State Key Lab of Crop Biology, College of Life Sciences, Shandong Agricultural University, Tai'an 271018, China.
Physiol Plant. 2010 Feb;138(2):164-75. doi: 10.1111/j.1399-3054.2009.01300.x. Epub 2009 Oct 6.
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(2) evolution and catalase (CAT, EC 1.11.1.6) activity as well as an increase in H(2)O(2) 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 (Q(A)) to secondary quinone electron acceptor of PS II (Q(B)) 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(2) evolution, which resulted in excess PSII excitation pressure and an overaccumulation of H(2)O(2) 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 H(2)O(2) levels and less antioxidant activity as reflected in lower CAT activity.
本研究旨在探索链格孢（Alternaria alternata）损伤烟草（Nicotiana tabacum）叶片的机制。链格孢代谢产物处理可加速不同叶龄叶片的衰老，表现为叶绿素、可溶性蛋白、光合 O2 释放和过氧化氢酶（CAT，EC 1.11.1.6）活性显著下降，H2O2 含量增加。随着叶片年龄的增加，链格孢代谢产物诱导的衰老程度增加。链格孢代谢产物极大地影响了叶片中光合系统 II（PSII）的行为：氧释放复合体（OEC）活性和电子从 PSII 的初级醌电子受体（Q(A))到 PSII 的次级醌电子受体（Q(B))的传递均受到显著抑制。这种抑制在较老的叶片中更为明显。离体实验表明，在不受自然衰老影响的情况下，链格孢代谢产物直接抑制了商业 CAT 溶液的活性，并抑制了光合 O2 的释放，这导致 PSII 激发压力过大，H2O2 在叶片段中过度积累。这些结果表明，链格孢代谢产物引起的光合作用和 CAT 活性的显著下降是活性氧（ROS）过度积累的重要原因，这加速了烟草叶片的衰老。随着烟草叶片年龄的增加，衰老增强的事实可能与较老叶片中 H2O2 水平较高和抗氧化剂活性较低（反映为 CAT 活性较低）有关。
