Yeast caspase 1 links messenger RNA stability to apoptosis in yeast
During the past years, yeasts have been successfully established as models to study the mechanisms of apoptotic regulation. We recently showed that mutations in the LSM4 gene, which is involved in messenger RNA decapping, lead to increased mRNA stability and apoptosis in yeast. Here, we show that mi...
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| Veröffentlicht in: | EMBO reports 2005-11, Vol.6 (11), p.1076-1081 |
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| creator | Mazzoni, Cristina Herker, Eva Palermo, Vanessa Jungwirth, Helmut Eisenberg, Tobias Madeo, Frank Falcone, Claudio |
| description | During the past years, yeasts have been successfully established as models to study the mechanisms of apoptotic regulation. We recently showed that mutations in the
LSM4
gene, which is involved in messenger RNA decapping, lead to increased mRNA stability and apoptosis in yeast. Here, we show that mitochondrial function and
YCA1
, which encodes a budding yeast metacaspase, are necessary for apoptosis triggered by stabilization of mRNAs. Deletion of
YCA1
in yeast cells mutated in the
LSM4
gene prevents mitochondrial fragmentation and rapid cell death during chronological ageing of the culture, diminishes reactive oxygen species accumulation and DNA breakage, and increases resistance to H
2
O
2
and acetic acid. mRNA levels in
lsm4
mutants deleted for
YCA1
are still increased, positioning the Yca1 budding yeast caspase as a downstream executor of cell death induced by mRNA perturbations. In addition, we show that mitochondrial function is necessary for fast death during chronological ageing, as well as in
LSM4
mutated and wild‐type cells. |
| doi_str_mv | 10.1038/sj.embor.7400514 |
| format | Article |
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LSM4
gene, which is involved in messenger RNA decapping, lead to increased mRNA stability and apoptosis in yeast. Here, we show that mitochondrial function and
YCA1
, which encodes a budding yeast metacaspase, are necessary for apoptosis triggered by stabilization of mRNAs. Deletion of
YCA1
in yeast cells mutated in the
LSM4
gene prevents mitochondrial fragmentation and rapid cell death during chronological ageing of the culture, diminishes reactive oxygen species accumulation and DNA breakage, and increases resistance to H
2
O
2
and acetic acid. mRNA levels in
lsm4
mutants deleted for
YCA1
are still increased, positioning the Yca1 budding yeast caspase as a downstream executor of cell death induced by mRNA perturbations. In addition, we show that mitochondrial function is necessary for fast death during chronological ageing, as well as in
LSM4
mutated and wild‐type cells.</description><identifier>ISSN: 1469-221X</identifier><identifier>EISSN: 1469-3178</identifier><identifier>EISSN: 1469-221X</identifier><identifier>DOI: 10.1038/sj.embor.7400514</identifier><identifier>PMID: 16170310</identifier><identifier>CODEN: ERMEAX</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Acetic acid ; Apoptosis ; Caspases - genetics ; Caspases - metabolism ; Cell Survival ; Deoxyribonucleic acid ; DNA ; Gene Silencing ; Hydrogen peroxide ; LSM4 ; mitochondria ; Mitochondria - metabolism ; Mortality ; Mutation ; Phenotype ; programmed cell death ; Reactive Oxygen Species - metabolism ; RNA Stability ; RNA, Messenger - metabolism ; Saccharomyces cerevisiae ; Saccharomyces cerevisiae - enzymology ; Saccharomyces cerevisiae Proteins - genetics ; Saccharomyces cerevisiae Proteins - metabolism ; Scientific Report ; Time Factors ; YCA1 ; Yeasts</subject><ispartof>EMBO reports, 2005-11, Vol.6 (11), p.1076-1081</ispartof><rights>European Molecular Biology Organization 2005</rights><rights>Copyright © 2005 European Molecular Biology Organization</rights><rights>Copyright Nature Publishing Group Nov 2005</rights><rights>Copyright © 2005, European Molecular Biology Organization 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6044-c6f936753da5bf9d07f9c764b47f6d28972c744cd5b180a14b5d224713641a7f3</citedby><cites>FETCH-LOGICAL-c6044-c6f936753da5bf9d07f9c764b47f6d28972c744cd5b180a14b5d224713641a7f3</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/PMC1371024/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1371024/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1417,1433,27924,27925,45574,45575,46409,46833,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16170310$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mazzoni, Cristina</creatorcontrib><creatorcontrib>Herker, Eva</creatorcontrib><creatorcontrib>Palermo, Vanessa</creatorcontrib><creatorcontrib>Jungwirth, Helmut</creatorcontrib><creatorcontrib>Eisenberg, Tobias</creatorcontrib><creatorcontrib>Madeo, Frank</creatorcontrib><creatorcontrib>Falcone, Claudio</creatorcontrib><title>Yeast caspase 1 links messenger RNA stability to apoptosis in yeast</title><title>EMBO reports</title><addtitle>EMBO Rep</addtitle><addtitle>EMBO Rep</addtitle><description>During the past years, yeasts have been successfully established as models to study the mechanisms of apoptotic regulation. We recently showed that mutations in the
LSM4
gene, which is involved in messenger RNA decapping, lead to increased mRNA stability and apoptosis in yeast. Here, we show that mitochondrial function and
YCA1
, which encodes a budding yeast metacaspase, are necessary for apoptosis triggered by stabilization of mRNAs. Deletion of
YCA1
in yeast cells mutated in the
LSM4
gene prevents mitochondrial fragmentation and rapid cell death during chronological ageing of the culture, diminishes reactive oxygen species accumulation and DNA breakage, and increases resistance to H
2
O
2
and acetic acid. mRNA levels in
lsm4
mutants deleted for
YCA1
are still increased, positioning the Yca1 budding yeast caspase as a downstream executor of cell death induced by mRNA perturbations. In addition, we show that mitochondrial function is necessary for fast death during chronological ageing, as well as in
LSM4
mutated and wild‐type cells.</description><subject>Acetic acid</subject><subject>Apoptosis</subject><subject>Caspases - genetics</subject><subject>Caspases - metabolism</subject><subject>Cell Survival</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Gene Silencing</subject><subject>Hydrogen peroxide</subject><subject>LSM4</subject><subject>mitochondria</subject><subject>Mitochondria - metabolism</subject><subject>Mortality</subject><subject>Mutation</subject><subject>Phenotype</subject><subject>programmed cell death</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>RNA Stability</subject><subject>RNA, Messenger - metabolism</subject><subject>Saccharomyces cerevisiae</subject><subject>Saccharomyces cerevisiae - enzymology</subject><subject>Saccharomyces cerevisiae Proteins - genetics</subject><subject>Saccharomyces cerevisiae Proteins - metabolism</subject><subject>Scientific Report</subject><subject>Time Factors</subject><subject>YCA1</subject><subject>Yeasts</subject><issn>1469-221X</issn><issn>1469-3178</issn><issn>1469-221X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkc9v0zAcxSMEYmNw5wKyduDW4l-x4wvSVm0dUhnSBhqcLCdxhrskDv4mjP73uCRqgQO72Jbe5z1_7ZckLwmeE8yyt7Ce2yb3YS45xinhj5JDwoWaMSKzx9OZUvLlIHkGsMaRUTJ7mhwQQSRmBB8mi6_WQI8KA50BiwiqXXsHqLEAtr21AV1dniDoTe5q129Q75HpfNd7cIBcizZb9_PkSWVqsC-m_Sj5fH72aXExW31cvl-crGaFwJzHtVJMyJSVJs0rVWJZqUIKnnNZiZJmStJCcl6UaU4ybAjP05JSLgkTnBhZsaPk3ZjbDXljy8K2fTC17oJrTNhob5z-W2ndN33rf2jCJMGUx4A3U0Dw3wcLvW4cFLauTWv9AFpkMqVSZQ-CFDNBOKcRPP4HXPshtPEXIpOllDKlIoRHqAgeINhqNzLBetujhrX-3aOeeoyW138-dW-YiouAGoF7V9vNg4H67MPp1T6cjF6Itm3J-6H_M9Cr0dOafgh2d-Fen426g97-3Mkm3GkhmUz1zeVSr64XFzeny2vN2S8FHNVR</recordid><startdate>20051101</startdate><enddate>20051101</enddate><creator>Mazzoni, Cristina</creator><creator>Herker, Eva</creator><creator>Palermo, Vanessa</creator><creator>Jungwirth, Helmut</creator><creator>Eisenberg, Tobias</creator><creator>Madeo, Frank</creator><creator>Falcone, Claudio</creator><general>John Wiley & Sons, Ltd</general><general>Nature Publishing Group UK</general><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>3V.</scope><scope>7QL</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20051101</creationdate><title>Yeast caspase 1 links messenger RNA stability to apoptosis in yeast</title><author>Mazzoni, Cristina ; Herker, Eva ; Palermo, Vanessa ; Jungwirth, Helmut ; Eisenberg, Tobias ; Madeo, Frank ; Falcone, Claudio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6044-c6f936753da5bf9d07f9c764b47f6d28972c744cd5b180a14b5d224713641a7f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Acetic acid</topic><topic>Apoptosis</topic><topic>Caspases - genetics</topic><topic>Caspases - metabolism</topic><topic>Cell Survival</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Gene Silencing</topic><topic>Hydrogen peroxide</topic><topic>LSM4</topic><topic>mitochondria</topic><topic>Mitochondria - metabolism</topic><topic>Mortality</topic><topic>Mutation</topic><topic>Phenotype</topic><topic>programmed cell death</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>RNA Stability</topic><topic>RNA, Messenger - metabolism</topic><topic>Saccharomyces cerevisiae</topic><topic>Saccharomyces cerevisiae - enzymology</topic><topic>Saccharomyces cerevisiae Proteins - genetics</topic><topic>Saccharomyces cerevisiae Proteins - metabolism</topic><topic>Scientific Report</topic><topic>Time Factors</topic><topic>YCA1</topic><topic>Yeasts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mazzoni, Cristina</creatorcontrib><creatorcontrib>Herker, Eva</creatorcontrib><creatorcontrib>Palermo, Vanessa</creatorcontrib><creatorcontrib>Jungwirth, Helmut</creatorcontrib><creatorcontrib>Eisenberg, Tobias</creatorcontrib><creatorcontrib>Madeo, Frank</creatorcontrib><creatorcontrib>Falcone, Claudio</creatorcontrib><collection>Istex</collection><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>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</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 Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</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>Research Library (Alumni Edition)</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>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</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>Research Library</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</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 Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>EMBO reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mazzoni, Cristina</au><au>Herker, Eva</au><au>Palermo, Vanessa</au><au>Jungwirth, Helmut</au><au>Eisenberg, Tobias</au><au>Madeo, Frank</au><au>Falcone, Claudio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Yeast caspase 1 links messenger RNA stability to apoptosis in yeast</atitle><jtitle>EMBO reports</jtitle><stitle>EMBO Rep</stitle><addtitle>EMBO Rep</addtitle><date>2005-11-01</date><risdate>2005</risdate><volume>6</volume><issue>11</issue><spage>1076</spage><epage>1081</epage><pages>1076-1081</pages><issn>1469-221X</issn><eissn>1469-3178</eissn><eissn>1469-221X</eissn><coden>ERMEAX</coden><abstract>During the past years, yeasts have been successfully established as models to study the mechanisms of apoptotic regulation. We recently showed that mutations in the
LSM4
gene, which is involved in messenger RNA decapping, lead to increased mRNA stability and apoptosis in yeast. Here, we show that mitochondrial function and
YCA1
, which encodes a budding yeast metacaspase, are necessary for apoptosis triggered by stabilization of mRNAs. Deletion of
YCA1
in yeast cells mutated in the
LSM4
gene prevents mitochondrial fragmentation and rapid cell death during chronological ageing of the culture, diminishes reactive oxygen species accumulation and DNA breakage, and increases resistance to H
2
O
2
and acetic acid. mRNA levels in
lsm4
mutants deleted for
YCA1
are still increased, positioning the Yca1 budding yeast caspase as a downstream executor of cell death induced by mRNA perturbations. In addition, we show that mitochondrial function is necessary for fast death during chronological ageing, as well as in
LSM4
mutated and wild‐type cells.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>16170310</pmid><doi>10.1038/sj.embor.7400514</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Wiley Free Content; PubMed Central |
| subjects | Acetic acid Apoptosis Caspases - genetics Caspases - metabolism Cell Survival Deoxyribonucleic acid DNA Gene Silencing Hydrogen peroxide LSM4 mitochondria Mitochondria - metabolism Mortality Mutation Phenotype programmed cell death Reactive Oxygen Species - metabolism RNA Stability RNA, Messenger - metabolism Saccharomyces cerevisiae Saccharomyces cerevisiae - enzymology Saccharomyces cerevisiae Proteins - genetics Saccharomyces cerevisiae Proteins - metabolism Scientific Report Time Factors YCA1 Yeasts |
| title | Yeast caspase 1 links messenger RNA stability to apoptosis in yeast |
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