Balk J, Leaver C J
University of Oxford, Department of Plant Sciences, South Parks Road, Oxford OX1 3RB, United Kingdom.
Plant Cell. 2001 Aug;13(8):1803-18. doi: 10.1105/tpc.010116.
In mammals, mitochondria have been shown to play a key intermediary role in apoptosis, a morphologically distinct form of programmed cell death (PCD), for example, through the release of cytochrome c, which activates a proteolytic enzyme cascade, resulting in specific nuclear DNA degradation and cell death. In plants, PCD is a feature of normal development, including the penultimate stage of anther development, leading to dehiscence and pollen release. However, there is little evidence that plant mitochondria are involved in PCD. In a wide range of plant species, anther and/or pollen development is disrupted in a class of mutants termed CMS (for cytoplasmic male sterility), which is associated with mutations in the mitochondrial genome. On the basis of the manifestation of a number of morphological and biochemical markers of apoptosis, we have shown that the PET1-CMS cytoplasm in sunflower causes premature PCD of the tapetal cells, which then extends to other anther tissues. These features included cell condensation, oligonucleosomal cleavage of nuclear DNA, separation of chromatin into delineated masses, and initial persistence of mitochondria. In addition, immunocytochemical analysis revealed that cytochrome c was released partially from the mitochondria into the cytosol of tapetal cells before the gross morphological changes associated with PCD. The decrease in cytochrome c content in mitochondria isolated from male sterile florets preceded a decrease in the integrity of the outer mitochondrial membrane and respiratory control ratio. Our data suggest that plant mitochondria, like mammalian mitochondria, play a key role in the induction of PCD. The tissue-specific nature of the CMS phenotype is discussed with regard to cellular respiratory demand and PCD during normal anther development.
在哺乳动物中，线粒体已被证明在细胞凋亡（一种形态上截然不同的程序性细胞死亡形式，即PCD）中起关键的中介作用，例如，通过细胞色素c的释放来激活蛋白水解酶级联反应，从而导致特定的核DNA降解和细胞死亡。在植物中，PCD是正常发育的一个特征，包括花药发育的倒数第二个阶段，最终导致花药开裂和花粉释放。然而，几乎没有证据表明植物线粒体参与PCD过程。在多种植物物种中，一类被称为CMS（细胞质雄性不育）的突变体中花药和/或花粉发育受到破坏，这与线粒体基因组中的突变有关。基于细胞凋亡的一些形态学和生化标志物的表现，我们已经表明向日葵中的PET1 - CMS细胞质会导致绒毡层细胞过早发生PCD，随后这种PCD会扩展到花药的其他组织。这些特征包括细胞浓缩、核DNA的寡核小体切割、染色质分离成界限分明的团块以及线粒体的最初持续性。此外，免疫细胞化学分析表明，在与PCD相关的总体形态变化之前，细胞色素c部分地从线粒体释放到绒毡层细胞的细胞质中。从雄性不育小花中分离得到的线粒体中细胞色素c含量的降低先于线粒体外膜完整性和呼吸控制率的降低。我们的数据表明，植物线粒体与哺乳动物线粒体一样，在PCD的诱导中起关键作用。我们还讨论了CMS表型的组织特异性与正常花药发育过程中的细胞呼吸需求和PCD的关系。
