A. N. Belozersky Institute of Physico-Chemical Biology, Moscow State University, Moscow, Russia.
PLoS Pathog. 2012;8(4):e1002640. doi: 10.1371/journal.ppat.1002640. Epub 2012 Apr 5.
Many plants release airborne volatile compounds in response to wounding due to pathogenic assault. These compounds serve as plant defenses and are involved in plant signaling. Here, we study the effects of pectin methylesterase (PME)-generated methanol release from wounded plants ("emitters") on the defensive reactions of neighboring "receiver" plants. Plant leaf wounding resulted in the synthesis of PME and a spike in methanol released into the air. Gaseous methanol or vapors from wounded PME-transgenic plants induced resistance to the bacterial pathogen Ralstonia solanacearum in the leaves of non-wounded neighboring "receiver" plants. In experiments with different volatile organic compounds, gaseous methanol was the only airborne factor that could induce antibacterial resistance in neighboring plants. In an effort to understand the mechanisms by which methanol stimulates the antibacterial resistance of "receiver" plants, we constructed forward and reverse suppression subtractive hybridization cDNA libraries from Nicotiana benthamiana plants exposed to methanol. We identified multiple methanol-inducible genes (MIGs), most of which are involved in defense or cell-to-cell trafficking. We then isolated the most affected genes for further analysis: β-1,3-glucanase (BG), a previously unidentified gene (MIG-21), and non-cell-autonomous pathway protein (NCAPP). Experiments with Tobacco mosaic virus (TMV) and a vector encoding two tandem copies of green fluorescent protein as a tracer of cell-to-cell movement showed the increased gating capacity of plasmodesmata in the presence of BG, MIG-21, and NCAPP. The increased gating capacity is accompanied by enhanced TMV reproduction in the "receivers". Overall, our data indicate that methanol emitted by a wounded plant acts as a signal that enhances antibacterial resistance and facilitates viral spread in neighboring plants.
许多植物在受到病原体攻击而受伤时会释放空气中的挥发性化合物。这些化合物作为植物防御物质，并参与植物信号转导。在这里，我们研究了果胶甲酯酶 (PME) 从受伤植物（“发射器”）中产生的甲醇释放对邻近“接收器”植物防御反应的影响。植物叶片受伤会导致 PME 的合成和空气中甲醇释放的激增。受伤的 PME 转基因植物释放的气态甲醇或蒸气会诱导非受伤邻近“接收器”植物叶片对细菌病原体丁香假单胞菌的抗性。在不同挥发性有机化合物的实验中，气态甲醇是唯一能诱导邻近植物产生抗细菌作用的空气传播因子。为了了解甲醇刺激“接收器”植物抗菌抗性的机制，我们构建了暴露于甲醇的黄花烟正向和反向抑制消减杂交 cDNA 文库。我们鉴定了多个甲醇诱导基因（MIGs），其中大多数与防御或细胞间运输有关。然后，我们分离了受影响最大的基因进行进一步分析：β-1,3-葡聚糖酶（BG），这是一个以前未被识别的基因（MIG-21）和非细胞自主途径蛋白（NCAPP）。用烟草花叶病毒（TMV）和一个编码两个串联绿色荧光蛋白拷贝的载体作为细胞间运动示踪剂的实验表明，在 BG、MIG-21 和 NCAPP 的存在下，胞间连丝的门控能力增加。门控能力的增加伴随着“接收器”中 TMV 繁殖的增加。总的来说，我们的数据表明，受伤植物释放的甲醇作为一种信号，增强了抗菌抗性，并促进了邻近植物中病毒的传播。
