Dissection of Arabidopsis Bax inhibitor-1 suppressing Bax-, hydrogen peroxide-, and salicylic acid-induced cell death
Dissection of Arabidopsis Bax inhibitor-1 suppressing Bax-, hydrogen peroxide-, and salicylic acid-induced cell death
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DOI：
10.1105/tpc.014613
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发表时间：
2004-01-01
期刊：
影响因子：
11.6
通讯作者：
Uchimiya, H
中科院分区：
文献类型：
--
作者：
Kawai-Yamada, M;Ohori, Y;Uchimiya, H
过表达植物Bax抑制剂-1（BI-1）能够抑制酵母和拟南芥中Bax介导的细胞死亡。在这里，我们证明了Bax异位表达诱导的活性氧产生对AtBI-1的共表达不敏感。同样，过氧化氢或水杨酸介导的细胞死亡也被抑制在烟草BY-2细胞过表达AtBI-1。为了确定AtBI-1作为细胞死亡抑制因子的功能结构域，在具有半乳糖诱导的哺乳动物Bax的酵母中分析了AtBI-1蛋白的截短系列。结果表明，DeltaC-AtBI-1（C-末端14个氨基酸缺失）失去了维持细胞生长的能力。此外，AtBI-1的C-末端7个氨基酸残基被其他缺乏卷曲螺旋结构的氨基酸残基取代的突变蛋白不能抑制细胞死亡，这表明C-末端区域对于抑制细胞死亡是必需的。我们还注意到，C-末端亲水区域在动物和植物Bax抑制剂之间是可互换的。
Overexpression of plant Bax Inhibitor-1 (BI-1) was able to suppress Bax-mediated cell death in yeast and Arabidopsis. Here, we demonstrate that reactive oxygen species production induced by the ectopic expression of Bax was insensitive to the coexpression of AtBI-1. Similarly, H2O2- or salicylic acid-mediated cell death also was suppressed in tobacco BY-2 cells overexpressing AtBI-1. To define the functional domain of AtBI-1 as a cell death suppressor, a truncated series of the AtBI-1 protein was analyzed in yeast possessing a galactose-inducible mammalian Bax. The results showed that DeltaC-AtBI-1 (with the C-terminal 14 amino acids deleted) lost the ability to sustain cell growth. Furthermore, a mutant protein in which the C-terminal seven amino acid residues of AtBI-1 were replaced with others lacking a coiled-coil structure failed to inhibit cell death, suggesting that the C-terminal region is essential for the inhibition of cell death. We also noted that the C-terminal hydrophilic region was interchangeable between animal and plant Bax inhibitors.