Neural Cell Type-Specific Expression of QKI Proteins Is Altered in quakingviable Mutant Mice
qkI, a newly cloned gene lying immediately proximal to the deletion in the quakingviable mutation, is transcribed into three messages of 5, 6, and 7 kb. Antibodies raised to the unique carboxy peptides of the resulting QKI proteins reveal that, in the nervous system, all three QKI proteins are expre...
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| Veröffentlicht in: | The Journal of neuroscience 1996-12, Vol.16 (24), p.7941-7949 |
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| container_issue | 24 |
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| container_title | The Journal of neuroscience |
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| creator | Hardy, Rebecca J Loushin, Carrie L Friedrich Jr., Victor L Chen, Qi Ebersole, Thomas A Lazzarini, Robert A Artzt, Karen |
| description | qkI, a newly cloned gene lying immediately proximal to the deletion in the quakingviable mutation, is transcribed into three messages of 5, 6, and 7 kb. Antibodies raised to the unique carboxy peptides of the resulting QKI proteins reveal that, in the nervous system, all three QKI proteins are expressed strongly in myelin-forming cells and also in astrocytes. Interestingly, individual isoforms show distinct intracellular distributions: QKI-6 and QKI-7 are localized to perikaryal cytoplasm, whereas QKI-5 invariably is restricted to the nucleus, consistent with the predicted role of QKI as an RNA-binding protein. In quakingviable mutants, which display severe dysmyelination, QKI-6 and QKI-7 are absent exclusively from myelin-forming cells. By contrast, QKI-5 is absent only in oligodendrocytes of severely affected tracts. These observations implicate QKI proteins as regulators of myelination and reveal key insights into the mechanisms of dysmyelination in the quakingviable mutant. |
| doi_str_mv | 10.1523/jneurosci.16-24-07941.1996 |
| format | Article |
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Antibodies raised to the unique carboxy peptides of the resulting QKI proteins reveal that, in the nervous system, all three QKI proteins are expressed strongly in myelin-forming cells and also in astrocytes. Interestingly, individual isoforms show distinct intracellular distributions: QKI-6 and QKI-7 are localized to perikaryal cytoplasm, whereas QKI-5 invariably is restricted to the nucleus, consistent with the predicted role of QKI as an RNA-binding protein. In quakingviable mutants, which display severe dysmyelination, QKI-6 and QKI-7 are absent exclusively from myelin-forming cells. By contrast, QKI-5 is absent only in oligodendrocytes of severely affected tracts. These observations implicate QKI proteins as regulators of myelination and reveal key insights into the mechanisms of dysmyelination in the quakingviable mutant.</description><identifier>ISSN: 0270-6474</identifier><identifier>EISSN: 1529-2401</identifier><identifier>DOI: 10.1523/jneurosci.16-24-07941.1996</identifier><identifier>PMID: 8987822</identifier><language>eng</language><publisher>United States: Soc Neuroscience</publisher><subject>Aging - metabolism ; Animals ; Astrocytes - metabolism ; Brain - cytology ; Brain - metabolism ; Demyelinating Diseases - genetics ; Demyelinating Diseases - metabolism ; Immune Sera ; Isomerism ; Mice ; Mice, Quaking ; Myelin Sheath - physiology ; Neuroglia - metabolism ; Neurons - metabolism ; Oligodendroglia - metabolism ; RNA, Messenger - metabolism ; RNA-Binding Proteins - genetics ; RNA-Binding Proteins - immunology ; RNA-Binding Proteins - metabolism ; Schwann Cells - metabolism ; Schwann Cells - physiology</subject><ispartof>The Journal of neuroscience, 1996-12, Vol.16 (24), p.7941-7949</ispartof><rights>Copyright © 1996 Society for Neuroscience 1996</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c370t-ed754d9143c6898a4c4a41db5bad767eda72c39280f8b2cd9a6d3c4b80e7edb53</citedby><cites>FETCH-LOGICAL-c370t-ed754d9143c6898a4c4a41db5bad767eda72c39280f8b2cd9a6d3c4b80e7edb53</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/PMC6579212/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6579212/$$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/8987822$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hardy, Rebecca J</creatorcontrib><creatorcontrib>Loushin, Carrie L</creatorcontrib><creatorcontrib>Friedrich Jr., Victor L</creatorcontrib><creatorcontrib>Chen, Qi</creatorcontrib><creatorcontrib>Ebersole, Thomas A</creatorcontrib><creatorcontrib>Lazzarini, Robert A</creatorcontrib><creatorcontrib>Artzt, Karen</creatorcontrib><title>Neural Cell Type-Specific Expression of QKI Proteins Is Altered in quakingviable Mutant Mice</title><title>The Journal of neuroscience</title><addtitle>J Neurosci</addtitle><description>qkI, a newly cloned gene lying immediately proximal to the deletion in the quakingviable mutation, is transcribed into three messages of 5, 6, and 7 kb. 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These observations implicate QKI proteins as regulators of myelination and reveal key insights into the mechanisms of dysmyelination in the quakingviable mutant.</description><subject>Aging - metabolism</subject><subject>Animals</subject><subject>Astrocytes - metabolism</subject><subject>Brain - cytology</subject><subject>Brain - metabolism</subject><subject>Demyelinating Diseases - genetics</subject><subject>Demyelinating Diseases - metabolism</subject><subject>Immune Sera</subject><subject>Isomerism</subject><subject>Mice</subject><subject>Mice, Quaking</subject><subject>Myelin Sheath - physiology</subject><subject>Neuroglia - metabolism</subject><subject>Neurons - metabolism</subject><subject>Oligodendroglia - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA-Binding Proteins - genetics</subject><subject>RNA-Binding Proteins - immunology</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Schwann Cells - metabolism</subject><subject>Schwann Cells - physiology</subject><issn>0270-6474</issn><issn>1529-2401</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkFtPwyAYhonR6Dz8BBPijVedQGkpXpiYZeo8H-9MCIWvG9q1tXRO_73MGaNXJLzf-_DxILRHSZ8mLD54qWDW1t64Pk0jxiMiJKd9KmW6gnphQoZLQldRjzBBopQLvoE2vX8hhAhCxTpaz2QmMsZ66Pk6oHSJB1CW-PGzgeihAeMKZ_Dwo2nBe1dXuC7w3cUI37Z1B67yeOTxcdlBCxa7Cr_N9Kurxu9O5yXgq1mnqw5fOQPbaK3QpYedn3MLPZ0MHwdn0eXN6WhwfBmZWJAuAisSbiXlsUnDYpobrjm1eZJrK1IBVgtmYskyUmQ5M1bq1MaG5xmBEOZJvIWOltxmlk_BGqi68CfVtG6q209Va6f-J5WbqHH9rtJESEZZABwuASZo9S0Uv11K1EK5Or8ePt3fPAxGiqaKcfWtXC2Uh_Lu39d_qz-OQ76_zCduPJm7FpSf6rIM01TN5_Mlb4GLvwBPqI9Z</recordid><startdate>19961215</startdate><enddate>19961215</enddate><creator>Hardy, Rebecca J</creator><creator>Loushin, Carrie L</creator><creator>Friedrich Jr., Victor L</creator><creator>Chen, Qi</creator><creator>Ebersole, Thomas A</creator><creator>Lazzarini, Robert A</creator><creator>Artzt, Karen</creator><general>Soc Neuroscience</general><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>5PM</scope></search><sort><creationdate>19961215</creationdate><title>Neural Cell Type-Specific Expression of QKI Proteins Is Altered in quakingviable Mutant Mice</title><author>Hardy, Rebecca J ; Loushin, Carrie L ; Friedrich Jr., Victor L ; Chen, Qi ; Ebersole, Thomas A ; Lazzarini, Robert A ; Artzt, Karen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c370t-ed754d9143c6898a4c4a41db5bad767eda72c39280f8b2cd9a6d3c4b80e7edb53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Aging - metabolism</topic><topic>Animals</topic><topic>Astrocytes - metabolism</topic><topic>Brain - cytology</topic><topic>Brain - metabolism</topic><topic>Demyelinating Diseases - genetics</topic><topic>Demyelinating Diseases - metabolism</topic><topic>Immune Sera</topic><topic>Isomerism</topic><topic>Mice</topic><topic>Mice, Quaking</topic><topic>Myelin Sheath - physiology</topic><topic>Neuroglia - metabolism</topic><topic>Neurons - metabolism</topic><topic>Oligodendroglia - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>RNA-Binding Proteins - genetics</topic><topic>RNA-Binding Proteins - immunology</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Schwann Cells - metabolism</topic><topic>Schwann Cells - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hardy, Rebecca J</creatorcontrib><creatorcontrib>Loushin, Carrie L</creatorcontrib><creatorcontrib>Friedrich Jr., Victor L</creatorcontrib><creatorcontrib>Chen, Qi</creatorcontrib><creatorcontrib>Ebersole, Thomas A</creatorcontrib><creatorcontrib>Lazzarini, Robert A</creatorcontrib><creatorcontrib>Artzt, Karen</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</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>Hardy, Rebecca J</au><au>Loushin, Carrie L</au><au>Friedrich Jr., Victor L</au><au>Chen, Qi</au><au>Ebersole, Thomas A</au><au>Lazzarini, Robert A</au><au>Artzt, Karen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neural Cell Type-Specific Expression of QKI Proteins Is Altered in quakingviable Mutant Mice</atitle><jtitle>The Journal of neuroscience</jtitle><addtitle>J Neurosci</addtitle><date>1996-12-15</date><risdate>1996</risdate><volume>16</volume><issue>24</issue><spage>7941</spage><epage>7949</epage><pages>7941-7949</pages><issn>0270-6474</issn><eissn>1529-2401</eissn><abstract>qkI, a newly cloned gene lying immediately proximal to the deletion in the quakingviable mutation, is transcribed into three messages of 5, 6, and 7 kb. Antibodies raised to the unique carboxy peptides of the resulting QKI proteins reveal that, in the nervous system, all three QKI proteins are expressed strongly in myelin-forming cells and also in astrocytes. Interestingly, individual isoforms show distinct intracellular distributions: QKI-6 and QKI-7 are localized to perikaryal cytoplasm, whereas QKI-5 invariably is restricted to the nucleus, consistent with the predicted role of QKI as an RNA-binding protein. In quakingviable mutants, which display severe dysmyelination, QKI-6 and QKI-7 are absent exclusively from myelin-forming cells. By contrast, QKI-5 is absent only in oligodendrocytes of severely affected tracts. These observations implicate QKI proteins as regulators of myelination and reveal key insights into the mechanisms of dysmyelination in the quakingviable mutant.</abstract><cop>United States</cop><pub>Soc Neuroscience</pub><pmid>8987822</pmid><doi>10.1523/jneurosci.16-24-07941.1996</doi><tpages>9</tpages></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Aging - metabolism Animals Astrocytes - metabolism Brain - cytology Brain - metabolism Demyelinating Diseases - genetics Demyelinating Diseases - metabolism Immune Sera Isomerism Mice Mice, Quaking Myelin Sheath - physiology Neuroglia - metabolism Neurons - metabolism Oligodendroglia - metabolism RNA, Messenger - metabolism RNA-Binding Proteins - genetics RNA-Binding Proteins - immunology RNA-Binding Proteins - metabolism Schwann Cells - metabolism Schwann Cells - physiology |
| title | Neural Cell Type-Specific Expression of QKI Proteins Is Altered in quakingviable Mutant Mice |
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