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首页> 外文期刊>Physiologia plantarum >Different enhancement of senescence induced by metabolic products of Alternaria alternata in tobacco leaves of different ages
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Different enhancement of senescence induced by metabolic products of Alternaria alternata in tobacco leaves of different ages

机译:不同年龄烟草叶片中交替链霉菌代谢产物诱导的衰老作用不同

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摘要

The purpose of this study was to explore the mechanisms by which Alternaria alternata damages tobacco (Nicotiana tabacum) leaves. Treatment with A. alternata metabolic products enhanced senescence in leaves of different ages, as indicated by the significant decrease in chlorophyll, soluble protein, photosynthetic O evolution and catalase (CAT, EC 1.11.1.6) activity as well as an increase in HO content. The induction of senescence by A. alternata metabolic products increased as the age of the leaves increased. A. alternata metabolic products greatly influenced the behavior of photosystem II (PSII) in the leaves: oxygen evolving complex (OEC) activity and electron transport from primary quinone electron acceptor of PS II (QA) to secondary quinone electron acceptor of PS II (QB) were both significantly inhibited. This inhibition also became more pronounced in older leaves. In vitro experiments revealed that, without the influence of natural senescence, the A. alternata metabolic products directly inhibited the activity of a commercial CAT solution and inhibited photosynthetic O evolution, which resulted in excess PSII excitation pressure and an overaccumulation of HO in leaf segments. These results suggest that the significant declines in photosynthesis and CAT activity induced by the metabolic products of A. alternata were important contributors to the overaccumulation of reactive oxygen species (ROS), which accelerated senescence in tobacco leaves. The fact that the enhancement of senescence was getting more pronounced with the age of tobacco leaves might be related to the fact that older leaves already had higher HO levels and less antioxidant activity as reflected in lower CAT activity.
机译:这项研究的目的是探讨链格孢菌损害烟草(Nicotiana tabacum)叶片的机制。叶绿素代谢产物的处理增强了不同年龄叶片的衰老,这表明叶绿素,可溶性蛋白,光合O的进化和过氧化氢酶(CAT,EC 1.11.1.6)活性显着降低以及HO含量增加表明。随着叶片年龄的增加,交替链霉菌代谢产物对衰老的诱导作用也增加。交链孢霉的代谢产物极大地影响了叶片中光系统II(PSII)的行为:放氧复合物(OEC)活性以及电子从PS II(QA)的初级醌电子受体转移到PS II(QB)的次级醌电子受体)均被显着抑制。这种抑制作用在老叶中也变得更加明显。体外实验表明,在没有自然衰老影响的情况下,交链孢霉的代谢产物直接抑制了商业CAT溶液的活性并抑制了光合作用O的进化,这导致了PSII激发压力过高和HO在叶节中的过度积累。这些结果表明,交替链霉菌的代谢产物引起的光合作用和CAT活性的显着下降是造成活性氧(ROS)过度积累的重要原因,而活性氧会加速烟草叶片的衰老。随着烟叶年龄的增长,衰老的增强越来越明显的事实可能与以下事实有关:较老的烟叶已经具有较高的HO水平和较低的抗氧化活性,这表现为较低的CAT活性。

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