I-BAR protein antagonism of endocytosis mediates directional sensing during guided cell migration
Although directed cellular migration facilitates the coordinated movement of cells during development and repair, the mechanisms regulating such migration remain poorly understood. Missing-in-metastasis (MIM) is a defining member of the inverse Bin/Amphiphysin/Rvs domain (I-BAR) subfamily of lipid b...
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| Veröffentlicht in: | The Journal of cell biology 2010-04, Vol.189 (2), p.353-367 |
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| container_title | The Journal of cell biology |
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| creator | Quinones, Gabriel A Jin, Janet Oro, Anthony E |
| description | Although directed cellular migration facilitates the coordinated movement of cells during development and repair, the mechanisms regulating such migration remain poorly understood. Missing-in-metastasis (MIM) is a defining member of the inverse Bin/Amphiphysin/Rvs domain (I-BAR) subfamily of lipid binding, cytoskeletal regulators whose levels are altered in a number of cancers. Here, we provide the first genetic evidence that an I-BAR protein regulates directed cell migration in vivo. Drosophila MIM (dmim) is involved in Drosophila border cell migration, with loss of dmim function resulting in a lack of directional movement by the border cell cluster. In vivo endocytosis assays combined with genetic analyses demonstrate that the dmim product regulates directed cell movement by inhibiting endocytosis and antagonizing the activities of the CD2-associated protein/cortactin complex in these cells. These studies demonstrate that DMIM antagonizes pro-endocytic components to facilitate polarity and localized guidance cue sensing during directional cell migration. |
| doi_str_mv | 10.1083/jcb.200910136 |
| format | Article |
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Missing-in-metastasis (MIM) is a defining member of the inverse Bin/Amphiphysin/Rvs domain (I-BAR) subfamily of lipid binding, cytoskeletal regulators whose levels are altered in a number of cancers. Here, we provide the first genetic evidence that an I-BAR protein regulates directed cell migration in vivo. Drosophila MIM (dmim) is involved in Drosophila border cell migration, with loss of dmim function resulting in a lack of directional movement by the border cell cluster. In vivo endocytosis assays combined with genetic analyses demonstrate that the dmim product regulates directed cell movement by inhibiting endocytosis and antagonizing the activities of the CD2-associated protein/cortactin complex in these cells. These studies demonstrate that DMIM antagonizes pro-endocytic components to facilitate polarity and localized guidance cue sensing during directional cell migration.</description><subject>Actins</subject><subject>Acyltransferases - genetics</subject><subject>Acyltransferases - metabolism</subject><subject>Animals</subject><subject>Animals, Genetically Modified</subject><subject>Cancer</subject><subject>Cell adhesion & migration</subject><subject>Cell lines</subject><subject>Cell membranes</subject><subject>Cell Movement - physiology</subject><subject>Cortactin - genetics</subject><subject>Cortactin - metabolism</subject><subject>Cytoskeleton</subject><subject>Drosophila</subject><subject>Drosophila melanogaster - anatomy & histology</subject><subject>Drosophila melanogaster - physiology</subject><subject>Drosophila Proteins - genetics</subject><subject>Drosophila Proteins - metabolism</subject><subject>Dyes</subject><subject>Eggs</subject><subject>Endocytosis</subject><subject>Endocytosis - physiology</subject><subject>Extracellular Signal-Regulated MAP Kinases - genetics</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Female</subject><subject>Gene expression regulation</subject><subject>Genetics</subject><subject>Germ cells</subject><subject>Germ Cells - cytology</subject><subject>Germ Cells - physiology</subject><subject>Humans</subject><subject>Insects</subject><subject>Lipids</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Microfilament Proteins - genetics</subject><subject>Microfilament Proteins - metabolism</subject><subject>Mutation</subject><subject>Protein Binding</subject><subject>Proteins</subject><subject>Receptor, Epidermal Growth Factor - genetics</subject><subject>Receptor, Epidermal Growth Factor - metabolism</subject><subject>Receptors</subject><issn>0021-9525</issn><issn>1540-8140</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc1v1DAQxS0EotvCkSPgnjiljL9i-1KpVHxUqoQE9Gw5jhO8ytqLnSD1v8fRllXhNIf305s38xB6ReCCgGLvt667oACaAGHtE7QhgkOjCIenaANASaMFFSfotJQtAHDJ2XN0QoEpIWW7Qfam-XD1De9zmn2I2MbZjimGssNpwD72yd3PqYSCd74PdvYF9yF7N4cU7YSLjyXEEfdLXse4hN732PlpwrswZrtiL9CzwU7Fv3yYZ-ju08cf11-a26-fb66vbhsnKJ8bKxjpvGipcGroCfdMkN5qp6hrW98pZZlmVChGhCOdAyk1cN8OXHWkZ1KyM3R58N0vXQ3rfJyzncw-h53N9ybZYP5VYvhpxvTbUCVaDbQavHswyOnX4stsdqGst9jo01KMZKxmlIRX8vw_cpuWXB9SjNJEc8ZXpjkwLqdSsh-OSQiYtTlTmzPH5ir_5nH8I_23qgq8PgDbMqf8SG-1gnZd-PagDzYZO-ZQzN13Wr2B1KdJqtkfR2OoAw</recordid><startdate>20100419</startdate><enddate>20100419</enddate><creator>Quinones, Gabriel A</creator><creator>Jin, Janet</creator><creator>Oro, Anthony E</creator><general>The Rockefeller University Press</general><general>Rockefeller University Press</general><scope>FBQ</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20100419</creationdate><title>I-BAR protein antagonism of endocytosis mediates directional sensing during guided cell migration</title><author>Quinones, Gabriel A ; 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Missing-in-metastasis (MIM) is a defining member of the inverse Bin/Amphiphysin/Rvs domain (I-BAR) subfamily of lipid binding, cytoskeletal regulators whose levels are altered in a number of cancers. Here, we provide the first genetic evidence that an I-BAR protein regulates directed cell migration in vivo. Drosophila MIM (dmim) is involved in Drosophila border cell migration, with loss of dmim function resulting in a lack of directional movement by the border cell cluster. In vivo endocytosis assays combined with genetic analyses demonstrate that the dmim product regulates directed cell movement by inhibiting endocytosis and antagonizing the activities of the CD2-associated protein/cortactin complex in these cells. 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| subjects | Actins Acyltransferases - genetics Acyltransferases - metabolism Animals Animals, Genetically Modified Cancer Cell adhesion & migration Cell lines Cell membranes Cell Movement - physiology Cortactin - genetics Cortactin - metabolism Cytoskeleton Drosophila Drosophila melanogaster - anatomy & histology Drosophila melanogaster - physiology Drosophila Proteins - genetics Drosophila Proteins - metabolism Dyes Eggs Endocytosis Endocytosis - physiology Extracellular Signal-Regulated MAP Kinases - genetics Extracellular Signal-Regulated MAP Kinases - metabolism Female Gene expression regulation Genetics Germ cells Germ Cells - cytology Germ Cells - physiology Humans Insects Lipids Mice Mice, Knockout Microfilament Proteins - genetics Microfilament Proteins - metabolism Mutation Protein Binding Proteins Receptor, Epidermal Growth Factor - genetics Receptor, Epidermal Growth Factor - metabolism Receptors |
| title | I-BAR protein antagonism of endocytosis mediates directional sensing during guided cell migration |
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