Mother–daughter precursor cell fate transformation after Cdc2 down-regulation in the Drosophila bristle lineage
The Drosophila bristle lineage is an excellent system in which to study how cell cycle and fate determination are synchronized in invariant cell lineages. In this model, five different cells arise from a single precursor cell, pI, after four asymmetric cell divisions. Cell diversity is achieved by t...
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Veröffentlicht in: | Developmental biology 2004-12, Vol.276 (2), p.367-377 |
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Drosophila bristle lineage is an excellent system in which to study how cell cycle and fate determination are synchronized in invariant cell lineages. In this model, five different cells arise from a single precursor cell, pI, after four asymmetric cell divisions. Cell diversity is achieved by the asymmetric segregation of cell determinants, such as Numb and Neuralized (Neur), resulting in differential activation of the Notch (N) pathway. We show that down-regulation of Cdc2, by over-expressing Tribbles, Dwee1, and Dmyt1 (three negative regulators of Cdc2) or by using thermo-sensitive Cdc2 mutant flies, delayed pI mitosis, and altered the polarity and the number of subsequent cell divisions. These modifications were associated with a mother–daughter cell fate transformation as the pI cell acquired the identity of the secondary precursor cell, pIIb. This type of change in cell identity only occurred when the N signaling pathway was inactive since ectopic N signaling transformed pI to pIIa-progeny fate. These transformations in cell identity suggest that, although synchronized, cell cycle and fate determination are independent phenomena in the bristle lineage. |
doi_str_mv | 10.1016/j.ydbio.2004.08.043 |
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Drosophila bristle lineage is an excellent system in which to study how cell cycle and fate determination are synchronized in invariant cell lineages. In this model, five different cells arise from a single precursor cell, pI, after four asymmetric cell divisions. Cell diversity is achieved by the asymmetric segregation of cell determinants, such as Numb and Neuralized (Neur), resulting in differential activation of the Notch (N) pathway. We show that down-regulation of Cdc2, by over-expressing Tribbles, Dwee1, and Dmyt1 (three negative regulators of Cdc2) or by using thermo-sensitive Cdc2 mutant flies, delayed pI mitosis, and altered the polarity and the number of subsequent cell divisions. These modifications were associated with a mother–daughter cell fate transformation as the pI cell acquired the identity of the secondary precursor cell, pIIb. This type of change in cell identity only occurred when the N signaling pathway was inactive since ectopic N signaling transformed pI to pIIa-progeny fate. These transformations in cell identity suggest that, although synchronized, cell cycle and fate determination are independent phenomena in the bristle lineage.</description><identifier>ISSN: 0012-1606</identifier><identifier>EISSN: 1095-564X</identifier><identifier>DOI: 10.1016/j.ydbio.2004.08.043</identifier><identifier>PMID: 15581871</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Asymmetric cell divisions ; CDC2 Protein Kinase - antagonists & inhibitors ; CDC2 Protein Kinase - genetics ; CDC2 Protein Kinase - metabolism ; Cell cycle ; Cell Cycle - physiology ; Cell Lineage ; Dmyt1 ; Down-Regulation ; Drosophila melanogaster - anatomy & histology ; Drosophila melanogaster - cytology ; Drosophila melanogaster - genetics ; Drosophila melanogaster - physiology ; Drosophila Proteins - genetics ; Drosophila Proteins - metabolism ; Dwee1 ; Fate determination ; Microchaete ; Neurons - cytology ; Neurons - physiology ; Notch ; Phenotype ; Recombinant Fusion Proteins - genetics ; Recombinant Fusion Proteins - metabolism ; SOP ; Stem Cells - cytology ; Stem Cells - physiology ; String ; Transgenes ; Tribbles</subject><ispartof>Developmental biology, 2004-12, Vol.276 (2), p.367-377</ispartof><rights>2004 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-35804315e18861a9bcb2e2086322c838e669f70976a29d462d74995a99b2fbd23</citedby><cites>FETCH-LOGICAL-c421t-35804315e18861a9bcb2e2086322c838e669f70976a29d462d74995a99b2fbd23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0012160604006141$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15581871$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fichelson, Pierre</creatorcontrib><creatorcontrib>Gho, Michel</creatorcontrib><title>Mother–daughter precursor cell fate transformation after Cdc2 down-regulation in the Drosophila bristle lineage</title><title>Developmental biology</title><addtitle>Dev Biol</addtitle><description>The
Drosophila bristle lineage is an excellent system in which to study how cell cycle and fate determination are synchronized in invariant cell lineages. In this model, five different cells arise from a single precursor cell, pI, after four asymmetric cell divisions. Cell diversity is achieved by the asymmetric segregation of cell determinants, such as Numb and Neuralized (Neur), resulting in differential activation of the Notch (N) pathway. We show that down-regulation of Cdc2, by over-expressing Tribbles, Dwee1, and Dmyt1 (three negative regulators of Cdc2) or by using thermo-sensitive Cdc2 mutant flies, delayed pI mitosis, and altered the polarity and the number of subsequent cell divisions. These modifications were associated with a mother–daughter cell fate transformation as the pI cell acquired the identity of the secondary precursor cell, pIIb. This type of change in cell identity only occurred when the N signaling pathway was inactive since ectopic N signaling transformed pI to pIIa-progeny fate. These transformations in cell identity suggest that, although synchronized, cell cycle and fate determination are independent phenomena in the bristle lineage.</description><subject>Animals</subject><subject>Asymmetric cell divisions</subject><subject>CDC2 Protein Kinase - antagonists & inhibitors</subject><subject>CDC2 Protein Kinase - genetics</subject><subject>CDC2 Protein Kinase - metabolism</subject><subject>Cell cycle</subject><subject>Cell Cycle - physiology</subject><subject>Cell Lineage</subject><subject>Dmyt1</subject><subject>Down-Regulation</subject><subject>Drosophila melanogaster - anatomy & histology</subject><subject>Drosophila melanogaster - cytology</subject><subject>Drosophila melanogaster - genetics</subject><subject>Drosophila melanogaster - physiology</subject><subject>Drosophila Proteins - genetics</subject><subject>Drosophila Proteins - metabolism</subject><subject>Dwee1</subject><subject>Fate determination</subject><subject>Microchaete</subject><subject>Neurons - cytology</subject><subject>Neurons - physiology</subject><subject>Notch</subject><subject>Phenotype</subject><subject>Recombinant Fusion Proteins - genetics</subject><subject>Recombinant Fusion Proteins - metabolism</subject><subject>SOP</subject><subject>Stem Cells - cytology</subject><subject>Stem Cells - physiology</subject><subject>String</subject><subject>Transgenes</subject><subject>Tribbles</subject><issn>0012-1606</issn><issn>1095-564X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kM1u1DAURi0EokPhCZCQV-wSru3EsRcs0LT8SK3YgMTOcuybGY8y8dR2qLrjHXjDPgkZZiR2rLy4536-3yHkNYOaAZPvdvWD70OsOUBTg6qhEU_IioFuq1Y2P56SFQDjFZMgL8iLnHcAIJQSz8kFa1vFVMdW5O42li2mx1-_vZ0324KJHhK6OeWYqMNxpIMtSEuyUx5i2tsS4kTtcATX3nHq4_1UJdzM42kUJroE0qsUczxsw2hpn0IuI9IxTGg3-JI8G-yY8dX5vSTfP15_W3-ubr5--rL-cFO5hrNSiVYthViLTCnJrO5dz5GDkoJzp4RCKfXQge6k5do3kvuu0bq1Wvd86D0Xl-TtKfeQ4t2MuZh9yMdGdsI4ZyM71grWwAKKE-iWm3PCwRxS2Nv0YBiYo2mzM39Nm6NpA8oshy1bb87xc79H_2_nrHYB3p8AXEr-DJhMdgEnhz4sgovxMfz3gz_OfpJR</recordid><startdate>20041215</startdate><enddate>20041215</enddate><creator>Fichelson, Pierre</creator><creator>Gho, Michel</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>7X8</scope></search><sort><creationdate>20041215</creationdate><title>Mother–daughter precursor cell fate transformation after Cdc2 down-regulation in the Drosophila bristle lineage</title><author>Fichelson, Pierre ; Gho, Michel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-35804315e18861a9bcb2e2086322c838e669f70976a29d462d74995a99b2fbd23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Asymmetric cell divisions</topic><topic>CDC2 Protein Kinase - antagonists & inhibitors</topic><topic>CDC2 Protein Kinase - genetics</topic><topic>CDC2 Protein Kinase - metabolism</topic><topic>Cell cycle</topic><topic>Cell Cycle - physiology</topic><topic>Cell Lineage</topic><topic>Dmyt1</topic><topic>Down-Regulation</topic><topic>Drosophila melanogaster - anatomy & histology</topic><topic>Drosophila melanogaster - cytology</topic><topic>Drosophila melanogaster - genetics</topic><topic>Drosophila melanogaster - physiology</topic><topic>Drosophila Proteins - genetics</topic><topic>Drosophila Proteins - metabolism</topic><topic>Dwee1</topic><topic>Fate determination</topic><topic>Microchaete</topic><topic>Neurons - cytology</topic><topic>Neurons - physiology</topic><topic>Notch</topic><topic>Phenotype</topic><topic>Recombinant Fusion Proteins - genetics</topic><topic>Recombinant Fusion Proteins - metabolism</topic><topic>SOP</topic><topic>Stem Cells - cytology</topic><topic>Stem Cells - physiology</topic><topic>String</topic><topic>Transgenes</topic><topic>Tribbles</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fichelson, Pierre</creatorcontrib><creatorcontrib>Gho, Michel</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>Developmental biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fichelson, Pierre</au><au>Gho, Michel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mother–daughter precursor cell fate transformation after Cdc2 down-regulation in the Drosophila bristle lineage</atitle><jtitle>Developmental biology</jtitle><addtitle>Dev Biol</addtitle><date>2004-12-15</date><risdate>2004</risdate><volume>276</volume><issue>2</issue><spage>367</spage><epage>377</epage><pages>367-377</pages><issn>0012-1606</issn><eissn>1095-564X</eissn><abstract>The
Drosophila bristle lineage is an excellent system in which to study how cell cycle and fate determination are synchronized in invariant cell lineages. In this model, five different cells arise from a single precursor cell, pI, after four asymmetric cell divisions. Cell diversity is achieved by the asymmetric segregation of cell determinants, such as Numb and Neuralized (Neur), resulting in differential activation of the Notch (N) pathway. We show that down-regulation of Cdc2, by over-expressing Tribbles, Dwee1, and Dmyt1 (three negative regulators of Cdc2) or by using thermo-sensitive Cdc2 mutant flies, delayed pI mitosis, and altered the polarity and the number of subsequent cell divisions. These modifications were associated with a mother–daughter cell fate transformation as the pI cell acquired the identity of the secondary precursor cell, pIIb. This type of change in cell identity only occurred when the N signaling pathway was inactive since ectopic N signaling transformed pI to pIIa-progeny fate. These transformations in cell identity suggest that, although synchronized, cell cycle and fate determination are independent phenomena in the bristle lineage.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>15581871</pmid><doi>10.1016/j.ydbio.2004.08.043</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Asymmetric cell divisions CDC2 Protein Kinase - antagonists & inhibitors CDC2 Protein Kinase - genetics CDC2 Protein Kinase - metabolism Cell cycle Cell Cycle - physiology Cell Lineage Dmyt1 Down-Regulation Drosophila melanogaster - anatomy & histology Drosophila melanogaster - cytology Drosophila melanogaster - genetics Drosophila melanogaster - physiology Drosophila Proteins - genetics Drosophila Proteins - metabolism Dwee1 Fate determination Microchaete Neurons - cytology Neurons - physiology Notch Phenotype Recombinant Fusion Proteins - genetics Recombinant Fusion Proteins - metabolism SOP Stem Cells - cytology Stem Cells - physiology String Transgenes Tribbles |
title | Mother–daughter precursor cell fate transformation after Cdc2 down-regulation in the Drosophila bristle lineage |
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