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Article: Thiol peroxidases mediate specific genome-wide regulation of gene expression in response to hydrogen peroxide

TitleThiol peroxidases mediate specific genome-wide regulation of gene expression in response to hydrogen peroxide
Authors
Issue Date2011
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
Citation
Proceedings Of The National Academy Of Sciences Of The United States Of America, 2011, v. 108 n. 7, p. 2729-2734 How to Cite?
AbstractHydrogen peroxide is thought to regulate cellular processes by direct oxidation of numerous cellular proteins, whereas antioxidants, most notably thiol peroxidases, are thought to reduce peroxides and inhibit H 2O 2 response. However, thiol peroxidases have also been implicated in activation of transcription factors and signaling. It remains unclear if these enzymes stimulate or inhibit redox regulation and whether this regulation is widespread or limited to a few cellular components. Herein, we found that Saccharomyces cerevisiae cells lacking all eight thiol peroxidases were viable and withstood redox stresses. They transcriptionally responded to various redox treatments, but were unable to activate and repress gene expression in response to H 2O 2. Further studies involving redox transcription factors suggested that thiol peroxidases are major regulators of global gene expression in response to H 2O 2. The data suggest that thiol peroxidases sense and transfer oxidative signals to the signaling proteins and regulate transcription, whereas a direct interaction between H 2O 2 and other cellular proteins plays a secondary role.
Persistent Identifierhttp://hdl.handle.net/10722/147629
ISSN
2023 Impact Factor: 9.4
2023 SCImago Journal Rankings: 3.737
ISI Accession Number ID
Funding AgencyGrant Number
National Institutes of Health (NIH)GM065204
GM083292
Funding Information:

We thank S. V. Avery (University of Nottingham, Nottingham, United Kingdom) and G. F. Merrill (Oregon State University, Corvallis, OR) for providing yeast strains, A. Bird for help with microarrays, and the University of Utah Microarray Core Facility for excellent technical assistance. This work was supported by National Institutes of Health (NIH) Grant GM065204 (to V.N.G.). J.C.R. was supported by NIH Grant GM083292 (to D.R.W.).

References

 

DC FieldValueLanguage
dc.contributor.authorFomenko, DEen_US
dc.contributor.authorKoc, Aen_US
dc.contributor.authorAgisheva, Nen_US
dc.contributor.authorJacobsen, Men_US
dc.contributor.authorKaya, Aen_US
dc.contributor.authorMalinouski, Men_US
dc.contributor.authorRutherford, JCen_US
dc.contributor.authorSiu, KLen_US
dc.contributor.authorJin, DYen_US
dc.contributor.authorWinge, DRen_US
dc.contributor.authorGladyshev, VNen_US
dc.date.accessioned2012-05-29T06:05:05Z-
dc.date.available2012-05-29T06:05:05Z-
dc.date.issued2011en_US
dc.identifier.citationProceedings Of The National Academy Of Sciences Of The United States Of America, 2011, v. 108 n. 7, p. 2729-2734en_US
dc.identifier.issn0027-8424en_US
dc.identifier.urihttp://hdl.handle.net/10722/147629-
dc.description.abstractHydrogen peroxide is thought to regulate cellular processes by direct oxidation of numerous cellular proteins, whereas antioxidants, most notably thiol peroxidases, are thought to reduce peroxides and inhibit H 2O 2 response. However, thiol peroxidases have also been implicated in activation of transcription factors and signaling. It remains unclear if these enzymes stimulate or inhibit redox regulation and whether this regulation is widespread or limited to a few cellular components. Herein, we found that Saccharomyces cerevisiae cells lacking all eight thiol peroxidases were viable and withstood redox stresses. They transcriptionally responded to various redox treatments, but were unable to activate and repress gene expression in response to H 2O 2. Further studies involving redox transcription factors suggested that thiol peroxidases are major regulators of global gene expression in response to H 2O 2. The data suggest that thiol peroxidases sense and transfer oxidative signals to the signaling proteins and regulate transcription, whereas a direct interaction between H 2O 2 and other cellular proteins plays a secondary role.en_US
dc.languageengen_US
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.orgen_US
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of Americaen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshGene Expression Regulation - Drug Effectsen_US
dc.subject.meshHydrogen Peroxide - Toxicityen_US
dc.subject.meshModels, Biologicalen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshMutagenesisen_US
dc.subject.meshOligonucleotide Array Sequence Analysisen_US
dc.subject.meshOxidative Stress - Geneticsen_US
dc.subject.meshPeroxidases - Deficiency - Metabolismen_US
dc.subject.meshPhenotypeen_US
dc.subject.meshRibosomal Proteins - Metabolismen_US
dc.subject.meshSaccharomyces Cerevisiae - Drug Effects - Enzymology - Geneticsen_US
dc.subject.meshSaccharomyces Cerevisiae Proteins - Metabolismen_US
dc.subject.meshSequence Analysis, Dnaen_US
dc.subject.meshSignal Transduction - Drug Effects - Physiologyen_US
dc.titleThiol peroxidases mediate specific genome-wide regulation of gene expression in response to hydrogen peroxideen_US
dc.typeArticleen_US
dc.identifier.emailJin, DY:dyjin@hkucc.hku.hken_US
dc.identifier.authorityJin, DY=rp00452en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1073/pnas.1010721108en_US
dc.identifier.pmid21282621-
dc.identifier.scopuseid_2-s2.0-79952582563en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79952582563&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume108en_US
dc.identifier.issue7en_US
dc.identifier.spage2729en_US
dc.identifier.epage2734en_US
dc.identifier.isiWOS:000287377000024-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridFomenko, DE=6602197028en_US
dc.identifier.scopusauthoridKoc, A=7006124626en_US
dc.identifier.scopusauthoridAgisheva, N=36672465400en_US
dc.identifier.scopusauthoridJacobsen, M=42761582100en_US
dc.identifier.scopusauthoridKaya, A=26424286000en_US
dc.identifier.scopusauthoridMalinouski, M=22835482500en_US
dc.identifier.scopusauthoridRutherford, JC=7101706816en_US
dc.identifier.scopusauthoridSiu, KL=35327996300en_US
dc.identifier.scopusauthoridJin, DY=7201973614en_US
dc.identifier.scopusauthoridWinge, DR=7006036381en_US
dc.identifier.scopusauthoridGladyshev, VN=35236886300en_US
dc.identifier.issnl0027-8424-

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