Differential Functions of G Protein and Baz-aPKC Signaling Pathways in Drosophila Neuroblast Asymmetric Division
Drosophila melanogaster neuroblasts (NBs) undergo asymmetric divisions during which cell-fate determinants localize asymmetrically, mitotic spindles orient along the apical-basal axis, and unequal-sized daughter cells appear. We identified here the first Drosophila mutant in the Gγ1 subunit of heter...
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| Veröffentlicht in: | The Journal of cell biology 2004-03, Vol.164 (5), p.729-738 |
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| creator | Izumi, Yasushi Ohta, Nao Itoh-Furuya, Asako Fuse, Naoyuki Matsuzaki, Fumio |
| description | Drosophila melanogaster neuroblasts (NBs) undergo asymmetric divisions during which cell-fate determinants localize asymmetrically, mitotic spindles orient along the apical-basal axis, and unequal-sized daughter cells appear. We identified here the first Drosophila mutant in the Gγ1 subunit of heterotrimeric G protein, which produces Gγ1 lacking its membrane anchor site and exhibits phenotypes identical to those of Gβ13F, including abnormal spindle asymmetry and spindle orientation in NB divisions. This mutant fails to bind Gβ13F to the membrane, indicating an essential role of cortical Gγ1-Gβ13F signaling in asymmetric divisions. In Gγ1 and Gβ13F mutant NBs, Pins-Gαi, which normally localize in the apical cortex, no longer distribute asymmetrically. However, the other apical components, Bazooka-atypical PKC-Par6-Inscuteable, still remain polarized and responsible for asymmetric Miranda localization, suggesting their dominant role in localizing cell-fate determinants. Further analysis of Gβγ and other mutants indicates a predominant role of Partner of Inscuteable-Gαi in spindle orientation. We thus suggest that the two apical signaling pathways have overlapping but different roles in asymmetric NB division. |
| doi_str_mv | 10.1083/jcb.200309162 |
| format | Article |
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We identified here the first Drosophila mutant in the Gγ1 subunit of heterotrimeric G protein, which produces Gγ1 lacking its membrane anchor site and exhibits phenotypes identical to those of Gβ13F, including abnormal spindle asymmetry and spindle orientation in NB divisions. This mutant fails to bind Gβ13F to the membrane, indicating an essential role of cortical Gγ1-Gβ13F signaling in asymmetric divisions. In Gγ1 and Gβ13F mutant NBs, Pins-Gαi, which normally localize in the apical cortex, no longer distribute asymmetrically. However, the other apical components, Bazooka-atypical PKC-Par6-Inscuteable, still remain polarized and responsible for asymmetric Miranda localization, suggesting their dominant role in localizing cell-fate determinants. Further analysis of Gβγ and other mutants indicates a predominant role of Partner of Inscuteable-Gαi in spindle orientation. We thus suggest that the two apical signaling pathways have overlapping but different roles in asymmetric NB division.</description><identifier>ISSN: 0021-9525</identifier><identifier>EISSN: 1540-8140</identifier><identifier>DOI: 10.1083/jcb.200309162</identifier><identifier>PMID: 14981094</identifier><identifier>CODEN: JCLBA3</identifier><language>eng</language><publisher>United States: Rockefeller University Press</publisher><subject>Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Carrier Proteins - metabolism ; Cell Cycle Proteins - metabolism ; Cell division ; Cell Division - physiology ; Cell Polarity ; Cell Size ; Cellular biology ; Cytoskeletal Proteins - genetics ; Cytoskeletal Proteins - metabolism ; Drosophila melanogaster - embryology ; Drosophila melanogaster - physiology ; Drosophila Proteins - metabolism ; Embryo, Nonmammalian - physiology ; GTP-Binding Protein alpha Subunits, Gq-G11 - genetics ; GTP-Binding Protein alpha Subunits, Gq-G11 - metabolism ; GTP-Binding Protein beta Subunits - genetics ; GTP-Binding Protein beta Subunits - metabolism ; Insects ; Intracellular Signaling Peptides and Proteins ; Isoenzymes - metabolism ; Macromolecular Substances ; Membranes ; Molecular Sequence Data ; Neurons - cytology ; Neurons - physiology ; Neuropeptides ; Point Mutation ; Protein Kinase C - metabolism ; Protein Subunits - genetics ; Protein Subunits - metabolism ; Proteins ; Proteins - genetics ; Proteins - metabolism ; Second Messenger Systems - physiology ; Spindle Apparatus - metabolism</subject><ispartof>The Journal of cell biology, 2004-03, Vol.164 (5), p.729-738</ispartof><rights>Copyright 2004 The Rockefeller University Press</rights><rights>Copyright Rockefeller University Press Mar 1, 2004</rights><rights>Copyright © 2004, The Rockefeller University Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c528t-a6086a998c99443950e58598b6f3472af05cccb3151acf8ef7ec7c5494143e683</citedby><cites>FETCH-LOGICAL-c528t-a6086a998c99443950e58598b6f3472af05cccb3151acf8ef7ec7c5494143e683</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14981094$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Izumi, Yasushi</creatorcontrib><creatorcontrib>Ohta, Nao</creatorcontrib><creatorcontrib>Itoh-Furuya, Asako</creatorcontrib><creatorcontrib>Fuse, Naoyuki</creatorcontrib><creatorcontrib>Matsuzaki, Fumio</creatorcontrib><title>Differential Functions of G Protein and Baz-aPKC Signaling Pathways in Drosophila Neuroblast Asymmetric Division</title><title>The Journal of cell biology</title><addtitle>J Cell Biol</addtitle><description>Drosophila melanogaster neuroblasts (NBs) undergo asymmetric divisions during which cell-fate determinants localize asymmetrically, mitotic spindles orient along the apical-basal axis, and unequal-sized daughter cells appear. We identified here the first Drosophila mutant in the Gγ1 subunit of heterotrimeric G protein, which produces Gγ1 lacking its membrane anchor site and exhibits phenotypes identical to those of Gβ13F, including abnormal spindle asymmetry and spindle orientation in NB divisions. This mutant fails to bind Gβ13F to the membrane, indicating an essential role of cortical Gγ1-Gβ13F signaling in asymmetric divisions. In Gγ1 and Gβ13F mutant NBs, Pins-Gαi, which normally localize in the apical cortex, no longer distribute asymmetrically. However, the other apical components, Bazooka-atypical PKC-Par6-Inscuteable, still remain polarized and responsible for asymmetric Miranda localization, suggesting their dominant role in localizing cell-fate determinants. Further analysis of Gβγ and other mutants indicates a predominant role of Partner of Inscuteable-Gαi in spindle orientation. We thus suggest that the two apical signaling pathways have overlapping but different roles in asymmetric NB division.</description><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Animals, Genetically Modified</subject><subject>Carrier Proteins - metabolism</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Cell division</subject><subject>Cell Division - physiology</subject><subject>Cell Polarity</subject><subject>Cell Size</subject><subject>Cellular biology</subject><subject>Cytoskeletal Proteins - genetics</subject><subject>Cytoskeletal Proteins - metabolism</subject><subject>Drosophila melanogaster - embryology</subject><subject>Drosophila melanogaster - physiology</subject><subject>Drosophila Proteins - metabolism</subject><subject>Embryo, Nonmammalian - physiology</subject><subject>GTP-Binding Protein alpha Subunits, Gq-G11 - genetics</subject><subject>GTP-Binding Protein alpha Subunits, Gq-G11 - metabolism</subject><subject>GTP-Binding Protein beta Subunits - genetics</subject><subject>GTP-Binding Protein beta Subunits - metabolism</subject><subject>Insects</subject><subject>Intracellular Signaling Peptides and Proteins</subject><subject>Isoenzymes - metabolism</subject><subject>Macromolecular Substances</subject><subject>Membranes</subject><subject>Molecular Sequence Data</subject><subject>Neurons - cytology</subject><subject>Neurons - physiology</subject><subject>Neuropeptides</subject><subject>Point Mutation</subject><subject>Protein Kinase C - metabolism</subject><subject>Protein Subunits - genetics</subject><subject>Protein Subunits - metabolism</subject><subject>Proteins</subject><subject>Proteins - genetics</subject><subject>Proteins - metabolism</subject><subject>Second Messenger Systems - physiology</subject><subject>Spindle Apparatus - metabolism</subject><issn>0021-9525</issn><issn>1540-8140</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1vEzEQhi0EomnhyA0hi0NvW_y5ti9IJaEFUUEk4Gx5XW_iaNcOtrco_HocJWqBC_JhDvPoHc88ALzA6AIjSd9sbHdBEKJI4ZY8AjPMGWokZugxmCFEcKM44SfgNOcNQogJRp-CE8yUxEixGdgufN-75ELxZoBXU7DFx5Bh7OE1XKZYnA_QhFv4zvxqzPLTHH71q2AGH1Zwacr6p9llWJFFijlu134w8LObUuwGkwu8zLtxdCV5Cxf-zuca_Qw86c2Q3fNjPQPfr95_m39obr5cf5xf3jSWE1ka0yLZGqWkVYoxqjhyXHIlu7anTBDTI26t7Sjm2Nheul44KyxnimFGXSvpGXh7yN1O3ehubd0wmUFvkx9N2ulovP67E_xar-KdJlgQ3LY14PwYkOKPyeWiR5-tGwYTXJyyFrg-ytV_QSxaRgTeg6__ATdxSvWYeT8UKV6dVKg5QLZeNCfX338ZI703rqtxfW-88q_-3POBPiquwMsDsMklpod-S7BSgv4GPJKw4A</recordid><startdate>20040301</startdate><enddate>20040301</enddate><creator>Izumi, Yasushi</creator><creator>Ohta, Nao</creator><creator>Itoh-Furuya, Asako</creator><creator>Fuse, Naoyuki</creator><creator>Matsuzaki, Fumio</creator><general>Rockefeller University Press</general><general>The Rockefeller University Press</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>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>7SS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20040301</creationdate><title>Differential Functions of G Protein and Baz-aPKC Signaling Pathways in Drosophila Neuroblast Asymmetric Division</title><author>Izumi, Yasushi ; Ohta, Nao ; Itoh-Furuya, Asako ; Fuse, Naoyuki ; Matsuzaki, Fumio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c528t-a6086a998c99443950e58598b6f3472af05cccb3151acf8ef7ec7c5494143e683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Amino Acid Sequence</topic><topic>Animals</topic><topic>Animals, Genetically Modified</topic><topic>Carrier Proteins - metabolism</topic><topic>Cell Cycle Proteins - metabolism</topic><topic>Cell division</topic><topic>Cell Division - physiology</topic><topic>Cell Polarity</topic><topic>Cell Size</topic><topic>Cellular biology</topic><topic>Cytoskeletal Proteins - genetics</topic><topic>Cytoskeletal Proteins - metabolism</topic><topic>Drosophila melanogaster - embryology</topic><topic>Drosophila melanogaster - physiology</topic><topic>Drosophila Proteins - metabolism</topic><topic>Embryo, Nonmammalian - physiology</topic><topic>GTP-Binding Protein alpha Subunits, Gq-G11 - genetics</topic><topic>GTP-Binding Protein alpha Subunits, Gq-G11 - metabolism</topic><topic>GTP-Binding Protein beta Subunits - genetics</topic><topic>GTP-Binding Protein beta Subunits - metabolism</topic><topic>Insects</topic><topic>Intracellular Signaling Peptides and Proteins</topic><topic>Isoenzymes - metabolism</topic><topic>Macromolecular Substances</topic><topic>Membranes</topic><topic>Molecular Sequence Data</topic><topic>Neurons - cytology</topic><topic>Neurons - physiology</topic><topic>Neuropeptides</topic><topic>Point Mutation</topic><topic>Protein Kinase C - metabolism</topic><topic>Protein Subunits - genetics</topic><topic>Protein Subunits - metabolism</topic><topic>Proteins</topic><topic>Proteins - genetics</topic><topic>Proteins - metabolism</topic><topic>Second Messenger Systems - physiology</topic><topic>Spindle Apparatus - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Izumi, Yasushi</creatorcontrib><creatorcontrib>Ohta, Nao</creatorcontrib><creatorcontrib>Itoh-Furuya, Asako</creatorcontrib><creatorcontrib>Fuse, Naoyuki</creatorcontrib><creatorcontrib>Matsuzaki, Fumio</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of cell biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Izumi, Yasushi</au><au>Ohta, Nao</au><au>Itoh-Furuya, Asako</au><au>Fuse, Naoyuki</au><au>Matsuzaki, Fumio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential Functions of G Protein and Baz-aPKC Signaling Pathways in Drosophila Neuroblast Asymmetric Division</atitle><jtitle>The Journal of cell biology</jtitle><addtitle>J Cell Biol</addtitle><date>2004-03-01</date><risdate>2004</risdate><volume>164</volume><issue>5</issue><spage>729</spage><epage>738</epage><pages>729-738</pages><issn>0021-9525</issn><eissn>1540-8140</eissn><coden>JCLBA3</coden><abstract>Drosophila melanogaster neuroblasts (NBs) undergo asymmetric divisions during which cell-fate determinants localize asymmetrically, mitotic spindles orient along the apical-basal axis, and unequal-sized daughter cells appear. We identified here the first Drosophila mutant in the Gγ1 subunit of heterotrimeric G protein, which produces Gγ1 lacking its membrane anchor site and exhibits phenotypes identical to those of Gβ13F, including abnormal spindle asymmetry and spindle orientation in NB divisions. This mutant fails to bind Gβ13F to the membrane, indicating an essential role of cortical Gγ1-Gβ13F signaling in asymmetric divisions. In Gγ1 and Gβ13F mutant NBs, Pins-Gαi, which normally localize in the apical cortex, no longer distribute asymmetrically. However, the other apical components, Bazooka-atypical PKC-Par6-Inscuteable, still remain polarized and responsible for asymmetric Miranda localization, suggesting their dominant role in localizing cell-fate determinants. Further analysis of Gβγ and other mutants indicates a predominant role of Partner of Inscuteable-Gαi in spindle orientation. We thus suggest that the two apical signaling pathways have overlapping but different roles in asymmetric NB division.</abstract><cop>United States</cop><pub>Rockefeller University Press</pub><pmid>14981094</pmid><doi>10.1083/jcb.200309162</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Amino Acid Sequence Animals Animals, Genetically Modified Carrier Proteins - metabolism Cell Cycle Proteins - metabolism Cell division Cell Division - physiology Cell Polarity Cell Size Cellular biology Cytoskeletal Proteins - genetics Cytoskeletal Proteins - metabolism Drosophila melanogaster - embryology Drosophila melanogaster - physiology Drosophila Proteins - metabolism Embryo, Nonmammalian - physiology GTP-Binding Protein alpha Subunits, Gq-G11 - genetics GTP-Binding Protein alpha Subunits, Gq-G11 - metabolism GTP-Binding Protein beta Subunits - genetics GTP-Binding Protein beta Subunits - metabolism Insects Intracellular Signaling Peptides and Proteins Isoenzymes - metabolism Macromolecular Substances Membranes Molecular Sequence Data Neurons - cytology Neurons - physiology Neuropeptides Point Mutation Protein Kinase C - metabolism Protein Subunits - genetics Protein Subunits - metabolism Proteins Proteins - genetics Proteins - metabolism Second Messenger Systems - physiology Spindle Apparatus - metabolism |
| title | Differential Functions of G Protein and Baz-aPKC Signaling Pathways in Drosophila Neuroblast Asymmetric Division |
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