有害疣孢霉菌与双孢蘑菇的互作关系

通过菌丝对峙、双重培养，以及对发病双孢蘑菇子实体的显微观察，探讨有害疣孢霉菌Mycogone perniciosa（MP0012）与双孢蘑菇Agaricus bisporus（As2796）之间的互作关系。结果表明，在菌丝对峙生长阶段有害疣孢霉菌菌丝不侵入双孢蘑菇菌丝体内，两者可交叉生长，对双孢蘑菇生长影响不显著；对峙与双重培养均显示有害疣孢霉菌菌丝会产生对双孢蘑菇菌丝生长的抑制作用的挥发性物质，造成双孢蘑菇菌丝扭结断裂。同时试验证实了双孢蘑菇菌丝会促进有害疣孢霉菌厚垣孢子的产生和萌发、菌丝生长和发育。侵染实验结果表明，有害疣孢霉菌可直接侵染双孢蘑菇子实体，引起双孢蘑菇子实体病害；对罹病子实体显微观察结果发现，发病前期双孢蘑菇子实体表面长出绒毛状病原菌丝，菌柄中空，菌褶褐变腐烂并长出病原菌丝；发病中期双孢蘑菇子实体内菌丝组织会出现萎缩裂解现象，在近有害疣孢霉菌菌丝一侧的双孢蘑菇子实体菌丝细胞壁被降解；发病后期双孢蘑菇子实体菌丝组织基本消失。由此初步判断有害疣孢霉菌对双孢蘑菇的寄生类型偏向于死体营养型。

The interactions between Mycogone perniciosa and Agaricus bisporus

Mycogone perniciosa MP0012 and Agaricus bisporus AS2796 were used as experimental materials, and the interactions between their mycelia of Mycogone perniciosa MP0012 and Agaricus bisporus AS2796 were investigated through confrontation culture, double culture and microscopic examination．The results of the confrontation culture test revealed that the mycelia of the two species were initially able to tolerate each other without any visually evident growth inhibition. However, both confrontation and double culture tests suggested that the volatile compounds produced by M. perniciosa eventually evidently inhibited the growth of A. bisporus and resulted in a large number of mycelial knots and fractures forming in the latter. On the other hand, the mycelia of A. bisporus had growth-promoting effects on M. perniciosa. The infection experiment revealed that M. perniciosa could directly infected and caused an infection in A. bisporus. Observations of the fruiting body of infected A. bisporus revealed that the mycelium of M. perniciosa appeared during the early stages of infection and was responsible for stalk hollowing and gill browning. During the intermediate stage, the mycelia of A. bisporus began to shrink and crack, while the cell walls in the vicinity of M. perniciosa exhibited signs of degradation. During the final stages of infection, the mycelia of A. bisporus almost completely disappeared. So it can be concluded that this pattern of parasitism is consistent with what is exhibited by necrotrophic mycoparasites.