Mutation of the Dictyostelium fbxA Gene Affects Cell-Fate Decisions and Spatial Patterning
Cell-fate decisions and spatial patterning in Dictyostelium are regulated by a number of genes. Our studies have implicated a gene called fbxA, which codes for an F-box protein, in these pathways. The FbxA protein is one of the controls on a cAMP phosphodiesterase called RegA, mediating its degradat...
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description | Cell-fate decisions and spatial patterning in
Dictyostelium are regulated by a number of genes. Our studies have implicated a gene called
fbxA, which codes for an F-box protein, in these pathways. The FbxA protein is one of the controls on a cAMP phosphodiesterase called RegA, mediating its degradation via ubiquitin-linked proteolysis. Using marked strains, we showed that the
fbxA
– mutant has defective cell-type proportioning, with a dearth of prestalk cells compared to prespore cells. In this work, we show that this effect occurs earlier during the 24 hour developmental cycle than previously thought. The normal sorting of the prestalk and prespore cells in aggregates and mounds is not affected by the mutation. The mutant cells sort abnormally at the tipped mound stage, when prespore and prestalk cells normally distribute into their proper compartments. The
fbxA
– mutant forms prestalk cells in low numbers when not in chimeras, but in the presence of wild-type amoebae the mutant preferentially forms viable spores, driving the wild type to form non-viable stalk cells. In an attempt to identify the signal transduction pathway that mediates proportionality in prestalk and prespore cells, we asked whether certain signal transduction mutants were immune to the effects of the
fbxA
–cells and formed spores in chimeras. |
doi_str_mv | 10.1078/143446103322454158 |
format | Article |
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Dictyostelium are regulated by a number of genes. Our studies have implicated a gene called
fbxA, which codes for an F-box protein, in these pathways. The FbxA protein is one of the controls on a cAMP phosphodiesterase called RegA, mediating its degradation via ubiquitin-linked proteolysis. Using marked strains, we showed that the
fbxA
– mutant has defective cell-type proportioning, with a dearth of prestalk cells compared to prespore cells. In this work, we show that this effect occurs earlier during the 24 hour developmental cycle than previously thought. The normal sorting of the prestalk and prespore cells in aggregates and mounds is not affected by the mutation. The mutant cells sort abnormally at the tipped mound stage, when prespore and prestalk cells normally distribute into their proper compartments. The
fbxA
– mutant forms prestalk cells in low numbers when not in chimeras, but in the presence of wild-type amoebae the mutant preferentially forms viable spores, driving the wild type to form non-viable stalk cells. In an attempt to identify the signal transduction pathway that mediates proportionality in prestalk and prespore cells, we asked whether certain signal transduction mutants were immune to the effects of the
fbxA
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Dictyostelium are regulated by a number of genes. Our studies have implicated a gene called
fbxA, which codes for an F-box protein, in these pathways. The FbxA protein is one of the controls on a cAMP phosphodiesterase called RegA, mediating its degradation via ubiquitin-linked proteolysis. Using marked strains, we showed that the
fbxA
– mutant has defective cell-type proportioning, with a dearth of prestalk cells compared to prespore cells. In this work, we show that this effect occurs earlier during the 24 hour developmental cycle than previously thought. The normal sorting of the prestalk and prespore cells in aggregates and mounds is not affected by the mutation. The mutant cells sort abnormally at the tipped mound stage, when prespore and prestalk cells normally distribute into their proper compartments. The
fbxA
– mutant forms prestalk cells in low numbers when not in chimeras, but in the presence of wild-type amoebae the mutant preferentially forms viable spores, driving the wild type to form non-viable stalk cells. In an attempt to identify the signal transduction pathway that mediates proportionality in prestalk and prespore cells, we asked whether certain signal transduction mutants were immune to the effects of the
fbxA
–cells and formed spores in chimeras.</description><subject>Animals</subject><subject>camp phosphodiesterase</subject><subject>cheaters</subject><subject>development</subject><subject>Dictyostelium</subject><subject>Dictyostelium - cytology</subject><subject>Dictyostelium - genetics</subject><subject>Dictyostelium - growth & development</subject><subject>evolution</subject><subject>F-box protein</subject><subject>F-Box Proteins - genetics</subject><subject>fbxA gene</subject><subject>Gene Expression Regulation, Developmental</subject><subject>Genes, Protozoan</subject><subject>Mutation</subject><subject>prespore cells</subject><subject>prestalk cells</subject><subject>Protozoan Proteins - genetics</subject><subject>Signal Transduction</subject><issn>1434-4610</issn><issn>1618-0941</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkcFrFDEYxYNYbF39BzxI8OBtNF-SySTgZVltFVoqqBcvIZt80ZTZmTXJSPvfm7ILgoKeEsjvPV7eI-QZsFfABv0apJBSAROCc9lL6PUDcgYKdMeMhIft3oDunjglj0u5YQykUfoROQWpei2NPiNfr5bqaponOkdavyN9m3y9m0vFMS07Gre3a3qBE9J1jOhroRscx-7c1UaiT6UpC3VToJ_2zcaN9KOrFfOUpm9PyEl0Y8Gnx3NFvpy_-7x5311eX3zYrC87L4HVTgDrow4ClOF9EJHx3oHygxgwKuMc16a9oQElAgbPXTCw9XJgygQHIMSKvDz47vP8Y8FS7S4V32K6Ceel2KHVwHvJ_wtCCwCM6Qa--AO8mZc8tU9YzgYjhW5hVoQfIJ_nUjJGu89p5_KdBWbv97F_79NEz4_Oy3aH4bfkOEgD3hwAbI39TJht8QknjyHl1r8Nc_qX_y-BqZsh</recordid><startdate>20031001</startdate><enddate>20031001</enddate><creator>Ennis, Herbert L.</creator><creator>Dao, Dee N.</creator><creator>Wu, Mary Y.</creator><creator>Kessin, Richard H.</creator><general>Elsevier GmbH</general><general>Elsevier Science Ltd</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>S0X</scope><scope>M7N</scope><scope>7X8</scope></search><sort><creationdate>20031001</creationdate><title>Mutation of the Dictyostelium fbxA Gene Affects Cell-Fate Decisions and Spatial Patterning</title><author>Ennis, Herbert L. ; Dao, Dee N. ; Wu, Mary Y. ; Kessin, Richard H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c410t-3105f8d316925d3f025a16c737ef69aa289316e9163dedc2ad91bc47069da1133</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>camp phosphodiesterase</topic><topic>cheaters</topic><topic>development</topic><topic>Dictyostelium</topic><topic>Dictyostelium - cytology</topic><topic>Dictyostelium - genetics</topic><topic>Dictyostelium - growth & development</topic><topic>evolution</topic><topic>F-box protein</topic><topic>F-Box Proteins - genetics</topic><topic>fbxA gene</topic><topic>Gene Expression Regulation, Developmental</topic><topic>Genes, Protozoan</topic><topic>Mutation</topic><topic>prespore cells</topic><topic>prestalk cells</topic><topic>Protozoan Proteins - genetics</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ennis, Herbert L.</creatorcontrib><creatorcontrib>Dao, Dee N.</creatorcontrib><creatorcontrib>Wu, Mary Y.</creatorcontrib><creatorcontrib>Kessin, Richard H.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>SIRS Editorial</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><jtitle>Protist</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ennis, Herbert L.</au><au>Dao, Dee N.</au><au>Wu, Mary Y.</au><au>Kessin, Richard H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mutation of the Dictyostelium fbxA Gene Affects Cell-Fate Decisions and Spatial Patterning</atitle><jtitle>Protist</jtitle><addtitle>Protist</addtitle><date>2003-10-01</date><risdate>2003</risdate><volume>154</volume><issue>3</issue><spage>419</spage><epage>429</epage><pages>419-429</pages><issn>1434-4610</issn><eissn>1618-0941</eissn><abstract>Cell-fate decisions and spatial patterning in
Dictyostelium are regulated by a number of genes. Our studies have implicated a gene called
fbxA, which codes for an F-box protein, in these pathways. The FbxA protein is one of the controls on a cAMP phosphodiesterase called RegA, mediating its degradation via ubiquitin-linked proteolysis. Using marked strains, we showed that the
fbxA
– mutant has defective cell-type proportioning, with a dearth of prestalk cells compared to prespore cells. In this work, we show that this effect occurs earlier during the 24 hour developmental cycle than previously thought. The normal sorting of the prestalk and prespore cells in aggregates and mounds is not affected by the mutation. The mutant cells sort abnormally at the tipped mound stage, when prespore and prestalk cells normally distribute into their proper compartments. The
fbxA
– mutant forms prestalk cells in low numbers when not in chimeras, but in the presence of wild-type amoebae the mutant preferentially forms viable spores, driving the wild type to form non-viable stalk cells. In an attempt to identify the signal transduction pathway that mediates proportionality in prestalk and prespore cells, we asked whether certain signal transduction mutants were immune to the effects of the
fbxA
–cells and formed spores in chimeras.</abstract><cop>Germany</cop><pub>Elsevier GmbH</pub><pmid>14658498</pmid><doi>10.1078/143446103322454158</doi><tpages>11</tpages></addata></record> |
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subjects | Animals camp phosphodiesterase cheaters development Dictyostelium Dictyostelium - cytology Dictyostelium - genetics Dictyostelium - growth & development evolution F-box protein F-Box Proteins - genetics fbxA gene Gene Expression Regulation, Developmental Genes, Protozoan Mutation prespore cells prestalk cells Protozoan Proteins - genetics Signal Transduction |
title | Mutation of the Dictyostelium fbxA Gene Affects Cell-Fate Decisions and Spatial Patterning |
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