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首页> 外文期刊>Biochemistry >Effect of Mitochondria-Targeted Antioxidant SkQ1 on Programmed Cell Death Induced by Viral Proteins in Tobacco Plants
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Effect of Mitochondria-Targeted Antioxidant SkQ1 on Programmed Cell Death Induced by Viral Proteins in Tobacco Plants

机译:线粒体抗氧化剂SkQ1对病毒蛋白诱导的烟草植物程序性细胞死亡的影响

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摘要

Programmed cell death (PCD) is the main defense mechanism in plants to fight various pathogens including viruses. The best-studied example of virus-induced PCD in plants is Tobacco mosaic virus (TMV)-elicited hypersensitive response in tobacco plants containing the N resistance gene. It was previously reported that the animal mitochondrial protein Bcl-xL, which lacks a homolog in plants, effectively suppresses plant PCD induced by TMV p50 — the elicitor of hypersensitive response in Nicotiana tabacum carrying the N gene. Our studies show that the mitochondria-targeted antioxidant SkQ 1 effectively suppresses p50-induced PCD in tobacco plants. On the other hand, SkQl did not affect Boa semilatent virus TGB3-induced endoplasmic reticulum stress, which is followed by PCD, in Nicotiana benthamiana epidermal cells. These data suggest that mitochondria-targeted antioxidant SkQl can be used to study molecular mechanisms of PCD suppression in plants.
机译:程序性细胞死亡(PCD)是植物对抗各种病原体(包括病毒)的主要防御机制。研究最深入的病毒诱导植物中PCD的例子是烟草花叶病毒(TMV)引起的含有N抗性基因的烟草植物的超敏反应。以前有报道说,动物线粒体蛋白Bcl-xL在植物中缺乏同源性,可有效抑制TMV p50诱导的植物PCD,TMV p50是烟草中带有N基因的超敏反应的引发剂。我们的研究表明,针对线粒体的抗氧化剂SkQ 1有效抑制烟草植物中p50诱导的PCD。另一方面,SkQ1在本氏烟草表皮细胞中不影响Boa半潜伏病毒TGB3诱导的内质网应激,随后是PCD。这些数据表明,针对线粒体的抗氧化剂SkQl可用于研究植物中PCD抑制的分子机制。

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