The binding protein BiP attenuates stress-induced cell death in soybean via modulation of the N-Rich protein-mediated signaling pathway
Autor(a) principal: | |
---|---|
Data de Publicação: | 2011 |
Outros Autores: | , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | LOCUS Repositório Institucional da UFV |
Texto Completo: | https://doi.org/10.1104/pp.111.179697 http://www.locus.ufv.br/handle/123456789/12573 |
Resumo: | The molecular chaperone binding protein (BiP) participates in the constitutive function of the endoplasmic reticulum (ER) and protects the cell against stresses. In this study, we investigated the underlying mechanism by which BiP protects plant cells from stress-induced cell death. We found that enhanced expression of BiP in soybean (Glycine max) attenuated ER stress- and osmotic stress-mediated cell death. Ectopic expression of BiP in transgenic lines attenuated the leaf necrotic lesions that are caused by the ER stress inducer tunicamycin and also maintained shoot turgidity upon polyethylene glycol-induced dehydration. BiP-mediated attenuation of stress-induced cell death was confirmed by the decreased percentage of dead cell, the reduced induction of the senescence-associated marker gene GmCystP, and reduced DNA fragmentation in BiP-overexpressing lines. These phenotypes were accompanied by a delay in the induction of the cell death marker genes N-RICH PROTEIN-A (NRP-A), NRP-B, and GmNAC6, which are involved in transducing a cell death signal generated by ER stress and osmotic stress through the NRP-mediated signaling pathway. The prosurvival effect of BiP was associated with modulation of the ER stress- and osmotic stress-induced NRP-mediated cell death signaling, as determined in transgenic tobacco (Nicotiana tabacum) lines with enhanced (sense) and suppressed (antisense) BiP levels. Enhanced expression of BiP prevented NRP- and NAC6-mediated chlorosis and the appearance of senescence-associated markers, whereas silencing of endogenous BiP accelerated the onset of leaf senescence mediated by NRPs and GmNAC6. Collectively, these results implicate BiP as a negative regulator of the stress-induced NRP-mediated cell death response. |
id |
UFV_36dc9c7982a1bcb893ad0330dbb4e431 |
---|---|
oai_identifier_str |
oai:locus.ufv.br:123456789/12573 |
network_acronym_str |
UFV |
network_name_str |
LOCUS Repositório Institucional da UFV |
repository_id_str |
2145 |
spelling |
Reis, Pedro A.A.Rosado, Gustavo L.Silva, Lucas A.C.Oliveira, Luciana C.Oliveira, Lucas B.Costa, Maximiller D.L.Alvim, Fátima C.Fontes, Elizabeth P.B.2017-10-31T10:01:18Z2017-10-31T10:01:18Z2011-121677-9452https://doi.org/10.1104/pp.111.179697http://www.locus.ufv.br/handle/123456789/12573The molecular chaperone binding protein (BiP) participates in the constitutive function of the endoplasmic reticulum (ER) and protects the cell against stresses. In this study, we investigated the underlying mechanism by which BiP protects plant cells from stress-induced cell death. We found that enhanced expression of BiP in soybean (Glycine max) attenuated ER stress- and osmotic stress-mediated cell death. Ectopic expression of BiP in transgenic lines attenuated the leaf necrotic lesions that are caused by the ER stress inducer tunicamycin and also maintained shoot turgidity upon polyethylene glycol-induced dehydration. BiP-mediated attenuation of stress-induced cell death was confirmed by the decreased percentage of dead cell, the reduced induction of the senescence-associated marker gene GmCystP, and reduced DNA fragmentation in BiP-overexpressing lines. These phenotypes were accompanied by a delay in the induction of the cell death marker genes N-RICH PROTEIN-A (NRP-A), NRP-B, and GmNAC6, which are involved in transducing a cell death signal generated by ER stress and osmotic stress through the NRP-mediated signaling pathway. The prosurvival effect of BiP was associated with modulation of the ER stress- and osmotic stress-induced NRP-mediated cell death signaling, as determined in transgenic tobacco (Nicotiana tabacum) lines with enhanced (sense) and suppressed (antisense) BiP levels. Enhanced expression of BiP prevented NRP- and NAC6-mediated chlorosis and the appearance of senescence-associated markers, whereas silencing of endogenous BiP accelerated the onset of leaf senescence mediated by NRPs and GmNAC6. Collectively, these results implicate BiP as a negative regulator of the stress-induced NRP-mediated cell death response.engPlant PhysiologyVol. 157, p. 1853–1865, Dec. 2011Protein BiPSoybean viaN-RichThe binding protein BiP attenuates stress-induced cell death in soybean via modulation of the N-Rich protein-mediated signaling pathwayinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfinfo:eu-repo/semantics/openAccessreponame:LOCUS Repositório Institucional da UFVinstname:Universidade Federal de Viçosa (UFV)instacron:UFVORIGINAL1853.full.pdf1853.full.pdftexto completoapplication/pdf1406130https://locus.ufv.br//bitstream/123456789/12573/1/1853.full.pdf94705f53167285d0acef467c14505816MD51LICENSElicense.txtlicense.txttext/plain; charset=utf-81748https://locus.ufv.br//bitstream/123456789/12573/2/license.txt8a4605be74aa9ea9d79846c1fba20a33MD52THUMBNAIL1853.full.pdf.jpg1853.full.pdf.jpgIM Thumbnailimage/jpeg5341https://locus.ufv.br//bitstream/123456789/12573/3/1853.full.pdf.jpgc3db615eebe74f43f454adfb6216da81MD53123456789/125732017-10-31 22:00:39.563oai:locus.ufv.br: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Repositório InstitucionalPUBhttps://www.locus.ufv.br/oai/requestfabiojreis@ufv.bropendoar:21452017-11-01T01:00:39LOCUS Repositório Institucional da UFV - Universidade Federal de Viçosa (UFV)false |
dc.title.en.fl_str_mv |
The binding protein BiP attenuates stress-induced cell death in soybean via modulation of the N-Rich protein-mediated signaling pathway |
title |
The binding protein BiP attenuates stress-induced cell death in soybean via modulation of the N-Rich protein-mediated signaling pathway |
spellingShingle |
The binding protein BiP attenuates stress-induced cell death in soybean via modulation of the N-Rich protein-mediated signaling pathway Reis, Pedro A.A. Protein BiP Soybean via N-Rich |
title_short |
The binding protein BiP attenuates stress-induced cell death in soybean via modulation of the N-Rich protein-mediated signaling pathway |
title_full |
The binding protein BiP attenuates stress-induced cell death in soybean via modulation of the N-Rich protein-mediated signaling pathway |
title_fullStr |
The binding protein BiP attenuates stress-induced cell death in soybean via modulation of the N-Rich protein-mediated signaling pathway |
title_full_unstemmed |
The binding protein BiP attenuates stress-induced cell death in soybean via modulation of the N-Rich protein-mediated signaling pathway |
title_sort |
The binding protein BiP attenuates stress-induced cell death in soybean via modulation of the N-Rich protein-mediated signaling pathway |
author |
Reis, Pedro A.A. |
author_facet |
Reis, Pedro A.A. Rosado, Gustavo L. Silva, Lucas A.C. Oliveira, Luciana C. Oliveira, Lucas B. Costa, Maximiller D.L. Alvim, Fátima C. Fontes, Elizabeth P.B. |
author_role |
author |
author2 |
Rosado, Gustavo L. Silva, Lucas A.C. Oliveira, Luciana C. Oliveira, Lucas B. Costa, Maximiller D.L. Alvim, Fátima C. Fontes, Elizabeth P.B. |
author2_role |
author author author author author author author |
dc.contributor.author.fl_str_mv |
Reis, Pedro A.A. Rosado, Gustavo L. Silva, Lucas A.C. Oliveira, Luciana C. Oliveira, Lucas B. Costa, Maximiller D.L. Alvim, Fátima C. Fontes, Elizabeth P.B. |
dc.subject.pt-BR.fl_str_mv |
Protein BiP Soybean via N-Rich |
topic |
Protein BiP Soybean via N-Rich |
description |
The molecular chaperone binding protein (BiP) participates in the constitutive function of the endoplasmic reticulum (ER) and protects the cell against stresses. In this study, we investigated the underlying mechanism by which BiP protects plant cells from stress-induced cell death. We found that enhanced expression of BiP in soybean (Glycine max) attenuated ER stress- and osmotic stress-mediated cell death. Ectopic expression of BiP in transgenic lines attenuated the leaf necrotic lesions that are caused by the ER stress inducer tunicamycin and also maintained shoot turgidity upon polyethylene glycol-induced dehydration. BiP-mediated attenuation of stress-induced cell death was confirmed by the decreased percentage of dead cell, the reduced induction of the senescence-associated marker gene GmCystP, and reduced DNA fragmentation in BiP-overexpressing lines. These phenotypes were accompanied by a delay in the induction of the cell death marker genes N-RICH PROTEIN-A (NRP-A), NRP-B, and GmNAC6, which are involved in transducing a cell death signal generated by ER stress and osmotic stress through the NRP-mediated signaling pathway. The prosurvival effect of BiP was associated with modulation of the ER stress- and osmotic stress-induced NRP-mediated cell death signaling, as determined in transgenic tobacco (Nicotiana tabacum) lines with enhanced (sense) and suppressed (antisense) BiP levels. Enhanced expression of BiP prevented NRP- and NAC6-mediated chlorosis and the appearance of senescence-associated markers, whereas silencing of endogenous BiP accelerated the onset of leaf senescence mediated by NRPs and GmNAC6. Collectively, these results implicate BiP as a negative regulator of the stress-induced NRP-mediated cell death response. |
publishDate |
2011 |
dc.date.issued.fl_str_mv |
2011-12 |
dc.date.accessioned.fl_str_mv |
2017-10-31T10:01:18Z |
dc.date.available.fl_str_mv |
2017-10-31T10:01:18Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
https://doi.org/10.1104/pp.111.179697 http://www.locus.ufv.br/handle/123456789/12573 |
dc.identifier.issn.none.fl_str_mv |
1677-9452 |
identifier_str_mv |
1677-9452 |
url |
https://doi.org/10.1104/pp.111.179697 http://www.locus.ufv.br/handle/123456789/12573 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartofseries.pt-BR.fl_str_mv |
Vol. 157, p. 1853–1865, Dec. 2011 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Plant Physiology |
publisher.none.fl_str_mv |
Plant Physiology |
dc.source.none.fl_str_mv |
reponame:LOCUS Repositório Institucional da UFV instname:Universidade Federal de Viçosa (UFV) instacron:UFV |
instname_str |
Universidade Federal de Viçosa (UFV) |
instacron_str |
UFV |
institution |
UFV |
reponame_str |
LOCUS Repositório Institucional da UFV |
collection |
LOCUS Repositório Institucional da UFV |
bitstream.url.fl_str_mv |
https://locus.ufv.br//bitstream/123456789/12573/1/1853.full.pdf https://locus.ufv.br//bitstream/123456789/12573/2/license.txt https://locus.ufv.br//bitstream/123456789/12573/3/1853.full.pdf.jpg |
bitstream.checksum.fl_str_mv |
94705f53167285d0acef467c14505816 8a4605be74aa9ea9d79846c1fba20a33 c3db615eebe74f43f454adfb6216da81 |
bitstream.checksumAlgorithm.fl_str_mv |
MD5 MD5 MD5 |
repository.name.fl_str_mv |
LOCUS Repositório Institucional da UFV - Universidade Federal de Viçosa (UFV) |
repository.mail.fl_str_mv |
fabiojreis@ufv.br |
_version_ |
1801212859717255168 |