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Participation of chloroplasts in plant apoptosis

机译:叶绿体参与植物细胞凋亡

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Milochondria are known to participate in the initiation of programmed cell death (PCD) in animals and in plants. The role of chloroplasts in PCD is still unknown. We describe a new system to study PCD in plants; namely, leaf epidermal peels. The peel represents a monolayer consisting of cells of two types: phototrophic (guard cells) and chemotrophic (epidermal cells). The peels from pea (Pisum sativum L.) leaves were treated by cyanide as an inducer of PCD. We found an apoptosis-enhancing effect ofillumination on chloroplastcontaining guard cells, but not on chloroplastless epidermal cells. Antioxidants and anaerobiosis prevented the CN~--induced apoptosis of cells of both types in the dark and in the light. On the other hand, methyl viologen andmenadione known as ROS-generating reagents as well as the Hill reaction electron acceptors (BQ, DAD, TMPD, or DPIP) that are not oxidized spontaneously by O_2 were shown to prevent the CN~--induced nucleus destruction in guard cells. Apoptosis of epidermal cells was potentiated by these reagents, and they had no influence on the CN effect. The light-dependent activation of CN~--induced apoptosis of guard cells was suppressed by DCMU, stigmatellin or DNP-INT, by a protein kinase inhibitor staurosporineas well as by cysteine and serine protease inhibitors. The above data suggest that apoptosis of guard cells is initiated upon a combined action of two factors, i.e., ROS and reduced plastoquinone of the photo synthetic electron transfer chain. As to reduction of ubiquinone in the mitochondrial respiratory chain, it seems to be antiapoptotic for the guard cell.
机译:已知线粒体参与动物和植物中程序性细胞死亡(PCD)的启动。叶绿体在PCD中的作用仍然未知。我们描述了一种用于研究植物中PCD的新系统;即叶表皮。果皮代表由两种类型的细胞组成的单层:光养性(保卫细胞)和化学营养性(表皮细胞)。用氰化物处理豌豆(Pisum sativum L.)叶片的果皮作为PCD的诱导剂。我们发现照明对含叶绿体的保卫细胞具有增强凋亡的作用,但对无叶绿体的表皮细胞却没有。抗氧化剂和厌氧菌阻止了CN_诱导的在黑暗和黑暗中两种细胞的凋亡。另一方面,已证明被称为ROS生成剂的甲基紫精和甲萘醌以及未被O_2自发氧化的Hill反应电子受体(BQ,DAD,TMPD或DPIP)可以防止CN〜诱导的核破坏保卫室。这些试剂增强了表皮细胞的凋亡,并且它们对CN作用没有影响。 CNMU诱导的保卫细胞凋亡的光依赖性激活被DCMU,柱头蛋白或DNP-INT,蛋白激酶抑制剂星形孢菌素以及半胱氨酸和丝氨酸蛋白酶抑制剂抑制。上述数据表明,保卫细胞的凋亡是由两个因素,即ROS和光合电子转移链的还原质体醌的组合作用而引发的。至于线粒体呼吸链中泛醌的还原,似乎对保卫细胞具有抗凋亡作用。

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