Induction of ASCORBATE PEROXIDASE 2 expression in wounded Arabidopsis leaves does not involve known wound-signalling pathways but is associated with changes in photosynthesis
Induction of ASCORBATE PEROXIDASE 2 expression in wounded Arabidopsis leaves does not involve known wound-signalling pathways but is associated with changes in photosynthesis
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DOI：
10.1111/j.1365-313x.2004.02066.x
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发表时间：
2004-05-01
期刊：
影响因子：
7.2
通讯作者：
Mullineaux, PM
中科院分区：
文献类型：
--
作者：
Chang, CCC;Ball, L;Mullineaux, PM
抗坏血酸过氧化物酶 2 (APX2) 编码抗氧化网络的关键酶。在过度光胁迫的拟南芥叶片中，光合电子传递 (PET)、过氧化氢 (H2O2) 和脱落酸 (ABA) 调节 APX2 表达。受伤的叶子对 APX2 表达的诱导作用较低，当暴露在过量的光线下时，APX2 的表达会协同增加。依赖于茉莉酸 (JA)、壳聚糖和 ABA 的信号通路不参与伤口诱导的 APX2 表达，但显示需要 PET，并且先于 CO2 固定率降低。这导致 H2O2 在静脉组织中积聚。二苯基碘 (DPI) 先前已被证明是受伤叶脉中 H2O2 积累的有效抑制剂，可能通过抑制 PET 来阻止 APX2 表达的诱导。因此，受伤叶片中 APX2 表达的弱诱导可能仅需要 H2O2 和 PET。与其他环境胁迫一样，叶子受伤会导致光合作用减少，从而导致活性氧（ROS）产生增加。这可能标志着许多不受 JA 依赖性或其他已知的 JA 独立途径调节的“伤口反应”基因的诱导。
ASCORBATE PEROXIDASE 2 (APX2) encodes a key enzyme of the antioxidant network. In excess light-stressed Arabidopsis leaves, photosynthetic electron transport (PET), hydrogen peroxide (H2O2) and abscisic acid (ABA) regulate APX2 expression. Wounded leaves showed low induction of APX2 expression, and when exposed to excess light, APX2 expression was increased synergistically. Signalling pathways dependent upon jasmonic acid (JA), chitosan and ABA were not involved in the wound-induced expression of APX2, but were shown to require PET and were preceded by a depressed rate of CO2 fixation. This led to an accumulation of H2O2 in veinal tissue. Diphenyl iodonium (DPI), which has been shown previously to be a potent inhibitor of H2O2 accumulation in the veins of wounded leaves, prevented induction of APX2 expression probably by inhibition of PET. Thus, the weak induction of APX2 expression in wounded leaves may require H2O2 and PET only. As in other environmental stresses, wounding of leaves resulted in decreased photosynthesis leading to increased reactive oxygen species (ROS) production. This may signal the induction of many 'wound-responsive' genes not regulated by JA-dependent or other known JA-independent pathways.