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IRE1- and HAC1 -independent transcriptional regulation in the unfolded protein response of yeast

dc.contributor.authorSchröder, Martinen_US
dc.contributor.authorClark, Roberten_US
dc.contributor.authorKaufman, Randal J.en_US
dc.date.accessioned2010-06-01T19:39:27Z
dc.date.available2010-06-01T19:39:27Z
dc.date.issued2003-08en_US
dc.identifier.citationSchrÖder, Martin; Clark, Robert; Kaufman, Randal J. (2003). " IRE1- and HAC1 -independent transcriptional regulation in the unfolded protein response of yeast." Molecular Microbiology 49(3): 591-606. <http://hdl.handle.net/2027.42/72792>en_US
dc.identifier.issn0950-382Xen_US
dc.identifier.issn1365-2958en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/72792
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=12864846&dopt=citationen_US
dc.description.abstractThe unfolded protein response (UPR) is a signalling pathway leading to transcriptional activation of genes that protect cells from accumulation of unfolded proteins in the lumen of the endoplasmic reticulum (ER). In yeast, the only known ER stress signalling pathway originates at the type I transmembrane protein kinase/endoribonuclease Ire1p. Ire1p regulates synthesis of the basic leucine-zipper (bZIP)-containing transcription factor Hac1p by controlling splicing of HAC1 mRNA. Only spliced HAC1 mRNA (HAC1 i ) is translated, and Hac1 i p activates transcription of genes that contain a conserved UPR element (UPRE) in their promoters. Here, we demonstrate that in addition to this well-understood ER stress signalling pathway, a second, IRE1, HAC1 and UPRE-independent mechanism for transcriptional activation upon ER stress, exists in yeast. A genetic screen identified recessive SIN4 alleles as suppressors of a defective UPR in ire1δ strains. Elevation of basal transcription in sin4 strains or by tethering the RNA polymerase II holoenzyme with LexAp-holoenzyme component fusion proteins to a promoter allowed for activation of the promoter by ER stress in an IRE1, HAC1 and UPRE-independent manner. We propose that this novel second ER-to-nucleus signal transduction pathway culminates in core promoter activation (CPA) through stimulation of RNA polymerase II holoenzyme activity. Core promoter activation was observed upon diverse cellular stresses, suggesting it represents a primordial stress-induced gene activation mechanism.en_US
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dc.format.extent3109 bytes
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dc.publisherBlackwell Science Ltden_US
dc.rights2003 Blackwell Publishing Ltden_US
dc.titleIRE1- and HAC1 -independent transcriptional regulation in the unfolded protein response of yeasten_US
dc.typeArticleen_US
dc.subject.hlbsecondlevelMicrobiology and Immunologyen_US
dc.subject.hlbtoplevelScienceen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Biological Chemistry, University of Michigan Medical Center, Ann Arbor, MI, USA.en_US
dc.contributor.affiliationotherHoward Hughes Medical Institute anden_US
dc.identifier.pmid12864846en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/72792/1/j.1365-2958.2003.03585.x.pdf
dc.identifier.doi10.1046/j.1365-2958.2003.03585.xen_US
dc.identifier.sourceMolecular Microbiologyen_US
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dc.owningcollnameInterdisciplinary and Peer-Reviewed


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