The mitochondrion--an organelle commonly involved in programmed cell death in Arabidopsis thaliana.
The mitochondrion--an organelle commonly involved in programmed cell death in Arabidopsis thaliana.
复制标题
DOI：
10.1111/j.1365-313x.2004.02239.x
复制
发表时间：
2004-11
期刊：
影响因子：
--
通讯作者：
N. Yao;B. Eisfelder;James Marvin;J. Greenberg
中科院分区：
文献类型：
--
作者：
N. Yao;B. Eisfelder;James Marvin;J. Greenberg
植物细胞在程序性细胞死亡（PCD）后期通常表现为染色质浓缩和核内分裂，然后出现明显的膜或细胞器超微结构变化。为了研究可能的早期PCD相关事件，我们利用拟南芥原生质体，在单细胞和群体水平上，利用显微镜观察和流式细胞术定量测定了PCD期间线粒体膜电位（DeltaPsim）的变化。DeltaPsim丢失通常在植物PCD的早期被诱导，这对PCD的执行很重要，环孢素A抑制动物细胞中线粒体通透性过渡孔，从而降低了DeltaPsim和PCD的变化。DeltaPsim丢失发生在细胞核形态改变之前，并且仅与线粒体细胞色素c释放（动物中的凋亡触发因子）有关，以响应三种PCD激发子之一。野生型中三种不同的刺激与PCD中的DeltaPsim变化有关：神经酰胺、原卟啉IX和超敏反应激发子AvrRpt2。此外，条件异位细胞死亡突变体的行为加速了细胞死亡2和过量产生acd2的植物也暗示DeltaPsim改变是PCD执行的关键。由于ACD2在成熟植物中主要是叶绿体成分，因此观察到ACD2突变体的细胞死亡需要线粒体功能的改变，这意味着叶绿体和线粒体之间的通信介导了PCD的激活。我们认为DeltaPsim缺失是植物PCD的常见早期标记，类似于在动物中记录的情况。然而，与动物细胞不同，在植物细胞中，线粒体细胞色素c的释放并不是控制PCD的必要步骤。
Plant cells undergoing programmed cell death (PCD) at late stages typically show chromatin condensation and endonucleolytic cleavage prior to obvious membrane or organelle ultrastructural changes. To investigate possible early PCD-associated events, we used microscopic observations and flow cytometry to quantitate mitochondrial membrane potential (DeltaPsim) changes during PCD at the single cell and population levels using Arabidopsis protoplasts. A DeltaPsim loss was commonly induced early during plant PCD and was important for PCD execution, as evidenced by the concomitant reduction of the change in DeltaPsim and PCD by cyclosporin A, which inhibits mitochondrial permeability transition pores in animal cells. DeltaPsim loss occurred prior to nuclear morphological changes and was only associated with mitochondrial cytochrome c release (an apoptotic trigger in animals) in response to one of three PCD elicitors. Three different stimuli in wild type implicated DeltaPsim changes in PCD: ceramide, protoporphyrin IX, and the hypersensitive response elicitor AvrRpt2. Additionally, the behavior of the conditional ectopic cell death mutant accelerated cell death2 and ACD2-overproducing plants also implicated DeltaPsim alteration as key for PCD execution. Because ACD2 is largely a chloroplast component in mature plants, the observation that the cell death in acd2 mutants requires changes in mitochondrial functions implicates communication between chloroplasts and mitochondria in mediating PCD activation. We suggest that DeltaPsim loss is a common early marker in plant PCD, similar to what has been documented in animals. However, unlike in animal cells, in plant cells, mitochondrial cytochrome c release is not an obligatory step in PCD control.