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A Novel Transcription Factor, ERD15 (Early Responsive to Dehydration 15), Connects Endoplasmic Reticulum Stress with an Osmotic Stress-induced Cell Death Signal

As in all other eukaryotic organisms, endoplasmic reticulum (ER) stress triggers the evolutionarily conserved unfolded protein response in soybean, but it also communicates with other adaptive signaling responses, such as osmotic stress-induced and ER stress-induced programmed cell death. These two...

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Autores principales: Alves, Murilo S., Reis, Pedro A. B., Dadalto, Silvana P., Faria, Jerusa A. Q. A., Fontes, Elizabeth P. B., Fietto, Luciano G.
Formato: Texto
Lenguaje:English
Publicado: American Society for Biochemistry and Molecular Biology 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3103375/
https://www.ncbi.nlm.nih.gov/pubmed/21482825
http://dx.doi.org/10.1074/jbc.M111.233494
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author Alves, Murilo S.
Reis, Pedro A. B.
Dadalto, Silvana P.
Faria, Jerusa A. Q. A.
Fontes, Elizabeth P. B.
Fietto, Luciano G.
author_facet Alves, Murilo S.
Reis, Pedro A. B.
Dadalto, Silvana P.
Faria, Jerusa A. Q. A.
Fontes, Elizabeth P. B.
Fietto, Luciano G.
author_sort Alves, Murilo S.
collection PubMed
description As in all other eukaryotic organisms, endoplasmic reticulum (ER) stress triggers the evolutionarily conserved unfolded protein response in soybean, but it also communicates with other adaptive signaling responses, such as osmotic stress-induced and ER stress-induced programmed cell death. These two signaling pathways converge at the level of gene transcription to activate an integrated cascade that is mediated by N-rich proteins (NRPs). Here, we describe a novel transcription factor, GmERD15 (Glycine max Early Responsive to Dehydration 15), which is induced by ER stress and osmotic stress to activate the expression of NRP genes. GmERD15 was isolated because of its capacity to stably associate with the NRP-B promoter in yeast. It specifically binds to a 187-bp fragment of the NRP-B promoter in vitro and activates the transcription of a reporter gene in yeast. Furthermore, GmERD15 was found in both the cytoplasm and the nucleus, and a ChIP assay revealed that it binds to the NRP-B promoter in vivo. Expression of GmERD15 in soybean protoplasts activated the NRP-B promoter and induced expression of the NRP-B gene. Collectively, these results support the interpretation that GmERD15 functions as an upstream component of stress-induced NRP-B-mediated signaling to connect stress in the ER to an osmotic stress-induced cell death signal.
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spelling pubmed-31033752011-06-07 A Novel Transcription Factor, ERD15 (Early Responsive to Dehydration 15), Connects Endoplasmic Reticulum Stress with an Osmotic Stress-induced Cell Death Signal Alves, Murilo S. Reis, Pedro A. B. Dadalto, Silvana P. Faria, Jerusa A. Q. A. Fontes, Elizabeth P. B. Fietto, Luciano G. J Biol Chem Plant Biology As in all other eukaryotic organisms, endoplasmic reticulum (ER) stress triggers the evolutionarily conserved unfolded protein response in soybean, but it also communicates with other adaptive signaling responses, such as osmotic stress-induced and ER stress-induced programmed cell death. These two signaling pathways converge at the level of gene transcription to activate an integrated cascade that is mediated by N-rich proteins (NRPs). Here, we describe a novel transcription factor, GmERD15 (Glycine max Early Responsive to Dehydration 15), which is induced by ER stress and osmotic stress to activate the expression of NRP genes. GmERD15 was isolated because of its capacity to stably associate with the NRP-B promoter in yeast. It specifically binds to a 187-bp fragment of the NRP-B promoter in vitro and activates the transcription of a reporter gene in yeast. Furthermore, GmERD15 was found in both the cytoplasm and the nucleus, and a ChIP assay revealed that it binds to the NRP-B promoter in vivo. Expression of GmERD15 in soybean protoplasts activated the NRP-B promoter and induced expression of the NRP-B gene. Collectively, these results support the interpretation that GmERD15 functions as an upstream component of stress-induced NRP-B-mediated signaling to connect stress in the ER to an osmotic stress-induced cell death signal. American Society for Biochemistry and Molecular Biology 2011-06-03 2011-04-11 /pmc/articles/PMC3103375/ /pubmed/21482825 http://dx.doi.org/10.1074/jbc.M111.233494 Text en © 2011 by The American Society for Biochemistry and Molecular Biology, Inc. Author's Choice—Final version full access. Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) applies to Author Choice Articles
spellingShingle Plant Biology
Alves, Murilo S.
Reis, Pedro A. B.
Dadalto, Silvana P.
Faria, Jerusa A. Q. A.
Fontes, Elizabeth P. B.
Fietto, Luciano G.
A Novel Transcription Factor, ERD15 (Early Responsive to Dehydration 15), Connects Endoplasmic Reticulum Stress with an Osmotic Stress-induced Cell Death Signal
title A Novel Transcription Factor, ERD15 (Early Responsive to Dehydration 15), Connects Endoplasmic Reticulum Stress with an Osmotic Stress-induced Cell Death Signal
title_full A Novel Transcription Factor, ERD15 (Early Responsive to Dehydration 15), Connects Endoplasmic Reticulum Stress with an Osmotic Stress-induced Cell Death Signal
title_fullStr A Novel Transcription Factor, ERD15 (Early Responsive to Dehydration 15), Connects Endoplasmic Reticulum Stress with an Osmotic Stress-induced Cell Death Signal
title_full_unstemmed A Novel Transcription Factor, ERD15 (Early Responsive to Dehydration 15), Connects Endoplasmic Reticulum Stress with an Osmotic Stress-induced Cell Death Signal
title_short A Novel Transcription Factor, ERD15 (Early Responsive to Dehydration 15), Connects Endoplasmic Reticulum Stress with an Osmotic Stress-induced Cell Death Signal
title_sort novel transcription factor, erd15 (early responsive to dehydration 15), connects endoplasmic reticulum stress with an osmotic stress-induced cell death signal
topic Plant Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3103375/
https://www.ncbi.nlm.nih.gov/pubmed/21482825
http://dx.doi.org/10.1074/jbc.M111.233494
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