title: The ER luminal binding protein (BiP) alleviates Cd(2+)-induced programmed cell death through endoplasmic reticulum stress-cell death signaling pathway in tobacco cells.
abstract: Cadmium (Cd) is very toxic to plant cells and Cd(2+) stress induces programmed cell death (PCD) in Nicotiana tabacum L. cv. bright yellow-2 (BY-2) cells. In plants, PCD can be regulated through the endoplasmic reticulum (ER) stress-cell death signaling pathway. However, the mechanism of Cd(2+)-induced PCD remains unclear. In this study, we found that Cd(2+) treatment induced ER stress in tobacco BY-2 cells. The expression of two ER stress markers NtBLP4 and NtPDI and an unfolded protein response related transcription factor NtbZIP60 were upregulated with Cd(2+) stress. Meanwhile, the PCD triggered by prolonged Cd(2+) stress could be relieved by two ER chemical chaperones, 4-phenylbutyric acid and tauroursodeoxycholic acid. These results demonstrate that the ER stress-cell death signaling pathway participates in the mediation of Cd(2+)-induced PCD. Furthermore, the ER chaperone AtBiP2 protein alleviated Cd(2+)-induced ER stress and PCD in BY-2 cells based on the fact that heterologous expression of AtBiP2 in tobacco BY-2 cells reduced the expression of NtBLP4 and a PCD-related gene NtHsr203J under Cd(2+) stress conditions. In summary, these results suggest that the ER stress-cell death signaling pathway regulates Cd(2+)-induced PCD in tobacco BY-2 cells, and that the AtBiP2 protein act as a negative regulator in this process.
authors.affiliation: Key Laboratory of Plant Resources, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, PR China; University of Chinese Academy of Sciences, Beijing 100049, PR China.
authors.forename: Hua
authors.initials: H
authors.lastname: Xu
authors.forename: Wenzhong
authors.initials: W
authors.lastname: Xu
authors.forename: Hongmei
authors.initials: H
authors.lastname: Xi
authors.forename: Wenwen
authors.initials: W
authors.lastname: Ma
authors.forename: Zhenyan
authors.initials: Z
authors.lastname: He
authors.forename: Mi
authors.initials: M
authors.lastname: Ma
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D017360:Arabidopsis / Q000235:genetics / Q000502:physiology; D002104:Cadmium / Q000633:toxicity*; D002352:Carrier Proteins / Q000235:genetics* / Q000378:metabolism; D059865:Endoplasmic Reticulum Stress; D010654:Phenylbutyrates / Q000378:metabolism; D059828:Plant Cells / Q000187:drug effects / Q000502:physiology; D010940:Plant Proteins / Q000235:genetics* / Q000378:metabolism; D030821:Plants, Genetically Modified / Q000187:drug effects / Q000235:genetics / Q000502:physiology; D015398:Signal Transduction; D013655:Taurochenodeoxycholic Acid / Q000378:metabolism; D014026:Nicotiana / Q000187:drug effects / Q000502:physiology*
chemical_list: D002352:Carrier Proteins; D010654:Phenylbutyrates; D010940:Plant Proteins; D002104:Cadmium; D013655:Taurochenodeoxycholic Acid; C031655:ursodoxicoltaurine; C075773:4-phenylbutyric acid
keywords: ATF/CREB homolog 1; ATF6; BY-2; BiP; BiP protein; Bright yellow-2 cells; Ca; Cadmium; Cd; ER; ER stress; GRP94; Hac1; IRE1; N-rich protein; NRP; PCD; PDI; PERK; PKR-like ER kinase; Programmed cell death; UPR; X-box binding protein 1; Xbp1; activating transcription factor 6; bZIP; basic-leucine zipper; bright yellow-2; cadmium; calcium; endoplasmic reticulum; glucose-regulated protein 94; inositol-requiring enzyme-1; luminal binding protein; programmed cell death; protein disulfide isomerase; unfolded protein response