dc.creatorReis, Pedro A.B.
dc.creatorFontes, Elizabeth P.B.
dc.date2018-04-26T18:15:48Z
dc.date2018-04-26T18:15:48Z
dc.date2012-06-01
dc.date.accessioned2023-09-27T21:07:34Z
dc.date.available2023-09-27T21:07:34Z
dc.identifier15592324
dc.identifierhttp://dx.doi.org/10.4161/psb.20111
dc.identifierhttp://www.locus.ufv.br/handle/123456789/19185
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8955059
dc.descriptionUpon disruption of ER homeostasis, plant cells activate at least two branches of the unfolded protein response (UPR) through IRE1-like and ATAF6-like transducers, resulting in the upregulation of ER-resident molecular chaperones and the activation of the ER-associated degradation protein system. Here, we discuss a new ER stress response pathway in plants that is associated with an osmotic stress response in transducing a cell death signal. Both ER and osmotic stress induce the expression of the novel transcription factor GmERD15, which binds and activates N-rich protein (NRP) promoters to induce NRP expression and cause the upregulation of GmNAC6, an effector of the cell death response. In contrast to this activation mechanism, the ER-resident molecular chaperone binding protein (BiP) attenuates the propagation of the cell death signal by modulating the expression and activity of components of the ER and osmotic stress-induced NRP-mediated cell death signaling. This interaction attenuates dehydration-induced cell death and promotes a better adaptation of BiP-overexpressing transgenic lines to drought.
dc.formatpdf
dc.formatapplication/pdf
dc.languageeng
dc.publisherPlant Signaling & Behavior
dc.relationv. 7, n. 6, p. 628-632, Junho 2012
dc.rightsLandes Bioscience
dc.subjectEndoplasmic reticulum stress
dc.subjectOsmotic stress
dc.subjectCell death response
dc.subjectN-rich proteins
dc.subjectGmNAC6
dc.subjectERD15
dc.subjectNRP-A
dc.subjectNRP-B
dc.titleN-rich protein (NRP)-mediated cell death signaling: a new branch of the ER stress response with implications for plant biotechnology
dc.typeArtigo


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