Shi Jiale, Jiang Mengyun, Wang He, Luo Zhi, Guo Yanjing, Chen Ying, Zhao Xiaoxi, Qiang Sheng, Strasser Reto Jörg, Kalaji Hazem M, Chen Shiguo
Weed Research Laboratory, Nanjing Agricultural University, Nanjing 210095, China.
Bioenergetics Laboratory, University of Geneva, CH-1254 Jussy, Geneva, Switzerland.
Plants (Basel). 2023 Feb 2;12(3):665. doi: 10.3390/plants12030665.
Mycotoxins are one of the most important sources for the discovery of new pesticides and drugs because of their chemical structural diversity and fascinating bioactivity as well as unique novel targets. Here, the effects of four mycotoxins, fumagillin, mevastatin, radicicol, and wortmannin, on photosynthesis were investigated to identify their precise sites of action on the photosynthetic apparatus of . Our results showed that these four mycotoxins have multiple targets, acting mainly on photosystem II (PSII). Their mode of action is similar to that of diuron, inhibiting electron flow beyond the primary quinone electron acceptor (Q) by binding to the secondary quinone electron acceptor (Q) site of the D1 protein, thereby affecting photosynthesis. The results of PSII oxygen evolution rate and chlorophyll (Chl) fluorescence imaging suggested that fumagillin strongly inhibited overall PSII activity; the other three toxins also exhibited a negative influence at the high concentration. Chl fluorescence kinetics and the JIP test showed that the inhibition of electron transport beyond Q was the most significant feature of the four mycotoxins. Fumagillin decreased the rate of O evolution by interrupting electron transfer on the PSII acceptor side, and had multiple negative effects on the primary photochemical reaction and PSII antenna size. Mevastatin caused a decrease in photosynthetic activity, mainly due to the inhibition of electron transport. Both radicicol and wortmannin decreased photosynthetic efficiency, mainly by inhibiting the electron transport efficiency of the PSII acceptor side and the activity of the PSII reaction centers. In addition, radicicol reduced the primary photochemical reaction efficiency and antenna size. The simulated molecular model of the four mycotoxins' binding to D1 protein indicated that the residue D1-Phe265 is their common site at the Q site. This is a novel target site different from those of commercial PSII herbicides. Thus, the interesting effects of the four mycotoxins on PSII suggested that they provide new ideas for the design of novel and efficient herbicide molecules.
由于霉菌毒素具有化学结构多样性、迷人的生物活性以及独特的新靶点,它们是发现新型农药和药物的最重要来源之一。在此,研究了四种霉菌毒素,即烟曲霉素、美伐他汀、放线菌酮和渥曼青霉素对光合作用的影响,以确定它们在光合装置上的确切作用位点。我们的结果表明,这四种霉菌毒素具有多个靶点,主要作用于光系统II(PSII)。它们的作用模式与敌草隆相似,通过与D1蛋白的次级醌电子受体(Q)位点结合,抑制初级醌电子受体(Q)之后的电子流动,从而影响光合作用。PSII放氧速率和叶绿素(Chl)荧光成像结果表明,烟曲霉素强烈抑制整体PSII活性;其他三种毒素在高浓度时也表现出负面影响。Chl荧光动力学和JIP测试表明,四种霉菌毒素对Q之后电子传递的抑制是最显著的特征。烟曲霉素通过中断PSII受体侧的电子传递降低了O释放速率,并对初级光化学反应和PSII天线大小产生多种负面影响。美伐他汀导致光合活性下降,主要是由于电子传递受到抑制。放线菌酮和渥曼青霉素都降低了光合效率,主要是通过抑制PSII受体侧的电子传递效率和PSII反应中心的活性。此外,放线菌酮降低了初级光化学反应效率和天线大小。四种霉菌毒素与D1蛋白结合的模拟分子模型表明,残基D1-Phe265是它们在Q位点的共同位点。这是一个与商业PSII除草剂不同的新靶点位点。因此,四种霉菌毒素对PSII的有趣作用表明,它们为设计新型高效除草剂分子提供了新思路。