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大豆疫霉菌对大豆下胚轴侵染过程的细胞学研究
引用本文:左豫虎,康振生,黄丽丽,韩青梅.大豆疫霉菌对大豆下胚轴侵染过程的细胞学研究[J].植物病理学报,2005,35(3):235-241.
作者姓名:左豫虎  康振生  黄丽丽  韩青梅
作者单位:1 西北农林科技大学植保学院, 陕西杨凌 712100;2 黑龙江八一农垦大学植物科技学院, 大庆 163319
基金项目:国家重点基础研究发展计划(973计划),国家自然科学基金,黑龙江省高校骨干教师创新能力资助计划
摘    要: 接种后1.5~24h,用光镜和电镜研究了2个大豆品种与大豆疫霉菌Ps411的亲和性和非亲和性互作。观察结果表明,大豆疫霉菌对大豆下胚轴的侵染过程可分为侵入前、侵入、皮层组织中的扩展和进入维管束组织4个连续阶段。大豆下胚轴接种后在25℃保湿培养,1.5h后游动孢子即形成休止孢并萌发产生附着孢,3h后侵入表皮细胞,6h后进入皮层组织,24h后进入维管束组织。病原菌主要以侵染菌丝直接侵入表皮,表皮细胞间隙是主要侵入部位。皮层细胞是病原菌定殖和发展的主要场所,胞间菌丝侵入皮层细胞并形成吸器。在菌丝与寄主细胞接触部位的寄主细胞壁与质膜之间常有胞壁沉积物的形成。在抗病品种上病菌的侵染事件与感病品种基本一致,但不能形成正常的吸器,胞壁沉积物明显多于感病品种,菌丝在寄主组织内的扩展明显受到抑制。利用β-1,3-葡聚糖免疫金标记单克隆抗体进行的免疫细胞化学的研究表明,胞壁沉积物内含有大量的β-1,3-葡聚糖,在大豆疫霉菌菌丝壁中也存在β-1,3-葡聚糖。以上结果表明,病原菌的侵染可诱导抗病寄主细胞内β-1,3-葡聚糖迅速的合成与积累、并形成胞壁沉积物,以抵御病菌的侵染与扩展。

关 键 词:大豆疫霉菌  大豆  侵染过程  超微结构  β-1  3-葡聚糖  
文章编号:0412-0914(2005)03-0235-07
修稿时间:2004年7月26日

Cytology on infection process of soybean hypocotyls by Phytophthora sojae
ZUO Yu-hu,KANG Zhen-sheng,HUANG Li-li,HAN Qing-mei.Cytology on infection process of soybean hypocotyls by Phytophthora sojae[J].Acta Phytopathologica Sinica,2005,35(3):235-241.
Authors:ZUO Yu-hu  KANG Zhen-sheng  HUANG Li-li  HAN Qing-mei
Institution:1 College of Plant Protection, Northwest A & F University, Yangling Shaanxi 712100, China;2 College of Plant Science and Technology, Heilongjiang August First Land Reclamation University, Daqing 163319, China
Abstract:Compatible and incompatible interactions of two soybean cultivars with isolate Ps411 of P. sojae were examined by light and electron microscopy, after inoculation 1.5 to 24 h. The infection process of soybean hypocotyls by P. sojae consists of 4 stages, i.e. pre-infection, penetration of epidermal cell, spreading in the cortex and colonization of vascular tissue. Zoospore encystment, germination and infection occurred within 1.5 h in all interactions. The fungus penetrated into epidermal cells after 3 h inoculation, entered cortex 6 h and reached vascular tissue by 24 h postinoculation. P. sojae penetrated epidermis by infection hyphae at the junction between periclinal host cell walls. The cortexes were very important for colonization and development for the pathogen. Intercellular hyphae penetrated cortical cell and formed haustoria in it. Cell wall appositions were usually formed in host cell adjacent to hyphae. The infection process in incompatible interactions was approximately the same as in compatible interaction. However, the incompatible interaction was charac-terized by the formation of abnormal haustoria, abundant wall appositions, inhibition of hyphael extention and absence of vascular tissue colonization in host cells. The resistant cultivars were not killed by P. sojae. Using immunogold labeling with monoclonal antibody against β-1,3-glucan and secondary antibody, β-1,3-glucan was localized in cell wall appositions and fungal cell walls. This result indicates that the formation and accumulation of the β-1,3-glucan was induced to constitute structure defense response in the incompatible interactions between soybean hypocotyls and P. sojae.
Keywords:Phytophthora sojae  soybean  infection process  ultrastructure  β-1  3-glucan  
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