Zimmermann Petra, Heinlein Christina, Orendi Gabriele, Zentgraf Ulrike
ZMBP (Centre of Molecular Biology of Plants), University of Tübingen, Auf der Morgenstelle 28, 72076 Tübingen, Germany.
Plant Cell Environ. 2006 Jun;29(6):1049-60. doi: 10.1111/j.1365-3040.2005.01459.x.
Oxygen free radicals are thought to play an essential role in senescence, especially those derived from peroxisomes. Therefore, the activities of different isoforms of the peroxisomal hydrogen peroxide (H2O2)-scavenging enzyme catalase (CAT) were analysed during senescence of Arabidopsis. CAT2 activity decreased with bolting time parallel with cytosolic ascorbate peroxidase 1 (APX1) activity before loss of chlorophyll could be measured. At the same time point, the H2O2 content increased. Subsequently, the stress-inducible CAT3 isoform was activated and APX1 activity was recovered, accompanied by a decline of the H2O2 content. In very late stages, low activities of the seed-specific CAT1 became detectable in leaves, but H2O2 increased again. Further analyses of CAT expression by promoter: beta-glucuronidase (GUS) fusions in transgenic plants revealed a vasculature-specific CAT3 expression, whereas CAT2 expression turned out to be specific for photosynthetic active tissues. CAT2 expression is down-regulated during leaf senescence, while CAT3 expression is induced with age and corresponds to an accumulation of H2O2 in the vascular bundles. CAT2 down-regulation on the transcriptional level appears as the initial step in creating the H2O2 peak during bolting time, while the decrease in APX1 activity might only be a secondary and amplifying effect.
氧自由基被认为在衰老过程中起着至关重要的作用,尤其是那些源自过氧化物酶体的自由基。因此,在拟南芥衰老过程中分析了过氧化物酶体过氧化氢(H₂O₂)清除酶过氧化氢酶(CAT)不同同工型的活性。在能够检测到叶绿素损失之前,CAT2活性随着抽薹时间下降,与胞质抗坏血酸过氧化物酶1(APX1)活性平行。在同一时间点,H₂O₂含量增加。随后,应激诱导的CAT3同工型被激活,APX1活性恢复,同时H₂O₂含量下降。在非常后期阶段,种子特异性的CAT1在叶片中可检测到低活性,但H₂O₂含量再次增加。通过启动子:β-葡萄糖醛酸酶(GUS)融合对转基因植物中CAT表达的进一步分析表明,CAT3在维管组织中特异性表达,而CAT2表达结果表明对光合活性组织具有特异性。在叶片衰老过程中CAT2表达下调,而CAT3表达随年龄诱导,并且与维管束中H₂O₂的积累相对应。CAT2在转录水平上的下调似乎是在抽薹期产生H₂O₂峰值的初始步骤,而APX1活性的下降可能只是一种次要的放大效应。