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Cell Wall and Protoplast Isoperoxidases in Tobacco Plants in Relation to Mechanical Injury and Infection with Tobacco Mosaic Virus

机译:烟草植物细胞壁和原生质体过氧化物酶与烟草花叶病毒的机械损伤和感染相关

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摘要

Leaves and pith of Turkish, Wisconsin 38, and Samsun NN tobacco (Nicotiana tabacum) varieties, which differ in their sensitivity to tobacco mosaic virus, showed the same qualitative isoperoxidase patterns and a similar distribution of distinctive isoperoxidases between the cell protoplast and wall-free, ionically, and covalently bound fractions. No changes in the qualitative isoenzyme spectrum were found in relation to age, mechanical injury, or leaf infection with tobacco mosaic virus. The distinctive isoperoxidases which reacted to infection were the same as those responsive to mechanical injury, confirming that the enzyme reaction to infection results from a nonspecific response to injury. The increase in peroxidase activity in response to infection or mechanical injury, or both, was greater in young tissue than in the older ones. The great increase in Samsun NN leaves and no increase in those of the two other varieties in response to infection may be due to differences in the degree to which the pathogen affected processes controlling the nonspecific peroxidase reaction to injury. Peroxidase development in the infected Samsun NN leaves was due to isoenzymes which form the wall-bound fraction in very young tissues, and to those which increase in activity with aging in the protoplast and wall-free fractions. In mechanically injured tissue, only the first group of isoenzymes increased in activity. In Samsun NN plants, the increased peroxidase activity in upper intact leaves above the infected ones was only due to isoenzymes whose activity increases with both normal and virus-accelerated senescence. Peroxidase reaction to challenge inoculation in these leaves was the same whether the lower ones were intact, infected and/or mechanically injured. Thus, the induced systemic resistance to tobacco mosaic virus may be due to other than peroxidase factors.In infected tissues, peroxidase was detected in the endoplasmic reticulum, Golgi apparatus, vacuole, cell wall, and intercellular spaces. The Golgi vesicles were often localized near the tonoplast and plasmalemma, fusing with membranes and secreting their contents. The possible “rejuvenating” effects of injury on synthesis and transport of distinctive isoperoxidases are discussed.
机译:土耳其,威斯康星州38和萨姆森(Samsun)NN烟草(Nicotiana tabacum)品种的叶和髓,其对烟草花叶病毒的敏感性不同,显示出相同的定性过氧化物酶模式,不同的过氧化物酶在细胞原生质体和无壁之间的分布相似,离子键和共价键结合的馏分。没有发现与年龄,机械损伤或烟草花叶病毒感染有关的定性同工酶谱变化。对感染反应的独特的过氧化物酶与对机械损伤的反应相同,证实对感染的酶反应是由对损伤的非特异性反应引起的。在年轻的组织中,响应感染或机械损伤或两者而引起的过氧化物酶活性的增加要大于老组织。由于感染,Samsun NN叶片的大量增加而其他两个品种的叶片没有增加,这可能是由于病原体影响控制非特异性过氧化物酶对伤害的反应的过程的程度不同所致。受感染的Samsun NN叶片中过氧化物酶的产生是由于同工酶在非常年轻的组织中形成了壁结合部分,以及那些随着原生质体和无壁部分的老化而增加的活性。在机械损伤的组织中,只有第一组同工酶的活性增加。在Samsun NN植物中,受感染叶片上方完整叶片中过氧化物酶活性的增加仅归因于同工酶,其活性随正常衰老和病毒加速衰老而增加。无论下部叶片是否完好无损,被感染和/或受到机械损伤,这些叶片中过氧化物酶对接种的反应都是相同的。因此,诱导的对烟草花叶病毒的全身抗性可能是由于过氧化物酶以外的因素引起的。在感染的组织中,在内质网,高尔基体,液泡,细胞壁和细胞间隙中检测到过氧化物酶。高尔基囊泡通常位于液泡膜和质膜附近,与膜融合并分泌其内容物。讨论了损伤对独特的过氧化物酶的合成和运输的可能的“恢复活力”作用。

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