Evidence That Helix-Loop-Helix Proteins Collaborate with Retinoblastoma Tumor Suppressor Protein to Regulate Cortical Neurogenesis
The retinoblastoma tumor suppressor protein (pRb) family is essential for cortical progenitors to exit the cell cycle and survive. In this report, we test the hypothesis that pRb collaborates with basic helix-loop-helix (bHLH) transcription factors to regulate cortical neurogenesis, taking advantage...
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| Veröffentlicht in: | The Journal of neuroscience 2000-10, Vol.20 (20), p.7648-7656 |
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| creator | Toma, Jean G El-Bizri, Hiba Barnabe-Heider, Fanie Aloyz, Raquel Miller, Freda D |
| description | The retinoblastoma tumor suppressor protein (pRb) family is essential for cortical progenitors to exit the cell cycle and survive. In this report, we test the hypothesis that pRb collaborates with basic helix-loop-helix (bHLH) transcription factors to regulate cortical neurogenesis, taking advantage of the naturally occurring dominant-inhibitory HLH protein Id2. Overexpression of Id2 in cortical progenitors completely inhibited the induction of neuron-specific genes and led to apoptosis, presumably as a consequence of conflicting differentiation signals. Both of these phenotypes were rescued by coexpression of a constitutively activated pRb mutant. In contrast, Id2 overexpression in postmitotic cortical neurons affected neither neuronal gene expression nor survival. Thus, pRb collaborates with HLHs to ensure the coordinate induction of terminal mitosis and neuronal gene expression as cortical progenitors become neurons. |
| doi_str_mv | 10.1523/jneurosci.20-20-07648.2000 |
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In this report, we test the hypothesis that pRb collaborates with basic helix-loop-helix (bHLH) transcription factors to regulate cortical neurogenesis, taking advantage of the naturally occurring dominant-inhibitory HLH protein Id2. Overexpression of Id2 in cortical progenitors completely inhibited the induction of neuron-specific genes and led to apoptosis, presumably as a consequence of conflicting differentiation signals. Both of these phenotypes were rescued by coexpression of a constitutively activated pRb mutant. In contrast, Id2 overexpression in postmitotic cortical neurons affected neither neuronal gene expression nor survival. Thus, pRb collaborates with HLHs to ensure the coordinate induction of terminal mitosis and neuronal gene expression as cortical progenitors become neurons.</description><identifier>ISSN: 0270-6474</identifier><identifier>EISSN: 1529-2401</identifier><identifier>DOI: 10.1523/jneurosci.20-20-07648.2000</identifier><identifier>PMID: 11027225</identifier><language>eng</language><publisher>United States: Soc Neuroscience</publisher><subject>Adenoviridae - genetics ; Animals ; Apoptosis ; Cell Differentiation - physiology ; Cell Survival - physiology ; Cells, Cultured ; Cerebral Cortex - cytology ; Cerebral Cortex - embryology ; Cerebral Cortex - metabolism ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; DNA-Binding Proteins - pharmacology ; Gene Expression - drug effects ; Genetic Vectors - genetics ; Genetic Vectors - metabolism ; Helix-Loop-Helix Motifs - physiology ; In Situ Nick-End Labeling ; Inhibitor of Differentiation Protein 2 ; Mice ; Neurons - cytology ; Neurons - metabolism ; Repressor Proteins ; Retinoblastoma Protein - metabolism ; Stem Cells - cytology ; Stem Cells - metabolism ; Transcription Factors - metabolism ; Transfection ; Tubulin - metabolism ; tumor suppressor proteins</subject><ispartof>The Journal of neuroscience, 2000-10, Vol.20 (20), p.7648-7656</ispartof><rights>Copyright © 2000 Society for Neuroscience 2000</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c542t-f31ac3e41529bfa77c57e2575569fc12666d7f055b25c6e9ef035044554e7d2b3</citedby><cites>FETCH-LOGICAL-c542t-f31ac3e41529bfa77c57e2575569fc12666d7f055b25c6e9ef035044554e7d2b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6772880/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6772880/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11027225$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Toma, Jean G</creatorcontrib><creatorcontrib>El-Bizri, Hiba</creatorcontrib><creatorcontrib>Barnabe-Heider, Fanie</creatorcontrib><creatorcontrib>Aloyz, Raquel</creatorcontrib><creatorcontrib>Miller, Freda D</creatorcontrib><title>Evidence That Helix-Loop-Helix Proteins Collaborate with Retinoblastoma Tumor Suppressor Protein to Regulate Cortical Neurogenesis</title><title>The Journal of neuroscience</title><addtitle>J Neurosci</addtitle><description>The retinoblastoma tumor suppressor protein (pRb) family is essential for cortical progenitors to exit the cell cycle and survive. In this report, we test the hypothesis that pRb collaborates with basic helix-loop-helix (bHLH) transcription factors to regulate cortical neurogenesis, taking advantage of the naturally occurring dominant-inhibitory HLH protein Id2. Overexpression of Id2 in cortical progenitors completely inhibited the induction of neuron-specific genes and led to apoptosis, presumably as a consequence of conflicting differentiation signals. Both of these phenotypes were rescued by coexpression of a constitutively activated pRb mutant. In contrast, Id2 overexpression in postmitotic cortical neurons affected neither neuronal gene expression nor survival. Thus, pRb collaborates with HLHs to ensure the coordinate induction of terminal mitosis and neuronal gene expression as cortical progenitors become neurons.</description><subject>Adenoviridae - genetics</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cell Differentiation - physiology</subject><subject>Cell Survival - physiology</subject><subject>Cells, Cultured</subject><subject>Cerebral Cortex - cytology</subject><subject>Cerebral Cortex - embryology</subject><subject>Cerebral Cortex - metabolism</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>DNA-Binding Proteins - pharmacology</subject><subject>Gene Expression - drug effects</subject><subject>Genetic Vectors - genetics</subject><subject>Genetic Vectors - metabolism</subject><subject>Helix-Loop-Helix Motifs - physiology</subject><subject>In Situ Nick-End Labeling</subject><subject>Inhibitor of Differentiation Protein 2</subject><subject>Mice</subject><subject>Neurons - cytology</subject><subject>Neurons - metabolism</subject><subject>Repressor Proteins</subject><subject>Retinoblastoma Protein - metabolism</subject><subject>Stem Cells - cytology</subject><subject>Stem Cells - metabolism</subject><subject>Transcription Factors - metabolism</subject><subject>Transfection</subject><subject>Tubulin - metabolism</subject><subject>tumor suppressor proteins</subject><issn>0270-6474</issn><issn>1529-2401</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU9v1DAQxS0EokvhK6CIA5xSbMeOdzkgoWihRasWtduz5XgnG1dOnNpOA1c-OU53xZ8T0kgeaX7vacYPoTcEnxFOi_d3PYzeBW3OKM5TYVGyZeoxfoIWiVjllGHyFC0wFTgvmWAn6EUIdwkQmIjn6ISQNKKUL9DP9YPZQa8h27YqZudgzfd849yQP7bZN-8imD5klbNW1c6rCNlkYptdQzS9q60K0XUq246d89nNOAweQkjtUZlFl9D9aGdh5Xw0Wtnscr5gDz0EE16iZ42yAV4d31N0-3m9rc7zzdWXi-rTJtec0Zg3BVG6ADYfWDdKCM0FUC44L1eNJrQsy51oMOc15bqEFTS44JgxzhmIHa2LU_Tx4DuMdQc7DX30ysrBm075H9IpI_-d9KaVe_cgSyHocomTwdujgXf3I4QoOxM0pH_pwY1BClpQRjH7L0jEknMqigR-OIA65Rk8NL-3IVjOWcuvl-vb66ub6kJSPNdj1nLOOolf_33PH-kx3AS8OwCt2beT8SBDp6xNOJHTNB0MZ7_iF3S5uH0</recordid><startdate>20001015</startdate><enddate>20001015</enddate><creator>Toma, Jean G</creator><creator>El-Bizri, Hiba</creator><creator>Barnabe-Heider, Fanie</creator><creator>Aloyz, Raquel</creator><creator>Miller, Freda D</creator><general>Soc Neuroscience</general><general>Society for Neuroscience</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>7TK</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20001015</creationdate><title>Evidence That Helix-Loop-Helix Proteins Collaborate with Retinoblastoma Tumor Suppressor Protein to Regulate Cortical Neurogenesis</title><author>Toma, Jean G ; El-Bizri, Hiba ; Barnabe-Heider, Fanie ; Aloyz, Raquel ; Miller, Freda D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c542t-f31ac3e41529bfa77c57e2575569fc12666d7f055b25c6e9ef035044554e7d2b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Adenoviridae - genetics</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Cell Differentiation - physiology</topic><topic>Cell Survival - physiology</topic><topic>Cells, Cultured</topic><topic>Cerebral Cortex - cytology</topic><topic>Cerebral Cortex - embryology</topic><topic>Cerebral Cortex - metabolism</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>DNA-Binding Proteins - pharmacology</topic><topic>Gene Expression - drug effects</topic><topic>Genetic Vectors - genetics</topic><topic>Genetic Vectors - metabolism</topic><topic>Helix-Loop-Helix Motifs - physiology</topic><topic>In Situ Nick-End Labeling</topic><topic>Inhibitor of Differentiation Protein 2</topic><topic>Mice</topic><topic>Neurons - cytology</topic><topic>Neurons - metabolism</topic><topic>Repressor Proteins</topic><topic>Retinoblastoma Protein - metabolism</topic><topic>Stem Cells - cytology</topic><topic>Stem Cells - metabolism</topic><topic>Transcription Factors - metabolism</topic><topic>Transfection</topic><topic>Tubulin - metabolism</topic><topic>tumor suppressor proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Toma, Jean G</creatorcontrib><creatorcontrib>El-Bizri, Hiba</creatorcontrib><creatorcontrib>Barnabe-Heider, Fanie</creatorcontrib><creatorcontrib>Aloyz, Raquel</creatorcontrib><creatorcontrib>Miller, Freda D</creatorcontrib><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><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Toma, Jean G</au><au>El-Bizri, Hiba</au><au>Barnabe-Heider, Fanie</au><au>Aloyz, Raquel</au><au>Miller, Freda D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evidence That Helix-Loop-Helix Proteins Collaborate with Retinoblastoma Tumor Suppressor Protein to Regulate Cortical Neurogenesis</atitle><jtitle>The Journal of neuroscience</jtitle><addtitle>J Neurosci</addtitle><date>2000-10-15</date><risdate>2000</risdate><volume>20</volume><issue>20</issue><spage>7648</spage><epage>7656</epage><pages>7648-7656</pages><issn>0270-6474</issn><eissn>1529-2401</eissn><abstract>The retinoblastoma tumor suppressor protein (pRb) family is essential for cortical progenitors to exit the cell cycle and survive. In this report, we test the hypothesis that pRb collaborates with basic helix-loop-helix (bHLH) transcription factors to regulate cortical neurogenesis, taking advantage of the naturally occurring dominant-inhibitory HLH protein Id2. Overexpression of Id2 in cortical progenitors completely inhibited the induction of neuron-specific genes and led to apoptosis, presumably as a consequence of conflicting differentiation signals. Both of these phenotypes were rescued by coexpression of a constitutively activated pRb mutant. In contrast, Id2 overexpression in postmitotic cortical neurons affected neither neuronal gene expression nor survival. Thus, pRb collaborates with HLHs to ensure the coordinate induction of terminal mitosis and neuronal gene expression as cortical progenitors become neurons.</abstract><cop>United States</cop><pub>Soc Neuroscience</pub><pmid>11027225</pmid><doi>10.1523/jneurosci.20-20-07648.2000</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenoviridae - genetics Animals Apoptosis Cell Differentiation - physiology Cell Survival - physiology Cells, Cultured Cerebral Cortex - cytology Cerebral Cortex - embryology Cerebral Cortex - metabolism DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism DNA-Binding Proteins - pharmacology Gene Expression - drug effects Genetic Vectors - genetics Genetic Vectors - metabolism Helix-Loop-Helix Motifs - physiology In Situ Nick-End Labeling Inhibitor of Differentiation Protein 2 Mice Neurons - cytology Neurons - metabolism Repressor Proteins Retinoblastoma Protein - metabolism Stem Cells - cytology Stem Cells - metabolism Transcription Factors - metabolism Transfection Tubulin - metabolism tumor suppressor proteins |
| title | Evidence That Helix-Loop-Helix Proteins Collaborate with Retinoblastoma Tumor Suppressor Protein to Regulate Cortical Neurogenesis |
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