Notch2, but not Notch1, is required for proximal fate acquisition in the mammalian nephron
The Notch pathway regulates cell fate determination in numerous developmental processes. Here we report that Notch2 acts non-redundantly to control the processes of nephron segmentation through an Rbp-J-dependent process. Notch1 and Notch2 are detected in the early renal vesicle. Genetic analysis re...
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| Veröffentlicht in: | Development (Cambridge) 2007-02, Vol.134 (4), p.801-811 |
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| container_title | Development (Cambridge) |
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| creator | Cheng, Hui-Teng Kim, Mijin Valerius, M Todd Surendran, Kameswaran Schuster-Gossler, Karin Gossler, Achim McMahon, Andrew P Kopan, Raphael |
| description | The Notch pathway regulates cell fate determination in numerous developmental processes. Here we report that Notch2 acts non-redundantly to control the processes of nephron segmentation through an Rbp-J-dependent process. Notch1 and Notch2 are detected in the early renal vesicle. Genetic analysis reveals that only Notch2 is required for the differentiation of proximal nephron structures (podocytes and proximal convoluted tubules) despite the presence of activated Notch1 in the nuclei of putative proximal progenitors. The inability of endogenous Notch1 to compensate for Notch2 deficiency may reflect sub-threshold Notch1 levels in the nucleus. In line with this view, forced expression of a γ-secretase-independent form of Notch1 intracellular domain drives the specification of proximal fates where all endogenous, ligand-dependent Notch signaling is blocked by aγ -secretase inhibitor. These results establish distinct (non-redundant), instructive roles for Notch receptors in nephron segmentation. |
| doi_str_mv | 10.1242/dev.02773 |
| format | Article |
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Here we report that Notch2 acts non-redundantly to control the processes of nephron segmentation through an Rbp-J-dependent process. Notch1 and Notch2 are detected in the early renal vesicle. Genetic analysis reveals that only Notch2 is required for the differentiation of proximal nephron structures (podocytes and proximal convoluted tubules) despite the presence of activated Notch1 in the nuclei of putative proximal progenitors. The inability of endogenous Notch1 to compensate for Notch2 deficiency may reflect sub-threshold Notch1 levels in the nucleus. In line with this view, forced expression of a γ-secretase-independent form of Notch1 intracellular domain drives the specification of proximal fates where all endogenous, ligand-dependent Notch signaling is blocked by aγ -secretase inhibitor. These results establish distinct (non-redundant), instructive roles for Notch receptors in nephron segmentation.</description><identifier>ISSN: 0950-1991</identifier><identifier>EISSN: 1477-9129</identifier><identifier>DOI: 10.1242/dev.02773</identifier><identifier>PMID: 17229764</identifier><language>eng</language><publisher>England: The Company of Biologists Limited</publisher><subject>Animals ; Embryo, Mammalian ; Embryonic Induction ; Immunoglobulin J Recombination Signal Sequence-Binding Protein - physiology ; Kidney Tubules, Proximal - embryology ; Kidney Tubules, Proximal - growth & development ; Mice ; Nephrons - embryology ; Nephrons - growth & development ; Organogenesis ; Receptor, Notch1 - physiology ; Receptor, Notch2 - physiology</subject><ispartof>Development (Cambridge), 2007-02, Vol.134 (4), p.801-811</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c386t-ee6291f13bb6e83faf7bbd0d553cff4e8b97db5bfc218e85ce2eb609d37f07163</citedby><cites>FETCH-LOGICAL-c386t-ee6291f13bb6e83faf7bbd0d553cff4e8b97db5bfc218e85ce2eb609d37f07163</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3665,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17229764$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cheng, Hui-Teng</creatorcontrib><creatorcontrib>Kim, Mijin</creatorcontrib><creatorcontrib>Valerius, M Todd</creatorcontrib><creatorcontrib>Surendran, Kameswaran</creatorcontrib><creatorcontrib>Schuster-Gossler, Karin</creatorcontrib><creatorcontrib>Gossler, Achim</creatorcontrib><creatorcontrib>McMahon, Andrew P</creatorcontrib><creatorcontrib>Kopan, Raphael</creatorcontrib><title>Notch2, but not Notch1, is required for proximal fate acquisition in the mammalian nephron</title><title>Development (Cambridge)</title><addtitle>Development</addtitle><description>The Notch pathway regulates cell fate determination in numerous developmental processes. Here we report that Notch2 acts non-redundantly to control the processes of nephron segmentation through an Rbp-J-dependent process. Notch1 and Notch2 are detected in the early renal vesicle. Genetic analysis reveals that only Notch2 is required for the differentiation of proximal nephron structures (podocytes and proximal convoluted tubules) despite the presence of activated Notch1 in the nuclei of putative proximal progenitors. The inability of endogenous Notch1 to compensate for Notch2 deficiency may reflect sub-threshold Notch1 levels in the nucleus. In line with this view, forced expression of a γ-secretase-independent form of Notch1 intracellular domain drives the specification of proximal fates where all endogenous, ligand-dependent Notch signaling is blocked by aγ -secretase inhibitor. These results establish distinct (non-redundant), instructive roles for Notch receptors in nephron segmentation.</description><subject>Animals</subject><subject>Embryo, Mammalian</subject><subject>Embryonic Induction</subject><subject>Immunoglobulin J Recombination Signal Sequence-Binding Protein - physiology</subject><subject>Kidney Tubules, Proximal - embryology</subject><subject>Kidney Tubules, Proximal - growth & development</subject><subject>Mice</subject><subject>Nephrons - embryology</subject><subject>Nephrons - growth & development</subject><subject>Organogenesis</subject><subject>Receptor, Notch1 - physiology</subject><subject>Receptor, Notch2 - physiology</subject><issn>0950-1991</issn><issn>1477-9129</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1P3DAQhi0EYre0B_5A5RMS0ob6I7HjY4WAVkJwaS-9WHEyJkZJnLUdCv8eL7tSjz2NRu-jVzMPQueUXFFWsm8dvFwRJiU_QmtaSlkoytQxWhNVkYIqRVfoU4zPhBAupDxFKyoZU1KUa_Tnwae2ZxtsloQnn_DHTjfYRRxgu7gAHbY-4Dn4Vzc2A7ZNAty0OYouOT9hN-HUAx6bMceumfAEcx_89Bmd2GaI8OUwz9Dv25tf1z-K-8e7n9ff74uW1yIVAIIpaik3RkDNbWOlMR3pqoq31pZQGyU7UxnbMlpDXbXAwAiiOi4tkVTwM3Sx780nbheISY8utjAMzQR-iVrUquJSqP-CNHOKyB14uQfb4GMMYPUc8u_hTVOid8Z1Nq4_jGf266F0MSN0_8iD4gxs9kDvnvq_2ac2zg_-ycUUdz0w-FlTXupS14Tyd81_jH8</recordid><startdate>200702</startdate><enddate>200702</enddate><creator>Cheng, Hui-Teng</creator><creator>Kim, Mijin</creator><creator>Valerius, M Todd</creator><creator>Surendran, Kameswaran</creator><creator>Schuster-Gossler, Karin</creator><creator>Gossler, Achim</creator><creator>McMahon, Andrew P</creator><creator>Kopan, Raphael</creator><general>The Company of Biologists Limited</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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>200702</creationdate><title>Notch2, but not Notch1, is required for proximal fate acquisition in the mammalian nephron</title><author>Cheng, Hui-Teng ; Kim, Mijin ; Valerius, M Todd ; Surendran, Kameswaran ; Schuster-Gossler, Karin ; Gossler, Achim ; McMahon, Andrew P ; Kopan, Raphael</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c386t-ee6291f13bb6e83faf7bbd0d553cff4e8b97db5bfc218e85ce2eb609d37f07163</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Embryo, Mammalian</topic><topic>Embryonic Induction</topic><topic>Immunoglobulin J Recombination Signal Sequence-Binding Protein - physiology</topic><topic>Kidney Tubules, Proximal - embryology</topic><topic>Kidney Tubules, Proximal - growth & development</topic><topic>Mice</topic><topic>Nephrons - embryology</topic><topic>Nephrons - growth & development</topic><topic>Organogenesis</topic><topic>Receptor, Notch1 - physiology</topic><topic>Receptor, Notch2 - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cheng, Hui-Teng</creatorcontrib><creatorcontrib>Kim, Mijin</creatorcontrib><creatorcontrib>Valerius, M Todd</creatorcontrib><creatorcontrib>Surendran, Kameswaran</creatorcontrib><creatorcontrib>Schuster-Gossler, Karin</creatorcontrib><creatorcontrib>Gossler, Achim</creatorcontrib><creatorcontrib>McMahon, Andrew P</creatorcontrib><creatorcontrib>Kopan, Raphael</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Development (Cambridge)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cheng, Hui-Teng</au><au>Kim, Mijin</au><au>Valerius, M Todd</au><au>Surendran, Kameswaran</au><au>Schuster-Gossler, Karin</au><au>Gossler, Achim</au><au>McMahon, Andrew P</au><au>Kopan, Raphael</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Notch2, but not Notch1, is required for proximal fate acquisition in the mammalian nephron</atitle><jtitle>Development (Cambridge)</jtitle><addtitle>Development</addtitle><date>2007-02</date><risdate>2007</risdate><volume>134</volume><issue>4</issue><spage>801</spage><epage>811</epage><pages>801-811</pages><issn>0950-1991</issn><eissn>1477-9129</eissn><abstract>The Notch pathway regulates cell fate determination in numerous developmental processes. Here we report that Notch2 acts non-redundantly to control the processes of nephron segmentation through an Rbp-J-dependent process. Notch1 and Notch2 are detected in the early renal vesicle. Genetic analysis reveals that only Notch2 is required for the differentiation of proximal nephron structures (podocytes and proximal convoluted tubules) despite the presence of activated Notch1 in the nuclei of putative proximal progenitors. The inability of endogenous Notch1 to compensate for Notch2 deficiency may reflect sub-threshold Notch1 levels in the nucleus. In line with this view, forced expression of a γ-secretase-independent form of Notch1 intracellular domain drives the specification of proximal fates where all endogenous, ligand-dependent Notch signaling is blocked by aγ -secretase inhibitor. These results establish distinct (non-redundant), instructive roles for Notch receptors in nephron segmentation.</abstract><cop>England</cop><pub>The Company of Biologists Limited</pub><pmid>17229764</pmid><doi>10.1242/dev.02773</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 0950-1991 1477-9129 |
| language | eng |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection; Company of Biologists |
| subjects | Animals Embryo, Mammalian Embryonic Induction Immunoglobulin J Recombination Signal Sequence-Binding Protein - physiology Kidney Tubules, Proximal - embryology Kidney Tubules, Proximal - growth & development Mice Nephrons - embryology Nephrons - growth & development Organogenesis Receptor, Notch1 - physiology Receptor, Notch2 - physiology |
| title | Notch2, but not Notch1, is required for proximal fate acquisition in the mammalian nephron |
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