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Article: Transcriptional regulation of yeast peroxiredoxin gene TSA2 through Hap1p, Rox1p, and Hap2/3/5p

TitleTranscriptional regulation of yeast peroxiredoxin gene TSA2 through Hap1p, Rox1p, and Hap2/3/5p
Authors
KeywordsFree radicals
Hap1p
Hap2/3/5p
Peroxiredoxins
Redox regulation
Rox1p
Tsa2p
Issue Date2003
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/freeradbiomed
Citation
Free Radical Biology and Medicine, 2003, v. 34 n. 5, p. 585-597 How to Cite?
AbstractIn Saccharomyces cerevisiae, the transcription of peroxiredoxin gene TSA2 is responsive to various reactive oxygen and nitrogen species. Redox-regulated transcriptional activators Yap1p, Skn7p, Msn2p/Msn4p have been shown to play a role in regulating TSA2 expression. In this study we show that the transcription of TSA2 is under complex control involving additional transcription factors Hap1p, Rox1p, and Hap2/3/5p. Deletion of HAP1 led to a 50% reduction of TSA2 transcriptional activity. As an intracellular oxygen sensor, heme stimulated TSA2 transcription by activating Hap1p. The induction of TSA2 by H2O2 is also mediated in part through Hap1p. Countering the effects of Hap1p was a transcriptional repressor Rox1p. Deletion of ROX1 or mutation of Rox1p-binding site significantly activated TSA2 transcription. In addition, TSA2 activity was diminished in hap2Δ, hap3Δ, hap4Δ, and hap5Δ strains, but was stimulated upon overexpression of Hap4p. Hap2/3/5p may cooperate with Msn2/4p to activate TSA2 after diauxic shift. Finally, we demonstrated a role for kinases Ras1/2p and Hog1p in Msn2/4p-dependent activation of TSA2. In particular, Hog1p mediated the response of TSA2 to osmotic and oxidative stress. Taken together, our findings suggest that the expression of TSA2 is regulated by a group of transcription factors responsive differentially to stress conditions. © 2003 Elsevier Science Inc.
Persistent Identifierhttp://hdl.handle.net/10722/147479
ISSN
2015 Impact Factor: 5.784
2015 SCImago Journal Rankings: 2.468
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, CMen_HK
dc.contributor.authorChing, YPen_HK
dc.contributor.authorZhou, Yen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorJin, DYen_HK
dc.date.accessioned2012-05-29T06:04:00Z-
dc.date.available2012-05-29T06:04:00Z-
dc.date.issued2003en_HK
dc.identifier.citationFree Radical Biology and Medicine, 2003, v. 34 n. 5, p. 585-597en_HK
dc.identifier.issn0891-5849en_HK
dc.identifier.urihttp://hdl.handle.net/10722/147479-
dc.description.abstractIn Saccharomyces cerevisiae, the transcription of peroxiredoxin gene TSA2 is responsive to various reactive oxygen and nitrogen species. Redox-regulated transcriptional activators Yap1p, Skn7p, Msn2p/Msn4p have been shown to play a role in regulating TSA2 expression. In this study we show that the transcription of TSA2 is under complex control involving additional transcription factors Hap1p, Rox1p, and Hap2/3/5p. Deletion of HAP1 led to a 50% reduction of TSA2 transcriptional activity. As an intracellular oxygen sensor, heme stimulated TSA2 transcription by activating Hap1p. The induction of TSA2 by H2O2 is also mediated in part through Hap1p. Countering the effects of Hap1p was a transcriptional repressor Rox1p. Deletion of ROX1 or mutation of Rox1p-binding site significantly activated TSA2 transcription. In addition, TSA2 activity was diminished in hap2Δ, hap3Δ, hap4Δ, and hap5Δ strains, but was stimulated upon overexpression of Hap4p. Hap2/3/5p may cooperate with Msn2/4p to activate TSA2 after diauxic shift. Finally, we demonstrated a role for kinases Ras1/2p and Hog1p in Msn2/4p-dependent activation of TSA2. In particular, Hog1p mediated the response of TSA2 to osmotic and oxidative stress. Taken together, our findings suggest that the expression of TSA2 is regulated by a group of transcription factors responsive differentially to stress conditions. © 2003 Elsevier Science Inc.en_HK
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/freeradbiomeden_HK
dc.relation.ispartofFree Radical Biology and Medicineen_HK
dc.subjectFree radicalsen_HK
dc.subjectHap1pen_HK
dc.subjectHap2/3/5pen_HK
dc.subjectPeroxiredoxinsen_HK
dc.subjectRedox regulationen_HK
dc.subjectRox1pen_HK
dc.subjectTsa2pen_HK
dc.subject.meshAntioxidants - Metabolismen_US
dc.subject.meshBinding Sitesen_US
dc.subject.meshCcaat-Binding Factor - Genetics - Metabolismen_US
dc.subject.meshDna-Binding Proteins - Genetics - Metabolismen_US
dc.subject.meshFree Radicals - Metabolismen_US
dc.subject.meshFungal Proteins - Genetics - Metabolismen_US
dc.subject.meshGene Expression Regulation, Enzymologicen_US
dc.subject.meshGene Expression Regulation, Fungalen_US
dc.subject.meshLac Operonen_US
dc.subject.meshMutagenesis, Site-Directeden_US
dc.subject.meshMutationen_US
dc.subject.meshOxidative Stressen_US
dc.subject.meshPeroxidases - Genetics - Metabolismen_US
dc.subject.meshPeroxiredoxinsen_US
dc.subject.meshPhospholipases A - Genetics - Metabolismen_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.subject.meshProtein Bindingen_US
dc.subject.meshRepressor Proteins - Genetics - Metabolismen_US
dc.subject.meshSaccharomyces Cerevisiae - Genetics - Growth & Development - Metabolismen_US
dc.subject.meshSaccharomyces Cerevisiae Proteins - Genetics - Metabolismen_US
dc.subject.meshTrans-Activators - Genetics - Metabolismen_US
dc.subject.meshTranscription Factors - Genetics - Metabolismen_US
dc.subject.meshTranscription, Geneticen_US
dc.subject.meshBeta-Galactosidase - Metabolismen_US
dc.titleTranscriptional regulation of yeast peroxiredoxin gene TSA2 through Hap1p, Rox1p, and Hap2/3/5pen_HK
dc.typeArticleen_HK
dc.identifier.emailWong, CM:wispwong@hkucc.hku.hken_HK
dc.identifier.emailChing, YP:ypching@hku.hken_HK
dc.identifier.emailJin, DY:dyjin@hkucc.hku.hken_HK
dc.identifier.authorityWong, CM=rp01489en_HK
dc.identifier.authorityChing, YP=rp00469en_HK
dc.identifier.authorityJin, DY=rp00452en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0891-5849(02)01354-0en_HK
dc.identifier.pmid12614847-
dc.identifier.scopuseid_2-s2.0-0037370205en_HK
dc.identifier.hkuros80469-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037370205&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume34en_HK
dc.identifier.issue5en_HK
dc.identifier.spage585en_HK
dc.identifier.epage597en_HK
dc.identifier.isiWOS:000181355400010-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, CM=18134632400en_HK
dc.identifier.scopusauthoridChing, YP=7005431277en_HK
dc.identifier.scopusauthoridZhou, Y=7405366890en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridJin, DY=7201973614en_HK

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