Evidence for Antagonistic Regulation of Cell Growth by the Calcineurin and High Osmolarity Glycerol Pathways in Saccharomyces cerevisiae
Because Ca 2+ signaling of budding yeast, through the activation of calcineurin and the Mpk1/Slt2 mitogen-activated protein kinase cascade, performs redundant function(s) in the events essential for growth, the simultaneous deletion of both these pathways (Î cnb1 Î mpk1 ) leads to lethality. A PTC...
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| Veröffentlicht in: | The Journal of biological chemistry 2004-01, Vol.279 (5), p.3651-3661 |
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| container_title | The Journal of biological chemistry |
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| creator | Shitamukai, Atsunori Hirata, Dai Sonobe, Shinya Miyakawa, Tokichi |
| description | Because Ca 2+ signaling of budding yeast, through the activation of calcineurin and the Mpk1/Slt2 mitogen-activated protein kinase cascade,
performs redundant function(s) in the events essential for growth, the simultaneous deletion of both these pathways (Î cnb1 Î mpk1 ) leads to lethality. A PTC4 cDNA that encodes a protein phosphatase belonging to the PP2C family was obtained as a high dosage suppressor of the lethality
of Î cnb1 Î mpk1 strain. Overexpression of PTC4 led to a decrease in the high osmolarity-induced Hog1 phosphorylation, and HOG1 deletion remarkably suppressed the synthetic lethality, indicating an antagonistic role of the high osmolarity glycerol (HOG)
pathway and the Ca 2+ signaling pathway in growth regulation. The calcineurin-Crz1 pathway was required for the down-regulation of the HOG pathway.
Analysis of the time course of actin polarization, bud formation, and the onset of mitosis in synchronous cell cultures demonstrated
that calcineurin negatively regulates actin polarization at the bud site, whereas the HOG pathway positively regulates bud
formation at a later step after actin has polarized. |
| doi_str_mv | 10.1074/jbc.M306098200 |
| format | Article |
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performs redundant function(s) in the events essential for growth, the simultaneous deletion of both these pathways (Î cnb1 Î mpk1 ) leads to lethality. A PTC4 cDNA that encodes a protein phosphatase belonging to the PP2C family was obtained as a high dosage suppressor of the lethality
of Î cnb1 Î mpk1 strain. Overexpression of PTC4 led to a decrease in the high osmolarity-induced Hog1 phosphorylation, and HOG1 deletion remarkably suppressed the synthetic lethality, indicating an antagonistic role of the high osmolarity glycerol (HOG)
pathway and the Ca 2+ signaling pathway in growth regulation. The calcineurin-Crz1 pathway was required for the down-regulation of the HOG pathway.
Analysis of the time course of actin polarization, bud formation, and the onset of mitosis in synchronous cell cultures demonstrated
that calcineurin negatively regulates actin polarization at the bud site, whereas the HOG pathway positively regulates bud
formation at a later step after actin has polarized.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M306098200</identifier><identifier>PMID: 14583627</identifier><language>eng</language><publisher>United States: American Society for Biochemistry and Molecular Biology</publisher><subject>Actins - metabolism ; Calcineurin - metabolism ; Calcium - metabolism ; Cell Cycle ; Cell Division ; Cell Separation ; DNA, Complementary - metabolism ; DNA-Binding Proteins ; Flow Cytometry ; G2 Phase ; Gene Deletion ; Genotype ; Glycerol - metabolism ; Hog1 protein ; Microscopy, Fluorescence ; Mitogen-Activated Protein Kinases - metabolism ; Mitosis ; Models, Biological ; Mutation ; Phenotype ; Phosphoprotein Phosphatases - metabolism ; Phosphorylation ; Plasmids - metabolism ; Protein Phosphatase 2C ; Saccharomyces cerevisiae ; Saccharomyces cerevisiae - metabolism ; Saccharomyces cerevisiae Proteins - metabolism ; Signal Transduction ; Time Factors ; Trans-Activators - metabolism ; Transcription Factors</subject><ispartof>The Journal of biological chemistry, 2004-01, Vol.279 (5), p.3651-3661</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-4d3b202b805e23290c3c1d01f39a094f60c88ec2bff1d98c30ec9a95d48131023</citedby><cites>FETCH-LOGICAL-c455t-4d3b202b805e23290c3c1d01f39a094f60c88ec2bff1d98c30ec9a95d48131023</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14583627$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shitamukai, Atsunori</creatorcontrib><creatorcontrib>Hirata, Dai</creatorcontrib><creatorcontrib>Sonobe, Shinya</creatorcontrib><creatorcontrib>Miyakawa, Tokichi</creatorcontrib><title>Evidence for Antagonistic Regulation of Cell Growth by the Calcineurin and High Osmolarity Glycerol Pathways in Saccharomyces cerevisiae</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Because Ca 2+ signaling of budding yeast, through the activation of calcineurin and the Mpk1/Slt2 mitogen-activated protein kinase cascade,
performs redundant function(s) in the events essential for growth, the simultaneous deletion of both these pathways (Î cnb1 Î mpk1 ) leads to lethality. A PTC4 cDNA that encodes a protein phosphatase belonging to the PP2C family was obtained as a high dosage suppressor of the lethality
of Î cnb1 Î mpk1 strain. Overexpression of PTC4 led to a decrease in the high osmolarity-induced Hog1 phosphorylation, and HOG1 deletion remarkably suppressed the synthetic lethality, indicating an antagonistic role of the high osmolarity glycerol (HOG)
pathway and the Ca 2+ signaling pathway in growth regulation. The calcineurin-Crz1 pathway was required for the down-regulation of the HOG pathway.
Analysis of the time course of actin polarization, bud formation, and the onset of mitosis in synchronous cell cultures demonstrated
that calcineurin negatively regulates actin polarization at the bud site, whereas the HOG pathway positively regulates bud
formation at a later step after actin has polarized.</description><subject>Actins - metabolism</subject><subject>Calcineurin - metabolism</subject><subject>Calcium - metabolism</subject><subject>Cell Cycle</subject><subject>Cell Division</subject><subject>Cell Separation</subject><subject>DNA, Complementary - metabolism</subject><subject>DNA-Binding Proteins</subject><subject>Flow Cytometry</subject><subject>G2 Phase</subject><subject>Gene Deletion</subject><subject>Genotype</subject><subject>Glycerol - metabolism</subject><subject>Hog1 protein</subject><subject>Microscopy, Fluorescence</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Mitosis</subject><subject>Models, Biological</subject><subject>Mutation</subject><subject>Phenotype</subject><subject>Phosphoprotein Phosphatases - metabolism</subject><subject>Phosphorylation</subject><subject>Plasmids - metabolism</subject><subject>Protein Phosphatase 2C</subject><subject>Saccharomyces cerevisiae</subject><subject>Saccharomyces cerevisiae - metabolism</subject><subject>Saccharomyces cerevisiae Proteins - metabolism</subject><subject>Signal Transduction</subject><subject>Time Factors</subject><subject>Trans-Activators - metabolism</subject><subject>Transcription Factors</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkMFq3DAQhkVpabZprz0W0UNv3o4kyysdw5JsCikpSQO5CVkerxVsK5XsLH6DPnZVdiFzmcP_zQ_zEfKZwZrBpvz-VLv1TwEVaMUB3pAVAyUKIdnjW7IC4KzQXKoz8iGlJ8hTavaenLFSKlHxzYr8vXzxDY4OaRsivRgnuw-jT5N39A73c28nH0YaWrrFvqe7GA5TR-uFTh3Sre2dH3GOfqR2bOi133f0Ng2ht9FPC931i8MYevrLTt3BLolm8N4619kYhpwlmnN88clb_EjetbZP-Om0z8nD1eXv7XVxc7v7sb24KVwp5VSUjag58FqBRC64Bicca4C1QlvQZVuBUwodr9uWNVo5Aei01bIpFRMMuDgn3469zzH8mTFNZvDJ5efsiGFOhmkuKmAig-sj6GJIKWJrnqMfbFwMA_Pfvcnuzav7fPDl1DzXAzav-El2Br4egS6LOviIpvbBdTgYvtFGGlFJJv4BloqM2Q</recordid><startdate>20040130</startdate><enddate>20040130</enddate><creator>Shitamukai, Atsunori</creator><creator>Hirata, Dai</creator><creator>Sonobe, Shinya</creator><creator>Miyakawa, Tokichi</creator><general>American Society for Biochemistry and Molecular Biology</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>M7N</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20040130</creationdate><title>Evidence for Antagonistic Regulation of Cell Growth by the Calcineurin and High Osmolarity Glycerol Pathways in Saccharomyces cerevisiae</title><author>Shitamukai, Atsunori ; Hirata, Dai ; Sonobe, Shinya ; Miyakawa, Tokichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-4d3b202b805e23290c3c1d01f39a094f60c88ec2bff1d98c30ec9a95d48131023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Actins - metabolism</topic><topic>Calcineurin - metabolism</topic><topic>Calcium - metabolism</topic><topic>Cell Cycle</topic><topic>Cell Division</topic><topic>Cell Separation</topic><topic>DNA, Complementary - metabolism</topic><topic>DNA-Binding Proteins</topic><topic>Flow Cytometry</topic><topic>G2 Phase</topic><topic>Gene Deletion</topic><topic>Genotype</topic><topic>Glycerol - metabolism</topic><topic>Hog1 protein</topic><topic>Microscopy, Fluorescence</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Mitosis</topic><topic>Models, Biological</topic><topic>Mutation</topic><topic>Phenotype</topic><topic>Phosphoprotein Phosphatases - metabolism</topic><topic>Phosphorylation</topic><topic>Plasmids - metabolism</topic><topic>Protein Phosphatase 2C</topic><topic>Saccharomyces cerevisiae</topic><topic>Saccharomyces cerevisiae - metabolism</topic><topic>Saccharomyces cerevisiae Proteins - metabolism</topic><topic>Signal Transduction</topic><topic>Time Factors</topic><topic>Trans-Activators - metabolism</topic><topic>Transcription Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shitamukai, Atsunori</creatorcontrib><creatorcontrib>Hirata, Dai</creatorcontrib><creatorcontrib>Sonobe, Shinya</creatorcontrib><creatorcontrib>Miyakawa, Tokichi</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>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shitamukai, Atsunori</au><au>Hirata, Dai</au><au>Sonobe, Shinya</au><au>Miyakawa, Tokichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evidence for Antagonistic Regulation of Cell Growth by the Calcineurin and High Osmolarity Glycerol Pathways in Saccharomyces cerevisiae</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>2004-01-30</date><risdate>2004</risdate><volume>279</volume><issue>5</issue><spage>3651</spage><epage>3661</epage><pages>3651-3661</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>Because Ca 2+ signaling of budding yeast, through the activation of calcineurin and the Mpk1/Slt2 mitogen-activated protein kinase cascade,
performs redundant function(s) in the events essential for growth, the simultaneous deletion of both these pathways (Î cnb1 Î mpk1 ) leads to lethality. A PTC4 cDNA that encodes a protein phosphatase belonging to the PP2C family was obtained as a high dosage suppressor of the lethality
of Î cnb1 Î mpk1 strain. Overexpression of PTC4 led to a decrease in the high osmolarity-induced Hog1 phosphorylation, and HOG1 deletion remarkably suppressed the synthetic lethality, indicating an antagonistic role of the high osmolarity glycerol (HOG)
pathway and the Ca 2+ signaling pathway in growth regulation. The calcineurin-Crz1 pathway was required for the down-regulation of the HOG pathway.
Analysis of the time course of actin polarization, bud formation, and the onset of mitosis in synchronous cell cultures demonstrated
that calcineurin negatively regulates actin polarization at the bud site, whereas the HOG pathway positively regulates bud
formation at a later step after actin has polarized.</abstract><cop>United States</cop><pub>American Society for Biochemistry and Molecular Biology</pub><pmid>14583627</pmid><doi>10.1074/jbc.M306098200</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Actins - metabolism Calcineurin - metabolism Calcium - metabolism Cell Cycle Cell Division Cell Separation DNA, Complementary - metabolism DNA-Binding Proteins Flow Cytometry G2 Phase Gene Deletion Genotype Glycerol - metabolism Hog1 protein Microscopy, Fluorescence Mitogen-Activated Protein Kinases - metabolism Mitosis Models, Biological Mutation Phenotype Phosphoprotein Phosphatases - metabolism Phosphorylation Plasmids - metabolism Protein Phosphatase 2C Saccharomyces cerevisiae Saccharomyces cerevisiae - metabolism Saccharomyces cerevisiae Proteins - metabolism Signal Transduction Time Factors Trans-Activators - metabolism Transcription Factors |
| title | Evidence for Antagonistic Regulation of Cell Growth by the Calcineurin and High Osmolarity Glycerol Pathways in Saccharomyces cerevisiae |
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