【作者】 王艳辉；

【导师】 董金皋； 李广敏； 商振清；

【作者基本信息】 河北农业大学 ， 植物学， 2003， 硕士

【摘要】 玉米大斑病（Northern Leaf Blight of Corn）是世界各地玉米的重要叶部病害，玉米大斑病菌所产毒素（HT-毒素）既是玉米大斑病菌的主要致病因子，又是诱导植物防卫反应的激发子。对HT-毒素的研究，将有助于研究玉米大斑病菌引发玉米抗病/感病的分子机制。 本试验用玉米大斑病菌不同小种毒素来处理不同Ht基因玉米植株后探讨钙调素（calmodulin,CaM）的变化。结果发现，在14个亲和组合的植株中，CaM在2～6h内迅速上升达到较高值，多数在数小时后下降，曲线呈现单峰状。而在另外14个非亲和组合的植株中，CaM在2～4小时内也迅速上升，但不久又迅速下降，此后会再次上升，总体上CaM曲线呈现升高—下降—再升高的趋势。 用HT-毒素胁迫针刺后的玉米离体叶片，非亲和组合的叶片上会出现较小的R（resistant）型病斑，亲和组合的叶片中出现较大的S（susceptible）型病斑。这是因为非亲和组合的叶片在受到HT-毒素胁迫后，激发了体内的抗病机制，产生了可阻碍毒素进一步扩展的物质，因而病斑较小。可见病斑的大小及类型可作为植株抗病/感病反应发生的指标。选取4个不同品种的玉米，用CaM抑制剂三氟啦嗪（Trifluoperazine,TFP）预处理离体叶片6～8h后，针刺叶片形成伤口，在伤口处滴加属于非亲和组合的HT-毒素后，叶片上出现S型病斑，标志玉米的抗病反应的激发受到了阻碍。 Ca²⁺-CaM途径是植物抗病反应的信号转导途径之一。在此途径中，植物受到刺激后，CaM含量明显上升，然后由Ca²⁺-CaM激活下游的抗病反应。CaM抑制剂可专一地抑制CaM活性，使信号转导受阻，抗病反应不能发生或延迟发生。在本试验中，玉米植株在受到毒素胁迫后，体内CaM迅速上升；而施用TFP后，在非亲和组合中未出现R型病斑，标志植株的抗病反应受到了抑制。由此证明，由玉米大斑病曲毒素激发的防卫反应的信号转导途径与CaM密切相关。更多还原

【Abstract】 The Northern Leaf Blight of Corn is one of the important leaf diseases of corn in the world. HT-toxin, which produced by Exserohilum turcicum, is not only a major toxigenic factor but also the elicitor to stimulate the defensive reaction of corn. To study the toxin will help to understand the moleculer of mechanism defensive reaction of plant.The change of CaM content in corn plants with different Ht gene, which were treated by HT-toxins from different turcicum races, had been studied. The experiment results showed that the CaM content in corn increased quickly at early 2~6 hours then decreased gradually after several hours in 14 compatible combinations and 14 controls treatments. But there was second ascending peak after the first ascending peak in incompatible combinations.There were different type lesions on corn leaves treated by HT-toxins in vitro through the acupuncture-wound bioassay: S type (susceptible) lesion-large and dark-green on compatible leaves but R type (resistant) lesion-small and yellow on incompatible leaves. This difference may be due to the defensive system could be stimulated or some substances could be produced which restrict the toxin’s spreading and lead to small lesion spot in incompatible plant but not in compatible plant. The R type disease spot could act as a symbol of resistant reaction. The interesting thing is that the R lesion type would turn into S type while incompatible leaves treated by toxin after exposing to Trifluoperazine (TFP, one of the depressor of CaM). This suggested that TFP could hinder the resistant reaction, in other word, CaM played aimportant role in signal transduction of resistant reaction.Ca2+-CaM was one of the major resistant signal transductions in plant, which typical character was CaM content in plant could go up evidently after being stimulated and activated downriver resistant reaction, the depressor of CaM could inhibit the activity of CaM specificity and restrain or delay defensive reaction. In the interactions between com plants with different Ht-gene and HT-toxins from different turcicum races, CaM’ quick changing and action of CaM depressor shared similar character. It was conclusion that the CaM was related to the plant defensive reaction.更多还原