Sall1 Regulates Mitral Cell Development and Olfactory Nerve Extension in the Developing Olfactory Bulb
Identifieur interne : 000352 ( Main/Corpus ); précédent : 000351; suivant : 000353Sall1 Regulates Mitral Cell Development and Olfactory Nerve Extension in the Developing Olfactory Bulb
Auteurs : Susan J. Harrison ; Ryuichi Nishinakamura ; A. Paula MonaghanSource :
- Cerebral Cortex [ 1047-3211 ] ; 2007-11-17.
Abstract
Sall1 is a zinc finger containing transcription factor that is highly expressed during mammalian embryogenesis. In humans, the developmental disorder Townes Brocks Syndrome is associated with mutations in the SALL1 gene. Sall1-deficient animals die at birth due to kidney deficits; however, its function in the nervous system has not been characterized. We examined the role of Sall1 in the developing olfactory system. We demonstrate that Sall1 is expressed by cells in the olfactory epithelium and olfactory bulb (OB). Sall1-deficient OBs are reduced in size and exhibit alterations in neurogenesis and mitral cell production. In addition, the olfactory nerve failed to extend past the ventralmedial region of the OB in Sall1-deficient animals. We observed intrinsic patterns of neurogenesis during olfactory development in control animals. In Sall1-mutant animals, these patterns of neurogenesis were disrupted. These findings suggest a role for Sall1 in regulating neuronal differentiation and maturation in developing neural structures.
Url:
DOI: 10.1093/cercor/bhm191
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Harrison</name><affiliation><mods:affiliation>Department of Neurobiology, University of Pittsburgh, Pittsburgh, PA 15261, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Biochemistry and Molecular Genetics Graduate Program, University of Pittsburgh, Pittsburgh, PA 15261, USA</mods:affiliation></affiliation></author><author><name sortKey="Nishinakamura, Ryuichi" sort="Nishinakamura, Ryuichi" uniqKey="Nishinakamura R" first="Ryuichi" last="Nishinakamura">Ryuichi Nishinakamura</name><affiliation><mods:affiliation>Division of Integrative Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan</mods:affiliation></affiliation></author><author><name sortKey="Monaghan, A Paula" sort="Monaghan, A Paula" uniqKey="Monaghan A" first="A. Paula" last="Monaghan">A. 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Harrison</name><affiliation><mods:affiliation>Department of Neurobiology, University of Pittsburgh, Pittsburgh, PA 15261, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Biochemistry and Molecular Genetics Graduate Program, University of Pittsburgh, Pittsburgh, PA 15261, USA</mods:affiliation></affiliation></author><author><name sortKey="Nishinakamura, Ryuichi" sort="Nishinakamura, Ryuichi" uniqKey="Nishinakamura R" first="Ryuichi" last="Nishinakamura">Ryuichi Nishinakamura</name><affiliation><mods:affiliation>Division of Integrative Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan</mods:affiliation></affiliation></author><author><name sortKey="Monaghan, A Paula" sort="Monaghan, A Paula" uniqKey="Monaghan A" first="A. Paula" last="Monaghan">A. Paula Monaghan</name><affiliation><mods:affiliation>Department of Neurobiology, University of Pittsburgh, Pittsburgh, PA 15261, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Biochemistry and Molecular Genetics Graduate Program, University of Pittsburgh, Pittsburgh, PA 15261, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA 15261, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: monaghan@pitt.edu</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Cerebral Cortex</title><idno type="ISSN">1047-3211</idno><idno type="eISSN">1460-2199</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2007-11-17">2007-11-17</date><biblScope unit="volume">18</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="1604">1604</biblScope><biblScope unit="page" to="1617">1617</biblScope></imprint><idno type="ISSN">1047-3211</idno></series><idno type="istex">3FD6E937B1CC76AB7D366AC374FBB193E191FCFC</idno><idno type="DOI">10.1093/cercor/bhm191</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1047-3211</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Sall1 is a zinc finger containing transcription factor that is highly expressed during mammalian embryogenesis. In humans, the developmental disorder Townes Brocks Syndrome is associated with mutations in the SALL1 gene. Sall1-deficient animals die at birth due to kidney deficits; however, its function in the nervous system has not been characterized. We examined the role of Sall1 in the developing olfactory system. We demonstrate that Sall1 is expressed by cells in the olfactory epithelium and olfactory bulb (OB). Sall1-deficient OBs are reduced in size and exhibit alterations in neurogenesis and mitral cell production. In addition, the olfactory nerve failed to extend past the ventralmedial region of the OB in Sall1-deficient animals. We observed intrinsic patterns of neurogenesis during olfactory development in control animals. In Sall1-mutant animals, these patterns of neurogenesis were disrupted. These findings suggest a role for Sall1 in regulating neuronal differentiation and maturation in developing neural structures.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>Susan J. Harrison</name><affiliations><json:string>Department of Neurobiology, University of Pittsburgh, Pittsburgh, PA 15261, USA</json:string><json:string>Department of Biochemistry and Molecular Genetics Graduate Program, University of Pittsburgh, Pittsburgh, PA 15261, USA</json:string></affiliations></json:item><json:item><name>Ryuichi Nishinakamura</name><affiliations><json:string>Division of Integrative Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan</json:string></affiliations></json:item><json:item><name>A. Paula Monaghan</name><affiliations><json:string>Department of Neurobiology, University of Pittsburgh, Pittsburgh, PA 15261, USA</json:string><json:string>Department of Biochemistry and Molecular Genetics Graduate Program, University of Pittsburgh, Pittsburgh, PA 15261, USA</json:string><json:string>Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA 15261, USA</json:string><json:string>E-mail: monaghan@pitt.edu</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Articles</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neurogenesis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>olfactory nerve innervation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>proliferation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>spalt</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Townes Brocks Syndrome</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Sall1 is a zinc finger containing transcription factor that is highly expressed during mammalian embryogenesis. In humans, the developmental disorder Townes Brocks Syndrome is associated with mutations in the SALL1 gene. Sall1-deficient animals die at birth due to kidney deficits; however, its function in the nervous system has not been characterized. We examined the role of Sall1 in the developing olfactory system. We demonstrate that Sall1 is expressed by cells in the olfactory epithelium and olfactory bulb (OB). Sall1-deficient OBs are reduced in size and exhibit alterations in neurogenesis and mitral cell production. In addition, the olfactory nerve failed to extend past the ventralmedial region of the OB in Sall1-deficient animals. We observed intrinsic patterns of neurogenesis during olfactory development in control animals. In Sall1-mutant animals, these patterns of neurogenesis were disrupted. 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Paula</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff2">2</xref><xref ref-type="aff" rid="aff4">4</xref></contrib></contrib-group><aff id="aff1"><label>1</label>Department of Neurobiology, University of Pittsburgh, Pittsburgh, PA 15261, USA</aff><aff id="aff2"><label>2</label>Department of Biochemistry and Molecular Genetics Graduate Program, University of Pittsburgh, Pittsburgh, PA 15261, USA</aff><aff id="aff3"><label>3</label>Division of Integrative Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan</aff><aff id="aff4"><label>4</label>Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA 15261, USA</aff><author-notes><corresp>Address correspondence to Dr A. Paula Monaghan, 6065 BST3, 3501 5th Avenue, Pittsburgh, PA 15261, USA. Email: <email>monaghan@pitt.edu</email>.</corresp></author-notes><pub-date pub-type="epub-ppub"><month>7</month><year>2008</year></pub-date><pub-date pub-type="epub"><day>17</day><month>11</month><year>2007</year></pub-date><volume>18</volume><issue>7</issue><fpage>1604</fpage><lpage>1617</lpage><permissions><copyright-statement>© The Author 2007. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org</copyright-statement><copyright-year>2008</copyright-year></permissions><abstract><p>Sall1 is a zinc finger containing transcription factor that is highly expressed during mammalian embryogenesis. In humans, the developmental disorder Townes Brocks Syndrome is associated with mutations in the SALL1 gene. Sall1-deficient animals die at birth due to kidney deficits; however, its function in the nervous system has not been characterized. We examined the role of Sall1 in the developing olfactory system. We demonstrate that Sall1 is expressed by cells in the olfactory epithelium and olfactory bulb (OB). Sall1-deficient OBs are reduced in size and exhibit alterations in neurogenesis and mitral cell production. In addition, the olfactory nerve failed to extend past the ventral–medial region of the OB in Sall1-deficient animals. We observed intrinsic patterns of neurogenesis during olfactory development in control animals. In Sall1-mutant animals, these patterns of neurogenesis were disrupted. These findings suggest a role for Sall1 in regulating neuronal differentiation and maturation in developing neural structures.</p></abstract><kwd-group><kwd>neurogenesis</kwd><kwd>olfactory nerve innervation</kwd><kwd>proliferation</kwd><kwd>spalt</kwd><kwd>Townes Brocks Syndrome</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Sall1 Regulates Mitral Cell Development and Olfactory Nerve Extension in the Developing Olfactory Bulb</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Sall1 Regulates Mitral Cell Development and Olfactory Nerve Extension in the Developing Olfactory Bulb</title></titleInfo><name type="personal"><namePart type="given">Susan J.</namePart><namePart type="family">Harrison</namePart><affiliation>Department of Neurobiology, University of Pittsburgh, Pittsburgh, PA 15261, USA</affiliation><affiliation>Department of Biochemistry and Molecular Genetics Graduate Program, University of Pittsburgh, Pittsburgh, PA 15261, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ryuichi</namePart><namePart type="family">Nishinakamura</namePart><affiliation>Division of Integrative Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">A. 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In humans, the developmental disorder Townes Brocks Syndrome is associated with mutations in the SALL1 gene. Sall1-deficient animals die at birth due to kidney deficits; however, its function in the nervous system has not been characterized. We examined the role of Sall1 in the developing olfactory system. We demonstrate that Sall1 is expressed by cells in the olfactory epithelium and olfactory bulb (OB). Sall1-deficient OBs are reduced in size and exhibit alterations in neurogenesis and mitral cell production. In addition, the olfactory nerve failed to extend past the ventralmedial region of the OB in Sall1-deficient animals. We observed intrinsic patterns of neurogenesis during olfactory development in control animals. In Sall1-mutant animals, these patterns of neurogenesis were disrupted. These findings suggest a role for Sall1 in regulating neuronal differentiation and maturation in developing neural structures.</abstract><subject><genre>Keywords</genre><topic>neurogenesis</topic><topic>olfactory nerve innervation</topic><topic>proliferation</topic><topic>spalt</topic><topic>Townes Brocks Syndrome</topic></subject><relatedItem type="host"><titleInfo><title>Cerebral Cortex</title></titleInfo><identifier type="ISSN">1047-3211</identifier><identifier type="eISSN">1460-2199</identifier><identifier type="JournalID">cercor</identifier><identifier type="JournalID-hwp">cercor</identifier><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>18</number></detail><detail type="issue"><caption>no.</caption><number>7</number></detail><extent unit="pages"><start>1604</start><end>1617</end></extent></part></relatedItem><identifier type="istex">3FD6E937B1CC76AB7D366AC374FBB193E191FCFC</identifier><identifier type="DOI">10.1093/cercor/bhm191</identifier><accessCondition type="use and reproduction" contentType="Copyright">The Author 2007. 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