Department of Systems Biology, Yonsei University, Seoul 120-749, Korea.
Mol Cells. 2012 Aug;34(2):185-91. doi: 10.1007/s10059-012-0096-0. Epub 2012 Jun 22.
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.
我们之前曾表明，沉默编码内质网（ER）定位蛋白的 NbBPS1 会导致烟草原生质体出现多种发育缺陷和细胞死亡[Kang 等人，2008]。在这项研究中，我们研究了由 NbBPS1 沉默引起的细胞死亡的机制。受影响的叶片细胞表现出程序性细胞死亡（PCD）的形态学标记，并积累了过量的活性氧。NbBPS1 沉默导致 ER 应激标记基因 BiP 样蛋白（BLP）基因、HSP70 和 Bax Inhibitor-1 的显著诱导。此外，NbBPS1 缺失导致 bZIP28 转录因子从 ER 膜重新定位到细胞核，类似于衣霉素诱导的 ER 应激过程中 bZIP28 的重新定位。受影响的叶片细胞中还观察到囊泡的异常积累和自噬活性的增加。这些结果表明，NbBPS1 在 ER 中的功能失活会导致烟草原生质体中 ER 应激、自噬和 PCD 的激活。
