Bax-induced cell death in tobacco is similar to the hypersensitive response
Bax-induced cell death in tobacco is similar to the hypersensitive response
复制标题
DOI：
10.1073/pnas.96.14.7956
复制
发表时间：
1999-07-06
影响因子：
11.1
通讯作者：
Cruz, SS
中科院分区：
文献类型：
--
作者：
Lacomme, C;Cruz, SS
Bax是一种促进死亡的蛋白质家族成员，当通过烟草花叶病毒载体在植物中表达时，它会引发细胞死亡。对Bax缺失突变体的分析表明，BH1和BH3结构域在促进细胞快速死亡方面是必需的，而羧基末端跨膜结构域的缺失则完全消除了Bax在植物中的致死性。Bax诱导的细胞死亡表型与野生型烟草花叶病毒在携带N基因的烟草植株中诱导的过敏反应非常相似。Bax在植物中促进细胞死亡的功能与防御相关蛋白PR1的积累有关，这表明Bax激活了植物的内源细胞死亡程序。为了支持这一观点，N基因和Bax介导的细胞死亡都被蛋白磷酸酶活性抑制剂冈田酸阻断。Bax在植物体内诱导细胞死亡和防御反应的能力表明，动物和植物细胞死亡过程的一些特征可能是相同的。
Bax, a death-promoting member of the Bcl-2 family of proteins, triggered cell death when expressed in plants from a tobacco mosaic virus vector. Analysis of Bax deletion mutants demonstrated a requirement for the BH1 and BH3 domains in promoting rapid cell death, whereas deletion of the carboxyl-terminal transmembrane domain completely abolished the lethality of Bax in plants. The phenotype of cell death induced by Bax closely resembled the hypersensitive response induced by wild-type tobacco mosaic virus in tobacco plants carrying the N gene. The cell death-promoting function of Bax in plants correlated with accumulation of the defense-related protein PR1, suggesting Bax activated an endogenous cell-death program in plants. In support of this view, both N gene- and Bax-mediated cell death was blocked by okadaic acid, an inhibitor of protein phosphatase activity. The ability of Bax to induce cell death and a defense reaction in plants suggests that some features of animal and plant cell death processes may be shared.