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Mol. Cells 2012; 34(2): 185-191

Published online August 31, 2012

https://doi.org/10.1007/s10059-012-0096-0

© The Korean Society for Molecular and Cellular Biology

Characterization of Cell Death Induced by NbBPS1 Silencing in Nicotiana benthamiana

Yong Won Kang1, Young Jeon1, and Hyun-Sook Pai*

Department of Systems Biology, Yonsei University, Seoul 120-749, Korea, 1These authors contributed equally to this work.

Correspondence to : *Correspondence: hspai@yonsei.ac.kr

Received: April 3, 2012; Revised: May 12, 2012; Accepted: May 14, 2012

Abstract

We previously showed that silencing of NbBPS1 encod-ing an endoplasmic reticulum (ER)-localized protein re-sults 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. ben-thamiana.

Keywords autophagy, bZIP28 transcription factor, ER stress, programmed cell death, vesicles, virus-induced gene silencing

Article

Research Article

Mol. Cells 2012; 34(2): 185-191

Published online August 31, 2012 https://doi.org/10.1007/s10059-012-0096-0

Copyright © The Korean Society for Molecular and Cellular Biology.

Characterization of Cell Death Induced by NbBPS1 Silencing in Nicotiana benthamiana

Yong Won Kang1, Young Jeon1, and Hyun-Sook Pai*

Department of Systems Biology, Yonsei University, Seoul 120-749, Korea, 1These authors contributed equally to this work.

Correspondence to:*Correspondence: hspai@yonsei.ac.kr

Received: April 3, 2012; Revised: May 12, 2012; Accepted: May 14, 2012

Abstract

We previously showed that silencing of NbBPS1 encod-ing an endoplasmic reticulum (ER)-localized protein re-sults 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. ben-thamiana.

Keywords: autophagy, bZIP28 transcription factor, ER stress, programmed cell death, vesicles, virus-induced gene silencing

Mol. Cells
May 31, 2022 Vol.45 No.5, pp. 273~352
COVER PICTURE
Fe2+ ion depletion-induced expression of BΔGFP at the early stage of leaf development (Choi et al., pp. 294-305).

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