BL Mice, Transgenic Mutation - genetics Myelin Basic Protein - metabolism Myelin Proteolipid Protein - metabolism Myelin-Oligodendrocyte Glycoprotein - metabolism Oligodendroglia - physiology Oligodendroglia - ultrastructure SOXB1 Transcription Factors - metabolism Spinal Cord - cytology Stem Cells - physiology |
title | Olig1 function is required for oligodendrocyte differentiation in the mouse brain |
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