BAX inhibitor-1 modulates endoplasmic reticulum stress-mediated programmed cell death in Arabidopsis
BAX inhibitor-1 modulates endoplasmic reticulum stress-mediated programmed cell death in Arabidopsis
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DOI：
10.1074/jbc.m706659200
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发表时间：
2008-02-08
影响因子：
4.8
通讯作者：
Lam, Eric
中科院分区：
文献类型：
--
作者：
Watanabe, Naohide;Lam, Eric
调控植物细胞程序性死亡（PCD）的组分和途径仍然知之甚少。在这里，我们描述了药物诱导的内质网（ER）应激对拟南芥幼苗的影响，并提出了拟南芥BAX抑制剂-1（AtBI 1）作为ER应激介导的PCD的调节剂的作用的证据。我们发现，处理拟南芥幼苗衣霉素（TM），N-连接的糖基化的抑制剂和诱导剂的ER应力触发积累的未折叠的蛋白质在ER，结果在强烈抑制根的生长和损失的生存伴随着典型的标志PCD，如积累的H2 O2，染色质凝聚，和oligonucleosomal核DNA片段。这些表型通过与两种不同的化学伴侣（4-苯基丁酸钠和牛磺熊去氧胆酸）中的任一种共治疗而减轻，这两种化学伴侣均具有伴侣特性，可以减少ER中错误折叠蛋白的负荷。在TM诱导的PCD开始之前，AtBI 1 mRNA的表达及其启动子活性显著增加。与野生型植株相比，AtBI 1突变体atbi 1 -1和atbi 1 -2表现出对TM的超敏反应，并加速了PCD进程。相反，过表达AtBI 1显着降低拟南芥幼苗对TM的敏感性。然而，AtBI 1基因表达水平的改变不会对典型的ER应激诱导基因（AtBip 2、AtPDI、AtCRT 1和AtCNX 1）的表达模式产生显著影响。我们认为AtBI 1在ER应激过程中作为一个高度保守的生存因子发挥着关键作用，与未折叠蛋白反应途径平行。
The components and pathways that regulate programmed cell death (PCD) in plants remain poorly understood. Here we describe the impact of drug-induced endoplasmic reticulum ( ER) stress on Arabidopsis seedlings and present evidence for the role of Arabidopsis BAX inhibitor-1 (AtBI1) as a modulator of ER stress-mediated PCD. We found that treatment of Arabidopsis seedlings with tunicamycin (TM), an inhibitor of N-linked glycosylation and an inducer of ER stress by triggering accumulation of unfolded proteins in the ER, results in strong inhibition of root growth and loss of survival accompanied by typical hallmarks of PCD such as accumulation of H2O2, chromatin condensation, and oligonucleosomal fragmentation of nuclear DNA. These phenotypes are alleviated by co-treatment with either of two different chemical chaperones, sodium 4-phenylbutyrate and tauroursodeoxycholic acid, both with chaperone properties that can reduce the load of misfolded protein in the ER. Expression of AtBI1 mRNA and its promoter activity are increased dramatically prior to initiation of TM-induced PCD. Compared with wild-type plants, two AtBI1 mutants (atbi1-1 and atbi1-2) exhibit hypersensitivity to TM with accelerated PCD progression. Conversely, overexpressing AtBI1 markedly reduces the sensitivity of Arabidopsis seedlings to TM. However, alterations in AtBI1 gene expression levels do not cause a significant effect on the expression patterns of typical ER stress-inducible genes (AtBip2, AtPDI, AtCRT1, and AtCNX1). We propose that AtBI1 plays a pivotal role as a highly conserved survival factor during ER stress that acts in parallel to the unfolded protein response pathway.