白僵菌和昆虫宿主在表皮上的相互作用机制研究

白僵菌是一种昆虫广谱致病真菌，不同于细菌和病毒等，白僵菌通过体表感染昆虫，在外表皮上随机锚定后，需突破由几丁质和蜡质层等组成的致密结构，最后进入昆虫体内。由于感染部位的随机性，难以通过显微手段追踪其在表皮层中的动态变化，给在表皮上的相互作用研究带来困难。鉴于此，前期通过对昆虫体表固定环节进行定点侵染，发现可以方便追踪入侵的菌丝体，同时观察到表皮黑化免疫反应发生在真菌侵入到几丁质层前，以及真皮细胞的DNA复制和细胞分裂等新的相互作用现象。为此，项目拟利用定点方法感染昆虫，筛选、鉴定来源于真菌的用于破坏宿主表皮层结构的酶类；通过抑制剂添食等手段，研究黑化反应产生的活性氧是否是宿主感知侵染早期的信号；结合宿主真皮细胞转录组变化，利用遗传操作手段等解析感染期间真皮细胞的增殖机制。项目采用定点感染技术，针对白僵菌和宿主在表皮上的相互作用机制进行研究，希望为遗传改造白僵菌来提高杀虫作用效率创造条件。

As one of the entomopathogenic fungi, Beauveria bassiana （B. bassiana） is a type of important biological pesticides. Different from the infection mechanism induced by bacteria and virus, B.bassiana has to break through the tough epicuticle that is composed of chitin and wax. B.bassiana has to pinpoint and locate on the larval surface randomly during the program of surficial infection. Normally it is very hard to tell the exact site of infection, which makes it impossible to observe the movement of B. bassiana in the cuticle under microscope. Due to it, we have very limited knowledge on the interaction of fungi and host on the interaction of fungi and host on the surficial epidermis. In order to solve the problem, we develop a new method of local infection on the fixed area of a larva. Eventually we found that it is very easy to trace B. bassiana in the cuticles. We also found that the immunity of melanization happens earlier before B.bassiana entering the cuticle. In the meanwhile, DNA duplication in epidermis cells was also observedunderneath of the local infection place. All these observations are unknown and deserve further study. To this end, we are going to study the mechanisms of cuticle degradation by B.bassiana epidermis melanization and immunity response of epidermal cells to B. bassiana infection. We believe that this study is helpful to genetically rebuild B. bassiana to improve its activity on cuticle degradation and inhibition on epidermis immunity responses, which will be useful to improve the efficiency of biological pesticide by B.bassiana.