Analysis of HeyL expression in wild-type and Notch pathway mutant mouse embryos
In vertebrates Notch signaling regulates cell fate decisions and boundary formation and it underlies several murine and human diseases. Gene targeting experiments point to key roles of Notch receptors, ligands, modulators and downstream targets in somitogenesis, neurogenesis and vascular development...
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| Veröffentlicht in: | Mechanisms of development 2000-11, Vol.98 (1), p.175-178 |
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| creator | Leimeister, Cornelia Schumacher, Nina Steidl, Christian Gessler, Manfred |
| description | In vertebrates Notch signaling regulates cell fate decisions and boundary formation and it underlies several murine and human diseases. Gene targeting experiments point to key roles of Notch receptors, ligands, modulators and downstream targets in somitogenesis, neurogenesis and vascular development. Here we report the embryonic expression of the
hairy-related basic helix-loop-helix gene
HeyL in wild-type and Notch pathway mutant mice. We show that
HeyL is strongly expressed in the presomitic mesoderm, the somites, the peripheral nervous system and smooth muscle of all arteries. Loss of
HeyL expression at the level of nascent somites in
Notch1 and
Delta-like1 knockout mutants implicates
HeyL as a Notch effector during somite formation. Furthermore,
HeyL expression in vascular smooth muscle cells and in the thymus strikingly overlaps with that of
Notch3, mutations of which underlie the CADASIL vascular disorder. |
| doi_str_mv | 10.1016/S0925-4773(00)00459-7 |
| format | Article |
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hairy-related basic helix-loop-helix gene
HeyL in wild-type and Notch pathway mutant mice. We show that
HeyL is strongly expressed in the presomitic mesoderm, the somites, the peripheral nervous system and smooth muscle of all arteries. Loss of
HeyL expression at the level of nascent somites in
Notch1 and
Delta-like1 knockout mutants implicates
HeyL as a Notch effector during somite formation. Furthermore,
HeyL expression in vascular smooth muscle cells and in the thymus strikingly overlaps with that of
Notch3, mutations of which underlie the CADASIL vascular disorder.</description><identifier>ISSN: 0925-4773</identifier><identifier>EISSN: 1872-6356</identifier><identifier>DOI: 10.1016/S0925-4773(00)00459-7</identifier><identifier>PMID: 11044625</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Animals ; Arteries ; Basic helix-loop-helix ; CADASIL ; Cranial ganglia ; Delta ; Embryonic and Fetal Development - genetics ; Gene Expression Regulation, Developmental ; Hairy ; Helix-Loop-Helix Motifs - genetics ; Hey ; Humans ; In Situ Hybridization ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins - genetics ; Mice ; Mice, Knockout ; Mouse ; Mutation ; Notch ; Presomititic mesoderm ; Receptor, Notch1 ; Receptors, Cell Surface ; Smooth muscles ; Somites ; Somitogenesis ; Spinal ganglia ; Thymus ; Transcription Factors - genetics ; Vasculature</subject><ispartof>Mechanisms of development, 2000-11, Vol.98 (1), p.175-178</ispartof><rights>2000 Elsevier Science Ireland Ltd</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-6cb4d522b104edb5b2e226acad682a98c472e65168328ad486f7234462509a413</citedby><cites>FETCH-LOGICAL-c526t-6cb4d522b104edb5b2e226acad682a98c472e65168328ad486f7234462509a413</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0925477300004597$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11044625$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Leimeister, Cornelia</creatorcontrib><creatorcontrib>Schumacher, Nina</creatorcontrib><creatorcontrib>Steidl, Christian</creatorcontrib><creatorcontrib>Gessler, Manfred</creatorcontrib><title>Analysis of HeyL expression in wild-type and Notch pathway mutant mouse embryos</title><title>Mechanisms of development</title><addtitle>Mech Dev</addtitle><description>In vertebrates Notch signaling regulates cell fate decisions and boundary formation and it underlies several murine and human diseases. Gene targeting experiments point to key roles of Notch receptors, ligands, modulators and downstream targets in somitogenesis, neurogenesis and vascular development. Here we report the embryonic expression of the
hairy-related basic helix-loop-helix gene
HeyL in wild-type and Notch pathway mutant mice. We show that
HeyL is strongly expressed in the presomitic mesoderm, the somites, the peripheral nervous system and smooth muscle of all arteries. Loss of
HeyL expression at the level of nascent somites in
Notch1 and
Delta-like1 knockout mutants implicates
HeyL as a Notch effector during somite formation. Furthermore,
HeyL expression in vascular smooth muscle cells and in the thymus strikingly overlaps with that of
Notch3, mutations of which underlie the CADASIL vascular disorder.</description><subject>Animals</subject><subject>Arteries</subject><subject>Basic helix-loop-helix</subject><subject>CADASIL</subject><subject>Cranial ganglia</subject><subject>Delta</subject><subject>Embryonic and Fetal Development - genetics</subject><subject>Gene Expression Regulation, Developmental</subject><subject>Hairy</subject><subject>Helix-Loop-Helix Motifs - genetics</subject><subject>Hey</subject><subject>Humans</subject><subject>In Situ Hybridization</subject><subject>Intracellular Signaling Peptides and Proteins</subject><subject>Membrane Proteins - genetics</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mouse</subject><subject>Mutation</subject><subject>Notch</subject><subject>Presomititic mesoderm</subject><subject>Receptor, Notch1</subject><subject>Receptors, Cell Surface</subject><subject>Smooth muscles</subject><subject>Somites</subject><subject>Somitogenesis</subject><subject>Spinal ganglia</subject><subject>Thymus</subject><subject>Transcription Factors - genetics</subject><subject>Vasculature</subject><issn>0925-4773</issn><issn>1872-6356</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMtOwzAQRS0EouXxCSCvECwCthM7yQpVFVCkii6AteXYU9UoL2yHkr8nfQiWrGZzZu6dg9AFJbeUUHH3SnLGoyRN42tCbghJeB6lB2hMs5RFIubiEI1_kRE68f6DEEKpoMdoRClJEsH4GC0mtSp7bz1ulngG_RzDd-vAe9vU2NZ4bUsThb4FrGqDX5qgV7hVYbVWPa66oOqAq6bzgKEqXN_4M3S0VKWH8_08Re-PD2_TWTRfPD1PJ_NIcyZCJHSRGM5YMRQBU_CCAWNCaWVExlSe6SRlIDgVWcwyZZJMLFMWbzuTXCU0PkVXu7utaz478EFW1msoS1XD0EcOtGB5ygeQ70DtGu8dLGXrbKVcLymRG5Nya1JuNElC5NakTIe9y31AV1Rg_rb26gbgfgfA8OaXBSe9tlBrMNaBDtI09p-IH08Ugjs</recordid><startdate>20001101</startdate><enddate>20001101</enddate><creator>Leimeister, Cornelia</creator><creator>Schumacher, Nina</creator><creator>Steidl, Christian</creator><creator>Gessler, Manfred</creator><general>Elsevier Ireland Ltd</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>7X8</scope></search><sort><creationdate>20001101</creationdate><title>Analysis of HeyL expression in wild-type and Notch pathway mutant mouse embryos</title><author>Leimeister, Cornelia ; Schumacher, Nina ; Steidl, Christian ; Gessler, Manfred</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-6cb4d522b104edb5b2e226acad682a98c472e65168328ad486f7234462509a413</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Arteries</topic><topic>Basic helix-loop-helix</topic><topic>CADASIL</topic><topic>Cranial ganglia</topic><topic>Delta</topic><topic>Embryonic and Fetal Development - genetics</topic><topic>Gene Expression Regulation, Developmental</topic><topic>Hairy</topic><topic>Helix-Loop-Helix Motifs - genetics</topic><topic>Hey</topic><topic>Humans</topic><topic>In Situ Hybridization</topic><topic>Intracellular Signaling Peptides and Proteins</topic><topic>Membrane Proteins - genetics</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mouse</topic><topic>Mutation</topic><topic>Notch</topic><topic>Presomititic mesoderm</topic><topic>Receptor, Notch1</topic><topic>Receptors, Cell Surface</topic><topic>Smooth muscles</topic><topic>Somites</topic><topic>Somitogenesis</topic><topic>Spinal ganglia</topic><topic>Thymus</topic><topic>Transcription Factors - genetics</topic><topic>Vasculature</topic><toplevel>online_resources</toplevel><creatorcontrib>Leimeister, Cornelia</creatorcontrib><creatorcontrib>Schumacher, Nina</creatorcontrib><creatorcontrib>Steidl, Christian</creatorcontrib><creatorcontrib>Gessler, Manfred</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>MEDLINE - Academic</collection><jtitle>Mechanisms of development</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Leimeister, Cornelia</au><au>Schumacher, Nina</au><au>Steidl, Christian</au><au>Gessler, Manfred</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Analysis of HeyL expression in wild-type and Notch pathway mutant mouse embryos</atitle><jtitle>Mechanisms of development</jtitle><addtitle>Mech Dev</addtitle><date>2000-11-01</date><risdate>2000</risdate><volume>98</volume><issue>1</issue><spage>175</spage><epage>178</epage><pages>175-178</pages><issn>0925-4773</issn><eissn>1872-6356</eissn><abstract>In vertebrates Notch signaling regulates cell fate decisions and boundary formation and it underlies several murine and human diseases. Gene targeting experiments point to key roles of Notch receptors, ligands, modulators and downstream targets in somitogenesis, neurogenesis and vascular development. Here we report the embryonic expression of the
hairy-related basic helix-loop-helix gene
HeyL in wild-type and Notch pathway mutant mice. We show that
HeyL is strongly expressed in the presomitic mesoderm, the somites, the peripheral nervous system and smooth muscle of all arteries. Loss of
HeyL expression at the level of nascent somites in
Notch1 and
Delta-like1 knockout mutants implicates
HeyL as a Notch effector during somite formation. Furthermore,
HeyL expression in vascular smooth muscle cells and in the thymus strikingly overlaps with that of
Notch3, mutations of which underlie the CADASIL vascular disorder.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>11044625</pmid><doi>10.1016/S0925-4773(00)00459-7</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Arteries Basic helix-loop-helix CADASIL Cranial ganglia Delta Embryonic and Fetal Development - genetics Gene Expression Regulation, Developmental Hairy Helix-Loop-Helix Motifs - genetics Hey Humans In Situ Hybridization Intracellular Signaling Peptides and Proteins Membrane Proteins - genetics Mice Mice, Knockout Mouse Mutation Notch Presomititic mesoderm Receptor, Notch1 Receptors, Cell Surface Smooth muscles Somites Somitogenesis Spinal ganglia Thymus Transcription Factors - genetics Vasculature |
| title | Analysis of HeyL expression in wild-type and Notch pathway mutant mouse embryos |
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