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Short-term salinity stress in tobacco plants leads to the onset of animal-like PCD hallmarks in planta in contrast to long-term stress

机译:与长期胁迫相反,烟草植物中的短期盐度胁迫导致植物体内出现动物样PCD标志

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Recent results have identified mitochondria as centers of stress-induced generation of reactive oxygen species in plants. Depolarization of plant mitochondrial membrane during stress results the release of programmed cell death (PCD)-inducing factors in the cytosol in a fashion similar to the onset of animal-like PCD. Herein, we report significant similarities of animal-like PCD and salinity stress-induced plant PCD. Short-term salinity stress (3 h) led to depolarization of the mitochondrial membrane, release of cytochrome c (CYT-c), which was visualized using a contemporary molecular technique, activation of caspase-3 type proteases and the onset of PCD in wild type tobacco plants, Nicotiana tabacum cv. Petit Havana. However, PCD was not manifested during long-term salinity stress (24 h). Interestingly long-term salinity stress led to necrotic-like features, which were accompanied by collapse of respiration, reduction of key components of the respiratory chain, such as CYT-c and alternative oxidase, ATP depletion and high proteolytic activity. The results suggest that salinity stress of tobacco plants in planta leads to the onset of animal-like PCD only during the early stages post-stress, while long-term stress leads to necrotic-like features. Keywords Abiotic stress - Alternative oxidase - Cytochrome c - Programmed cell death - Salinity
机译:最近的研究结果表明,线粒体是胁迫诱导植物中活性氧生成的中心。胁迫期间植物线粒体膜的去极化导致以类似于动物类PCD发作的方式在细胞质中释放程序性细胞死亡(PCD)诱导因子。在本文中,我们报道了动物样PCD和盐度胁迫诱导的植物PCD的显着相似性。短期盐度胁迫(3 h)导致线粒体膜去极化,释放细胞色素c(CYT-c)(使用现代分子技术可观察到),激活caspase-3型蛋白酶并在野生环境中发生PCD型烟草植物,Nicotiana tabacum cv。小哈瓦那。然而,在长期盐度胁迫(24 h)中未表现出PCD。有趣的是,长期盐度胁迫导致了坏死样特征,伴随着呼吸衰竭,呼吸链关键成分减少,例如CYT-c和替代氧化酶,ATP耗竭和高蛋白水解活性。结果表明,烟草植物中的盐分胁迫仅在胁迫后的早期导致动物样PCD的发作,而长期胁迫则导致坏死样特征。非生物胁迫-替代氧化酶-细胞色素c-程序性细胞死亡-盐度

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