Characterization of cell death induced by NbBPS1 silencing in nicotiana benthamiana

Yong Won Kang; Young Jeon; Hyun Sook Pai

doi:10.1007/s10059-012-0096-0

Characterization of cell death induced by NbBPS1 silencing in nicotiana benthamiana

Yong Won Kang, Young Jeon, Hyun Sook Pai

Research output: Contribution to journal › Article › peer-review

3 Citations (Scopus)

Abstract

We previously showed that silencing of NbBPS1 encoding an endoplasmic reticulum (ER)-localized protein results in pleiotrophic developmental defects and cell death in Nicotiana benthamiana [Kang et al. (2008)]. In this study, we investigated the mechanism of the cell death caused by NbBPS1 silencing. Affected leaf cells exhibited morphological markers of programmed cell death (PCD) and accumulated excessive amounts of reactive oxygen species. NbBPS1 silencing caused dramatic induction of the ER stress marker genes BiP-like protein (BLP) genes, HSP70, and Bax Inhibitor-1. Furthermore, NbBPS1 deficiency led to relocalization of bZIP28 transcription factor from the ER membrane to the nucleus, similar to the bZIP28 relocalization during tunicamycin-induced ER stress. Abnormal accumulation of vesicles and increased autophagy activity were also observed in the affected leaf cells. These results suggest that inactivation of NbBPS1 function in the ER leads to ER stress, autophagy, and PCD activation in N. benthamiana.

Original language	English
Pages (from-to)	185-191
Number of pages	7
Journal	Molecules and cells
Volume	34
Issue number	2
DOIs	https://doi.org/10.1007/s10059-012-0096-0
Publication status	Published - 2012 Aug

Bibliographical note

Funding Information:
This research was supported by the Next-Generation BioGreen 21 Program (PMBC, No. PJ009079/SSAC, No. PJ008214) from Rural Development Administration (RDA) of Korea.

All Science Journal Classification (ASJC) codes

Molecular Biology
Cell Biology

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title = "Characterization of cell death induced by NbBPS1 silencing in nicotiana benthamiana",

abstract = "We previously showed that silencing of NbBPS1 encoding an endoplasmic reticulum (ER)-localized protein results in pleiotrophic developmental defects and cell death in Nicotiana benthamiana [Kang et al. (2008)]. In this study, we investigated the mechanism of the cell death caused by NbBPS1 silencing. Affected leaf cells exhibited morphological markers of programmed cell death (PCD) and accumulated excessive amounts of reactive oxygen species. NbBPS1 silencing caused dramatic induction of the ER stress marker genes BiP-like protein (BLP) genes, HSP70, and Bax Inhibitor-1. Furthermore, NbBPS1 deficiency led to relocalization of bZIP28 transcription factor from the ER membrane to the nucleus, similar to the bZIP28 relocalization during tunicamycin-induced ER stress. Abnormal accumulation of vesicles and increased autophagy activity were also observed in the affected leaf cells. These results suggest that inactivation of NbBPS1 function in the ER leads to ER stress, autophagy, and PCD activation in N. benthamiana.",

author = "Kang, {Yong Won} and Young Jeon and Pai, {Hyun Sook}",

note = "Funding Information: This research was supported by the Next-Generation BioGreen 21 Program (PMBC, No. PJ009079/SSAC, No. PJ008214) from Rural Development Administration (RDA) of Korea.",

year = "2012",

month = aug,

doi = "10.1007/s10059-012-0096-0",

language = "English",

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AU - Kang, Yong Won

AU - Jeon, Young

AU - Pai, Hyun Sook

N1 - Funding Information: This research was supported by the Next-Generation BioGreen 21 Program (PMBC, No. PJ009079/SSAC, No. PJ008214) from Rural Development Administration (RDA) of Korea.

PY - 2012/8

Y1 - 2012/8

N2 - We previously showed that silencing of NbBPS1 encoding an endoplasmic reticulum (ER)-localized protein results in pleiotrophic developmental defects and cell death in Nicotiana benthamiana [Kang et al. (2008)]. In this study, we investigated the mechanism of the cell death caused by NbBPS1 silencing. Affected leaf cells exhibited morphological markers of programmed cell death (PCD) and accumulated excessive amounts of reactive oxygen species. NbBPS1 silencing caused dramatic induction of the ER stress marker genes BiP-like protein (BLP) genes, HSP70, and Bax Inhibitor-1. Furthermore, NbBPS1 deficiency led to relocalization of bZIP28 transcription factor from the ER membrane to the nucleus, similar to the bZIP28 relocalization during tunicamycin-induced ER stress. Abnormal accumulation of vesicles and increased autophagy activity were also observed in the affected leaf cells. These results suggest that inactivation of NbBPS1 function in the ER leads to ER stress, autophagy, and PCD activation in N. benthamiana.

AB - We previously showed that silencing of NbBPS1 encoding an endoplasmic reticulum (ER)-localized protein results in pleiotrophic developmental defects and cell death in Nicotiana benthamiana [Kang et al. (2008)]. In this study, we investigated the mechanism of the cell death caused by NbBPS1 silencing. Affected leaf cells exhibited morphological markers of programmed cell death (PCD) and accumulated excessive amounts of reactive oxygen species. NbBPS1 silencing caused dramatic induction of the ER stress marker genes BiP-like protein (BLP) genes, HSP70, and Bax Inhibitor-1. Furthermore, NbBPS1 deficiency led to relocalization of bZIP28 transcription factor from the ER membrane to the nucleus, similar to the bZIP28 relocalization during tunicamycin-induced ER stress. Abnormal accumulation of vesicles and increased autophagy activity were also observed in the affected leaf cells. These results suggest that inactivation of NbBPS1 function in the ER leads to ER stress, autophagy, and PCD activation in N. benthamiana.

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Characterization of cell death induced by NbBPS1 silencing in nicotiana benthamiana

Abstract

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