Mena Is Required for Neurulation and Commissure Formation
Mammalian enabled (Mena) is a member of a protein family thought to link signal transduction pathways to localized remodeling of the actin cytoskeleton. Mena binds directly to Profilin, an actin-binding protein that modulates actin polymerization. In primary neurons, Mena is concentrated at the tips...
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| Veröffentlicht in: | Neuron (Cambridge, Mass.) Mass.), 1999-02, Vol.22 (2), p.313-325 |
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| container_title | Neuron (Cambridge, Mass.) |
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| creator | Lanier, Lorene M Gates, Monte A Witke, Walter Menzies, A.Sheila Wehman, Ann M Macklis, Jeffrey D Kwiatkowski, David Soriano, Philippe Gertler, Frank B |
| description | Mammalian enabled (Mena) is a member of a protein family thought to link signal transduction pathways to localized remodeling of the actin cytoskeleton. Mena binds directly to Profilin, an actin-binding protein that modulates actin polymerization. In primary neurons, Mena is concentrated at the tips of growth cone filopodia. Mena-deficient mice are viable; however, axons projecting from interhemispheric cortico-cortical neurons are misrouted in early neonates, and failed decussation of the corpus callosum as well as defects in the hippocampal commissure and the pontocerebellar pathway are evident in the adult. Mena-deficient mice that are heterozygous for a Profilin I deletion die in utero and display defects in neurulation, demonstrating an important functional role for Mena in regulation of the actin cytoskeleton. |
| doi_str_mv | 10.1016/S0896-6273(00)81092-2 |
| format | Article |
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Mena binds directly to Profilin, an actin-binding protein that modulates actin polymerization. In primary neurons, Mena is concentrated at the tips of growth cone filopodia. Mena-deficient mice are viable; however, axons projecting from interhemispheric cortico-cortical neurons are misrouted in early neonates, and failed decussation of the corpus callosum as well as defects in the hippocampal commissure and the pontocerebellar pathway are evident in the adult. 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Mena-deficient mice that are heterozygous for a Profilin I deletion die in utero and display defects in neurulation, demonstrating an important functional role for Mena in regulation of the actin cytoskeleton.</description><subject>Animals</subject><subject>Animals, Newborn - physiology</subject><subject>Axons - physiology</subject><subject>Brain - embryology</subject><subject>Carrier Proteins - genetics</subject><subject>Carrier Proteins - physiology</subject><subject>Contractile Proteins</subject><subject>Cytoskeletal Proteins</subject><subject>Embryo, Mammalian - physiology</subject><subject>Embryonic and Fetal Development - physiology</subject><subject>Gene Deletion</subject><subject>Growth Cones - physiology</subject><subject>Mice - embryology</subject><subject>Microfilament Proteins - genetics</subject><subject>Mutation - physiology</subject><subject>Nervous System - embryology</subject><subject>Profilins</subject><subject>Tissue Distribution</subject><issn>0896-6273</issn><issn>1097-4199</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMtKAzEUhoMotlYfQZmV6GI0t0malUixWqgKXtYhkzmBkbm0yYzg25t2irjr6hz4v3PhQ-ic4BuCibh9x1MlUkElu8L4ekqwoik9QOPYyJQTpQ7R-A8ZoZMQvjAmPFPkGI0IxkIxJsdIPUNjkkVI3mDdlx6KxLU-eYHe95XpyrZJTFMks7auyxB6D8m89fU2OEVHzlQBznZ1gj7nDx-zp3T5-riY3S9TyxXpUpdzlTtluKEFkcoITKZZnktpDGVCUKAxsJzTLIbYKuK4dVNhMwcsM1ayCboc9q58u-4hdDq-YqGqTANtH7RQgnDM2F6QSMpllokIZgNofRuCB6dXvqyN_9EE641cvZWrN-Y0xnorV9M4d7E70Oc1FP-mBpsRuBsAiD6-S_A62BIaC0U0aztdtOWeE79_zIhf</recordid><startdate>19990201</startdate><enddate>19990201</enddate><creator>Lanier, Lorene M</creator><creator>Gates, Monte A</creator><creator>Witke, Walter</creator><creator>Menzies, A.Sheila</creator><creator>Wehman, Ann M</creator><creator>Macklis, Jeffrey D</creator><creator>Kwiatkowski, David</creator><creator>Soriano, Philippe</creator><creator>Gertler, Frank B</creator><general>Elsevier Inc</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>7TK</scope><scope>7X8</scope></search><sort><creationdate>19990201</creationdate><title>Mena Is Required for Neurulation and Commissure Formation</title><author>Lanier, Lorene M ; Gates, Monte A ; Witke, Walter ; Menzies, A.Sheila ; Wehman, Ann M ; Macklis, Jeffrey D ; Kwiatkowski, David ; Soriano, Philippe ; Gertler, Frank B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c491t-fb49bf9a4a2d179a60185bb77aa23662e2a2dc442579a0c91f4cf86c5fe35ac73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Animals, Newborn - physiology</topic><topic>Axons - physiology</topic><topic>Brain - embryology</topic><topic>Carrier Proteins - genetics</topic><topic>Carrier Proteins - physiology</topic><topic>Contractile Proteins</topic><topic>Cytoskeletal Proteins</topic><topic>Embryo, Mammalian - physiology</topic><topic>Embryonic and Fetal Development - physiology</topic><topic>Gene Deletion</topic><topic>Growth Cones - physiology</topic><topic>Mice - embryology</topic><topic>Microfilament Proteins - genetics</topic><topic>Mutation - physiology</topic><topic>Nervous System - embryology</topic><topic>Profilins</topic><topic>Tissue Distribution</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lanier, Lorene M</creatorcontrib><creatorcontrib>Gates, Monte A</creatorcontrib><creatorcontrib>Witke, Walter</creatorcontrib><creatorcontrib>Menzies, A.Sheila</creatorcontrib><creatorcontrib>Wehman, Ann M</creatorcontrib><creatorcontrib>Macklis, Jeffrey D</creatorcontrib><creatorcontrib>Kwiatkowski, David</creatorcontrib><creatorcontrib>Soriano, Philippe</creatorcontrib><creatorcontrib>Gertler, Frank B</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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuron (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lanier, Lorene M</au><au>Gates, Monte A</au><au>Witke, Walter</au><au>Menzies, A.Sheila</au><au>Wehman, Ann M</au><au>Macklis, Jeffrey D</au><au>Kwiatkowski, David</au><au>Soriano, Philippe</au><au>Gertler, Frank B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mena Is Required for Neurulation and Commissure Formation</atitle><jtitle>Neuron (Cambridge, Mass.)</jtitle><addtitle>Neuron</addtitle><date>1999-02-01</date><risdate>1999</risdate><volume>22</volume><issue>2</issue><spage>313</spage><epage>325</epage><pages>313-325</pages><issn>0896-6273</issn><eissn>1097-4199</eissn><abstract>Mammalian enabled (Mena) is a member of a protein family thought to link signal transduction pathways to localized remodeling of the actin cytoskeleton. 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| subjects | Animals Animals, Newborn - physiology Axons - physiology Brain - embryology Carrier Proteins - genetics Carrier Proteins - physiology Contractile Proteins Cytoskeletal Proteins Embryo, Mammalian - physiology Embryonic and Fetal Development - physiology Gene Deletion Growth Cones - physiology Mice - embryology Microfilament Proteins - genetics Mutation - physiology Nervous System - embryology Profilins Tissue Distribution |
| title | Mena Is Required for Neurulation and Commissure Formation |
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