bHLH Transcription Factor Olig1 Is Required to Repair Demyelinated Lesions in the CNS
Olig1 and Olig2 are closely related basic helix-loop-helix (bHLH) transcription factors that are expressed in myelinating oligodendrocytes and their progenitor cells in the developing central nervous system (CNS). Olig2 is necessary for the specification of oligodendrocytes, but the biological funct...
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| Veröffentlicht in: | Science (American Association for the Advancement of Science) 2004-12, Vol.306 (5704), p.2111-2115 |
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| container_title | Science (American Association for the Advancement of Science) |
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| creator | Arnett, Heather A Fancy, Stephen P. J Alberta, John A Zhao, Chao Plant, Sheila R Kaing, Sovann Raine, Cedric S Rowitch, David H Franklin, Robin J. M Stiles, Charles D |
| description | Olig1 and Olig2 are closely related basic helix-loop-helix (bHLH) transcription factors that are expressed in myelinating oligodendrocytes and their progenitor cells in the developing central nervous system (CNS). Olig2 is necessary for the specification of oligodendrocytes, but the biological functions of Olig1 during oligodendrocyte lineage development are poorly understood. We show here that Olig1 function in mice is required not to develop the brain but to repair it. Specifically, we demonstrate a genetic requirement for Olig1 in repairing the types of lesions that occur in patients with multiple sclerosis. |
| doi_str_mv | 10.1126/science.1103709 |
| format | Article |
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J ; Alberta, John A ; Zhao, Chao ; Plant, Sheila R ; Kaing, Sovann ; Raine, Cedric S ; Rowitch, David H ; Franklin, Robin J. M ; Stiles, Charles D</creator><creatorcontrib>Arnett, Heather A ; Fancy, Stephen P. J ; Alberta, John A ; Zhao, Chao ; Plant, Sheila R ; Kaing, Sovann ; Raine, Cedric S ; Rowitch, David H ; Franklin, Robin J. M ; Stiles, Charles D</creatorcontrib><description>Olig1 and Olig2 are closely related basic helix-loop-helix (bHLH) transcription factors that are expressed in myelinating oligodendrocytes and their progenitor cells in the developing central nervous system (CNS). Olig2 is necessary for the specification of oligodendrocytes, but the biological functions of Olig1 during oligodendrocyte lineage development are poorly understood. We show here that Olig1 function in mice is required not to develop the brain but to repair it. Specifically, we demonstrate a genetic requirement for Olig1 in repairing the types of lesions that occur in patients with multiple sclerosis.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.1103709</identifier><identifier>PMID: 15604411</identifier><identifier>CODEN: SCIEAS</identifier><language>eng</language><publisher>Washington, DC: American Association for the Advancement of Science</publisher><subject>Adults ; Anatomy ; Animals ; Animals, Newborn ; Basic Helix-Loop-Helix Transcription Factors ; Biological and medical sciences ; Brain ; Brain - growth & development ; Brain - physiology ; Cell Nucleus - metabolism ; Central nervous system ; Cuprizone - pharmacology ; Cytoplasm - metabolism ; Demyelinating diseases ; Demyelinating Diseases - physiopathology ; Developmental Stages ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Ethidium - pharmacology ; Genetic aspects ; Genetic research ; Genetic transcription ; Humans ; Injuries ; Lesions ; Lysophosphatidylcholines - pharmacology ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Microscopy ; Multiple sclerosis ; Multiple Sclerosis - physiopathology ; Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis ; Myelin Sheath - physiology ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Nerve Tissue Proteins - physiology ; Nervous system ; Neurology ; Neuroscience ; Oligodendrocyte Transcription Factor 2 ; Oligodendroglia ; Oligodendroglia - physiology ; Patients ; Progenitor cells ; Rats ; Rats, Sprague-Dawley ; Rodents ; Spinal Cord - growth & development ; Spinal Cord - physiology ; Stem Cells - physiology ; Transcription (Genetics) ; Transcription Factors - genetics ; Transcription Factors - metabolism ; White matter</subject><ispartof>Science (American Association for the Advancement of Science), 2004-12, Vol.306 (5704), p.2111-2115</ispartof><rights>Copyright 2004 American Association for the Advancement of Science</rights><rights>2005 INIST-CNRS</rights><rights>COPYRIGHT 2004 American Association for the Advancement of Science</rights><rights>COPYRIGHT 2004 American Association for the Advancement of Science</rights><rights>Copyright American Association for the Advancement of Science Dec 17, 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c808t-a8f76492fb3105fd808d461389a74a56f8ac3d59b59ad6cce56bca266bf2be883</citedby><cites>FETCH-LOGICAL-c808t-a8f76492fb3105fd808d461389a74a56f8ac3d59b59ad6cce56bca266bf2be883</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/3839726$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3839726$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,776,780,799,2871,2872,27901,27902,57992,58225</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16380418$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15604411$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Arnett, Heather A</creatorcontrib><creatorcontrib>Fancy, Stephen P. J</creatorcontrib><creatorcontrib>Alberta, John A</creatorcontrib><creatorcontrib>Zhao, Chao</creatorcontrib><creatorcontrib>Plant, Sheila R</creatorcontrib><creatorcontrib>Kaing, Sovann</creatorcontrib><creatorcontrib>Raine, Cedric S</creatorcontrib><creatorcontrib>Rowitch, David H</creatorcontrib><creatorcontrib>Franklin, Robin J. M</creatorcontrib><creatorcontrib>Stiles, Charles D</creatorcontrib><title>bHLH Transcription Factor Olig1 Is Required to Repair Demyelinated Lesions in the CNS</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>Olig1 and Olig2 are closely related basic helix-loop-helix (bHLH) transcription factors that are expressed in myelinating oligodendrocytes and their progenitor cells in the developing central nervous system (CNS). Olig2 is necessary for the specification of oligodendrocytes, but the biological functions of Olig1 during oligodendrocyte lineage development are poorly understood. We show here that Olig1 function in mice is required not to develop the brain but to repair it. Specifically, we demonstrate a genetic requirement for Olig1 in repairing the types of lesions that occur in patients with multiple sclerosis.</description><subject>Adults</subject><subject>Anatomy</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Basic Helix-Loop-Helix Transcription Factors</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Brain - growth & development</subject><subject>Brain - physiology</subject><subject>Cell Nucleus - metabolism</subject><subject>Central nervous system</subject><subject>Cuprizone - pharmacology</subject><subject>Cytoplasm - metabolism</subject><subject>Demyelinating diseases</subject><subject>Demyelinating Diseases - physiopathology</subject><subject>Developmental Stages</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Ethidium - pharmacology</subject><subject>Genetic aspects</subject><subject>Genetic research</subject><subject>Genetic transcription</subject><subject>Humans</subject><subject>Injuries</subject><subject>Lesions</subject><subject>Lysophosphatidylcholines - pharmacology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microscopy</subject><subject>Multiple sclerosis</subject><subject>Multiple Sclerosis - physiopathology</subject><subject>Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. 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J ; Alberta, John A ; Zhao, Chao ; Plant, Sheila R ; Kaing, Sovann ; Raine, Cedric S ; Rowitch, David H ; Franklin, Robin J. 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Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis</topic><topic>Myelin Sheath - physiology</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Nerve Tissue Proteins - physiology</topic><topic>Nervous system</topic><topic>Neurology</topic><topic>Neuroscience</topic><topic>Oligodendrocyte Transcription Factor 2</topic><topic>Oligodendroglia</topic><topic>Oligodendroglia - physiology</topic><topic>Patients</topic><topic>Progenitor cells</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rodents</topic><topic>Spinal Cord - growth & development</topic><topic>Spinal Cord - physiology</topic><topic>Stem Cells - physiology</topic><topic>Transcription (Genetics)</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>White matter</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Arnett, Heather A</creatorcontrib><creatorcontrib>Fancy, Stephen P. 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Olig2 is necessary for the specification of oligodendrocytes, but the biological functions of Olig1 during oligodendrocyte lineage development are poorly understood. We show here that Olig1 function in mice is required not to develop the brain but to repair it. Specifically, we demonstrate a genetic requirement for Olig1 in repairing the types of lesions that occur in patients with multiple sclerosis.</abstract><cop>Washington, DC</cop><pub>American Association for the Advancement of Science</pub><pmid>15604411</pmid><doi>10.1126/science.1103709</doi><tpages>5</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0036-8075 |
| ispartof | Science (American Association for the Advancement of Science), 2004-12, Vol.306 (5704), p.2111-2115 |
| issn | 0036-8075 1095-9203 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_743089551 |
| source | American Association for the Advancement of Science; Jstor Complete Legacy; MEDLINE |
| subjects | Adults Anatomy Animals Animals, Newborn Basic Helix-Loop-Helix Transcription Factors Biological and medical sciences Brain Brain - growth & development Brain - physiology Cell Nucleus - metabolism Central nervous system Cuprizone - pharmacology Cytoplasm - metabolism Demyelinating diseases Demyelinating Diseases - physiopathology Developmental Stages DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Ethidium - pharmacology Genetic aspects Genetic research Genetic transcription Humans Injuries Lesions Lysophosphatidylcholines - pharmacology Medical sciences Mice Mice, Inbred C57BL Microscopy Multiple sclerosis Multiple Sclerosis - physiopathology Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis Myelin Sheath - physiology Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Nerve Tissue Proteins - physiology Nervous system Neurology Neuroscience Oligodendrocyte Transcription Factor 2 Oligodendroglia Oligodendroglia - physiology Patients Progenitor cells Rats Rats, Sprague-Dawley Rodents Spinal Cord - growth & development Spinal Cord - physiology Stem Cells - physiology Transcription (Genetics) Transcription Factors - genetics Transcription Factors - metabolism White matter |
| title | bHLH Transcription Factor Olig1 Is Required to Repair Demyelinated Lesions in the CNS |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-13T23%3A13%3A47IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=bHLH%20Transcription%20Factor%20Olig1%20Is%20Required%20to%20Repair%20Demyelinated%20Lesions%20in%20the%20CNS&rft.jtitle=Science%20(American%20Association%20for%20the%20Advancement%20of%20Science)&rft.au=Arnett,%20Heather%20A&rft.date=2004-12-17&rft.volume=306&rft.issue=5704&rft.spage=2111&rft.epage=2115&rft.pages=2111-2115&rft.issn=0036-8075&rft.eissn=1095-9203&rft.coden=SCIEAS&rft_id=info:doi/10.1126/science.1103709&rft_dat=%3Cgale_proqu%3EA127196216%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=213604218&rft_id=info:pmid/15604411&rft_galeid=A127196216&rft_jstor_id=3839726&rfr_iscdi=true |