Overexpression of the yap1, PDE2, and STB3 genes enhances the tolerance of yeast to oxidative stress induced by 7-chlorotetrazolo[5,1-c]benzo[1,2,4]triazine
Abstract 7-chlorotetrazolo[5,1-c]benzo[1,2,4]triazine (CTBT) is an antifungal agent that induces oxidative stress and enhances the activity of other antifungals with different modes of action. A genome-wide screening of Saccharomyces cerevisiae genomic library in the high-copy-number plasmid reveale...
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creator | Drobna, Eva Gazdag, Zoltan Culakova, Hana Dzugasova, Vladimira Gbelska, Yvetta Pesti, Miklos Subik, Julius |
description | Abstract
7-chlorotetrazolo[5,1-c]benzo[1,2,4]triazine (CTBT) is an antifungal agent that induces oxidative stress and enhances the activity of other antifungals with different modes of action. A genome-wide screening of Saccharomyces cerevisiae genomic library in the high-copy-number plasmid revealed three genes, yap1, PDE2, and STB3, which increased the CTBT tolerance of the parental strain. The yap1 gene is known to activate many genes in response to oxidants. The PDE2 and STB3 genes encode the high-affinity cAMP phosphodiesterase and the transcription factor recognizing the ribosomal RNA processing element in promoter sequences, respectively. The protective effects of their overexpression against CTBT toxicity was observed in the absence of certain proteins involved in stress responses, cell wall integrity signaling, and chromatin remodeling. The enhanced CTBT tolerance of the yap1, PDE2. and STB3 transformants was a consequence of their high antioxidant enzyme activities at the beginning of CTBT treatment in comparison with that of the parental strain, for that they inactivated the CTBT-induced reactive oxygen species. These results point to the complex interplay among the oxidant sensing, cAMP-protein kinase A signaling, and transcription reprogramming of yeast cells, leading to their better adaptation to the stress imposed by CTBT. |
doi_str_mv | 10.1111/j.1567-1364.2012.00845.x |
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7-chlorotetrazolo[5,1-c]benzo[1,2,4]triazine (CTBT) is an antifungal agent that induces oxidative stress and enhances the activity of other antifungals with different modes of action. A genome-wide screening of Saccharomyces cerevisiae genomic library in the high-copy-number plasmid revealed three genes, yap1, PDE2, and STB3, which increased the CTBT tolerance of the parental strain. The yap1 gene is known to activate many genes in response to oxidants. The PDE2 and STB3 genes encode the high-affinity cAMP phosphodiesterase and the transcription factor recognizing the ribosomal RNA processing element in promoter sequences, respectively. The protective effects of their overexpression against CTBT toxicity was observed in the absence of certain proteins involved in stress responses, cell wall integrity signaling, and chromatin remodeling. The enhanced CTBT tolerance of the yap1, PDE2. and STB3 transformants was a consequence of their high antioxidant enzyme activities at the beginning of CTBT treatment in comparison with that of the parental strain, for that they inactivated the CTBT-induced reactive oxygen species. These results point to the complex interplay among the oxidant sensing, cAMP-protein kinase A signaling, and transcription reprogramming of yeast cells, leading to their better adaptation to the stress imposed by CTBT.</description><identifier>ISSN: 1567-1356</identifier><identifier>EISSN: 1567-1364</identifier><identifier>DOI: 10.1111/j.1567-1364.2012.00845.x</identifier><identifier>PMID: 22909133</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Antifungal Agents - pharmacology ; Antioxidants ; Cell walls ; Cellular Reprogramming ; Cellular stress response ; Chromatin remodeling ; Cyclic AMP ; deletion mutants ; DNA, Fungal - genetics ; Drug Tolerance ; Enzymatic activity ; Gene Expression Regulation, Fungal - drug effects ; Genomes ; Kinases ; Oligonucleotide Array Sequence Analysis ; overexpressed genes ; Oxidants ; Oxidative stress ; Oxidative Stress - drug effects ; Phosphodiesterase ; Protein kinase A ; Reactive Oxygen Species ; resistance ; RNA processing ; rRNA ; Saccharomyces cerevisiae ; Saccharomyces cerevisiae - drug effects ; Saccharomyces cerevisiae - genetics ; Saccharomyces cerevisiae - metabolism ; Saccharomyces cerevisiae Proteins - genetics ; Saccharomyces cerevisiae Proteins - metabolism ; Sequence Analysis, DNA ; Signal Transduction ; superoxide ; susceptibility ; Toxicity ; Trans-Activators - genetics ; Trans-Activators - metabolism ; transcription ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Triazine ; Triazines - pharmacology</subject><ispartof>FEMS yeast research, 2012-12, Vol.12 (8), p.958-968</ispartof><rights>Copyright © 2012 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved 2012</rights><rights>2012 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved</rights><rights>2012 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved.</rights><rights>Copyright © 2012 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4405-9bb95b81ab88e77c9bff58d6b1a1a8af8d22528393f39208368cbf12b845f2523</citedby><cites>FETCH-LOGICAL-c4405-9bb95b81ab88e77c9bff58d6b1a1a8af8d22528393f39208368cbf12b845f2523</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1567-1364.2012.00845.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1567-1364.2012.00845.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22909133$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Drobna, Eva</creatorcontrib><creatorcontrib>Gazdag, Zoltan</creatorcontrib><creatorcontrib>Culakova, Hana</creatorcontrib><creatorcontrib>Dzugasova, Vladimira</creatorcontrib><creatorcontrib>Gbelska, Yvetta</creatorcontrib><creatorcontrib>Pesti, Miklos</creatorcontrib><creatorcontrib>Subik, Julius</creatorcontrib><title>Overexpression of the yap1, PDE2, and STB3 genes enhances the tolerance of yeast to oxidative stress induced by 7-chlorotetrazolo[5,1-c]benzo[1,2,4]triazine</title><title>FEMS yeast research</title><addtitle>FEMS Yeast Res</addtitle><description>Abstract
7-chlorotetrazolo[5,1-c]benzo[1,2,4]triazine (CTBT) is an antifungal agent that induces oxidative stress and enhances the activity of other antifungals with different modes of action. A genome-wide screening of Saccharomyces cerevisiae genomic library in the high-copy-number plasmid revealed three genes, yap1, PDE2, and STB3, which increased the CTBT tolerance of the parental strain. The yap1 gene is known to activate many genes in response to oxidants. The PDE2 and STB3 genes encode the high-affinity cAMP phosphodiesterase and the transcription factor recognizing the ribosomal RNA processing element in promoter sequences, respectively. The protective effects of their overexpression against CTBT toxicity was observed in the absence of certain proteins involved in stress responses, cell wall integrity signaling, and chromatin remodeling. The enhanced CTBT tolerance of the yap1, PDE2. and STB3 transformants was a consequence of their high antioxidant enzyme activities at the beginning of CTBT treatment in comparison with that of the parental strain, for that they inactivated the CTBT-induced reactive oxygen species. These results point to the complex interplay among the oxidant sensing, cAMP-protein kinase A signaling, and transcription reprogramming of yeast cells, leading to their better adaptation to the stress imposed by CTBT.</description><subject>Antifungal Agents - pharmacology</subject><subject>Antioxidants</subject><subject>Cell walls</subject><subject>Cellular Reprogramming</subject><subject>Cellular stress response</subject><subject>Chromatin remodeling</subject><subject>Cyclic AMP</subject><subject>deletion mutants</subject><subject>DNA, Fungal - genetics</subject><subject>Drug Tolerance</subject><subject>Enzymatic activity</subject><subject>Gene Expression Regulation, Fungal - drug effects</subject><subject>Genomes</subject><subject>Kinases</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>overexpressed genes</subject><subject>Oxidants</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Phosphodiesterase</subject><subject>Protein kinase A</subject><subject>Reactive Oxygen Species</subject><subject>resistance</subject><subject>RNA processing</subject><subject>rRNA</subject><subject>Saccharomyces cerevisiae</subject><subject>Saccharomyces cerevisiae - drug effects</subject><subject>Saccharomyces cerevisiae - genetics</subject><subject>Saccharomyces cerevisiae - metabolism</subject><subject>Saccharomyces cerevisiae Proteins - genetics</subject><subject>Saccharomyces cerevisiae Proteins - metabolism</subject><subject>Sequence Analysis, DNA</subject><subject>Signal Transduction</subject><subject>superoxide</subject><subject>susceptibility</subject><subject>Toxicity</subject><subject>Trans-Activators - genetics</subject><subject>Trans-Activators - metabolism</subject><subject>transcription</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Triazine</subject><subject>Triazines - pharmacology</subject><issn>1567-1356</issn><issn>1567-1364</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</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>eNqNUctu1DAUtRCIPuAXkCW2SfAjD0diA6UFpEqtoCxQVVl2csNklNrBdtrJfAsfi8O0s0FIeON7fc851zoHIUxJRuN5s85oUVYp5WWeMUJZRojIi2zzBB3uB0_3dVEeoCPv14TQKgKfowPGalJTzg_Rr4s7cLAZHXjfW4Nth8MK8KxGmuDLD6cswcq0-OvVe45_gAGPwayUaWKx4IIdwC3tQpxB-RCfsN30rQr9HWAfFmHcm3ZqoMV6xlXarAbrbIDg1NYO9rpIaNrcaDBbe00TluQ3wfVq2xt4gZ51avDw8uE-Rt_OTq9OPqXnFx8_n7w7T5s8J0Vaa10XWlClhYCqamrddYVoS00VVUJ1omWsYILXvOM1I4KXotEdZTp61sUJP0avd7qjsz8n8EGu7eRMXCkZ53mVF9GwiBI7VOOs9w46Obr-VrlZUiKXWORaLo7LxX25xCL_xCI3kfrqYcGkb6HdEx9ziIC3O8B9P8D838Ly7PuXWEQ639HtNP6DnP79q986vqow</recordid><startdate>20121201</startdate><enddate>20121201</enddate><creator>Drobna, Eva</creator><creator>Gazdag, Zoltan</creator><creator>Culakova, Hana</creator><creator>Dzugasova, Vladimira</creator><creator>Gbelska, Yvetta</creator><creator>Pesti, Miklos</creator><creator>Subik, Julius</creator><general>Blackwell Publishing Ltd</general><general>Oxford 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>3V.</scope><scope>7X7</scope><scope>7XB</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></search><sort><creationdate>20121201</creationdate><title>Overexpression of the yap1, PDE2, and STB3 genes enhances the tolerance of yeast to oxidative stress induced by 7-chlorotetrazolo[5,1-c]benzo[1,2,4]triazine</title><author>Drobna, Eva ; Gazdag, Zoltan ; Culakova, Hana ; Dzugasova, Vladimira ; Gbelska, Yvetta ; Pesti, Miklos ; Subik, Julius</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4405-9bb95b81ab88e77c9bff58d6b1a1a8af8d22528393f39208368cbf12b845f2523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Antifungal Agents - pharmacology</topic><topic>Antioxidants</topic><topic>Cell walls</topic><topic>Cellular Reprogramming</topic><topic>Cellular stress response</topic><topic>Chromatin remodeling</topic><topic>Cyclic AMP</topic><topic>deletion mutants</topic><topic>DNA, Fungal - genetics</topic><topic>Drug Tolerance</topic><topic>Enzymatic activity</topic><topic>Gene Expression Regulation, Fungal - drug effects</topic><topic>Genomes</topic><topic>Kinases</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>overexpressed genes</topic><topic>Oxidants</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Phosphodiesterase</topic><topic>Protein kinase A</topic><topic>Reactive Oxygen Species</topic><topic>resistance</topic><topic>RNA processing</topic><topic>rRNA</topic><topic>Saccharomyces cerevisiae</topic><topic>Saccharomyces cerevisiae - drug effects</topic><topic>Saccharomyces cerevisiae - genetics</topic><topic>Saccharomyces cerevisiae - metabolism</topic><topic>Saccharomyces cerevisiae Proteins - genetics</topic><topic>Saccharomyces cerevisiae Proteins - metabolism</topic><topic>Sequence Analysis, DNA</topic><topic>Signal Transduction</topic><topic>superoxide</topic><topic>susceptibility</topic><topic>Toxicity</topic><topic>Trans-Activators - genetics</topic><topic>Trans-Activators - metabolism</topic><topic>transcription</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Triazine</topic><topic>Triazines - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Drobna, Eva</creatorcontrib><creatorcontrib>Gazdag, Zoltan</creatorcontrib><creatorcontrib>Culakova, Hana</creatorcontrib><creatorcontrib>Dzugasova, Vladimira</creatorcontrib><creatorcontrib>Gbelska, Yvetta</creatorcontrib><creatorcontrib>Pesti, Miklos</creatorcontrib><creatorcontrib>Subik, Julius</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>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><jtitle>FEMS yeast research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Drobna, Eva</au><au>Gazdag, Zoltan</au><au>Culakova, Hana</au><au>Dzugasova, Vladimira</au><au>Gbelska, Yvetta</au><au>Pesti, Miklos</au><au>Subik, Julius</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of the yap1, PDE2, and STB3 genes enhances the tolerance of yeast to oxidative stress induced by 7-chlorotetrazolo[5,1-c]benzo[1,2,4]triazine</atitle><jtitle>FEMS yeast research</jtitle><addtitle>FEMS Yeast Res</addtitle><date>2012-12-01</date><risdate>2012</risdate><volume>12</volume><issue>8</issue><spage>958</spage><epage>968</epage><pages>958-968</pages><issn>1567-1356</issn><eissn>1567-1364</eissn><abstract>Abstract
7-chlorotetrazolo[5,1-c]benzo[1,2,4]triazine (CTBT) is an antifungal agent that induces oxidative stress and enhances the activity of other antifungals with different modes of action. A genome-wide screening of Saccharomyces cerevisiae genomic library in the high-copy-number plasmid revealed three genes, yap1, PDE2, and STB3, which increased the CTBT tolerance of the parental strain. The yap1 gene is known to activate many genes in response to oxidants. The PDE2 and STB3 genes encode the high-affinity cAMP phosphodiesterase and the transcription factor recognizing the ribosomal RNA processing element in promoter sequences, respectively. The protective effects of their overexpression against CTBT toxicity was observed in the absence of certain proteins involved in stress responses, cell wall integrity signaling, and chromatin remodeling. The enhanced CTBT tolerance of the yap1, PDE2. and STB3 transformants was a consequence of their high antioxidant enzyme activities at the beginning of CTBT treatment in comparison with that of the parental strain, for that they inactivated the CTBT-induced reactive oxygen species. These results point to the complex interplay among the oxidant sensing, cAMP-protein kinase A signaling, and transcription reprogramming of yeast cells, leading to their better adaptation to the stress imposed by CTBT.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>22909133</pmid><doi>10.1111/j.1567-1364.2012.00845.x</doi><tpages>11</tpages></addata></record> |
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subjects | Antifungal Agents - pharmacology Antioxidants Cell walls Cellular Reprogramming Cellular stress response Chromatin remodeling Cyclic AMP deletion mutants DNA, Fungal - genetics Drug Tolerance Enzymatic activity Gene Expression Regulation, Fungal - drug effects Genomes Kinases Oligonucleotide Array Sequence Analysis overexpressed genes Oxidants Oxidative stress Oxidative Stress - drug effects Phosphodiesterase Protein kinase A Reactive Oxygen Species resistance RNA processing rRNA Saccharomyces cerevisiae Saccharomyces cerevisiae - drug effects Saccharomyces cerevisiae - genetics Saccharomyces cerevisiae - metabolism Saccharomyces cerevisiae Proteins - genetics Saccharomyces cerevisiae Proteins - metabolism Sequence Analysis, DNA Signal Transduction superoxide susceptibility Toxicity Trans-Activators - genetics Trans-Activators - metabolism transcription Transcription Factors - genetics Transcription Factors - metabolism Triazine Triazines - pharmacology |
title | Overexpression of the yap1, PDE2, and STB3 genes enhances the tolerance of yeast to oxidative stress induced by 7-chlorotetrazolo[5,1-c]benzo[1,2,4]triazine |
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