多堆柄锈菌侵染玉米的细胞学及超微结构特征
Histology and ultrastructure of maize lines infected by Puccinia polysora

为明确玉米对多堆柄锈菌Puccinia polysora侵染后病理反应的细胞学特征,利用扫描和透射电镜技术分析了玉米自交系与多堆柄锈菌互作中二者的细胞变化过程。多堆柄锈菌对玉米的侵染主要以直接穿透叶片表皮侵入为主,少量可从气孔和细胞间隙侵入。接种后,病菌夏孢子在感病自交系叶片上快速并大量萌发,在叶表生长蔓延并侵入表皮组织细胞,7 d后形成夏孢子堆;在抗病自交系上,病菌萌发、菌丝生长均受到明显抑制,少量入侵的病菌也由于寄主细胞死亡而导致菌丝和夏孢子干瘪死亡。侵染早期在感病寄主细胞间隙出现菌丝并穿透细胞壁,在胞内产生分枝菌丝,此时寄主细胞结构正常;随着菌丝进一步扩展,叶绿体等结构发生紊乱,被侵染细胞逐渐死亡。在抗病自交系上,接菌24 h后寄主即出现过敏性坏死反应,侵入位点与周围细胞快速坏死,抑制菌丝生长蔓延;叶绿体中清晰可见深色颗粒状物质;72 h后细胞壁外侧产生大量致密的深色结晶体,应为与抗病反应相关的酚类物质。表明抗多堆柄锈菌的玉米材料可能存在2种抗病途径,即寄主与病菌互作中由分子识别引起的免疫反应和病菌侵入后的系统防卫反应。
Histology and ultrastructure of maize leaves infected by Puccinia polysora were analyzed by using scanning and transmission electron microscopes. The rust pathogen infection of maize leaves was mainly caused by hyphae penetrating directly through cell walls of epidermis, and some infections were initiated through stoma and intercellular space. In susceptible lines the uredospores germinated soon after inoculation and the hyphae grew fast and infected the leaf cells. At the 7th day after inoculation the uredia developed. In resistant lines the uredospores germination and hyphal growth were inhibited and a few uredospores that were successfully penetrated into host cells also die soon because of host resistance reaction in infected cells. In early stage after inoculation, the cell and organelle architectures were regular in susceptible lines. After 24 h the fungal hyphae could be found in cells; intercellular space and chloroplast structure and other organelles were deranged that caused cell death. In the resistant lines the cell structure was integrate, and the hypersensitive response appeared around the infection cells and black particles were found in the chloroplast after 24 h inoculation, which inhibited rust hyphal growth and development in the cells. After 72 h there were a lot of dense and black crystal substances accumulated in intercellular space, which should be phenolic compounds. It indicated that the resistance in P. polysora-resistant maize lines might be controlled by immune response after molecular recognition during pathogen-maize interaction and by defense system after successful infection of the pathogen.