光学分子成像技术研究伏马毒素B1诱导植物光依赖性超敏反应的机制

Using Optical Molecular Imaging to Study Mechanism of Fumonisin B1-Induced Light-dependent Hypersensitive Cell Death

伏马毒素B1(FB1)是一种来源于串珠镰刀菌的可以引起植物光依赖性超敏反应的病原激发子,但这种超敏反应的机制研究尚不清楚。运用光学分子成像技术,并借助调制叶绿素荧光和激光共聚焦成像系统对拟南芥叶片在FB1侵染早期的光化学效率和叶绿体形态变化进行了分析,研究了FB1诱导的光依赖性超敏反应过程中的分子机制。结果发现,在光参与下,FB1明显降低了拟南芥叶片叶绿体的光化学效率,促进了叶绿体来源的活性氧大量产生和绿色荧光蛋白(GFP)标记的叶绿体基质蛋白的降解,而过氧化氢酶或抗坏血酸预处理则抑制了这一过程,说明活性氧参与促进了GFP标记的叶绿体基质蛋白的降解。总之,本文借助光学分子成像技术发现叶绿体在FB1诱发的植物光依赖性的超敏反应早期发挥着重要作用。

Fumonisin B1 （ FB1 ） , an elicitor produced by the Fusarium monilrme, can induce light-dependem hypersensitive cell death in plant, but the underlying molecular mechanism remains unclear. In this study, base on optical molecular imaging, we studied the molecular mechanism of light-dependent hypersensitive cell death in the initial stage of FB1 stress by measuring chlorophyll fluorescence and confocal laser scanning imaging analysis. Our resuhs suggested that FB1 reduced photosynthetic activity in Arabidopsis thaliana leaves. Moreover, FBI promoted light-dependent chloroplastic ROS production and stroma-targeted green fluorescent protein （GFP） degradation, while CAT or AsA pre-treat- ment reversed this trend, suggesting that ROS are involved in FBl-induced chloroplast degradation. In conclusion, using optical molecular imaging technique, our study found that chloroplast played a vital role in FB1-induced light-dependent hypersensitive cell death in plant.