中文摘要：

【目的】通过研究促分裂原活化蛋白酶（MAPK）途径对玉米大斑病菌HT-毒素产生及生物学活性的影响，探索该途径对玉米大斑病菌致病性的调控机制。【方法】利用MAPK途径特异性抑制剂U0126分析该途径对玉米大斑病菌HT-毒素产生及活性的影响。【结果】1～20μmol·L^-1 U0126处理后，菌株01—23的HT-毒素组成和含量均发生了变化，部分组分的合成受到抑制，并诱导产生了一些新的毒素组分。1～20μmol·L^-1 U0126处理后获得的HT-毒素在感病寄主B37和B37Ht1玉米自交系上的生物学活性都受到了显著抑制，在B37玉米叶片上的抑制程度强于B37Ht1。随着U0126浓度的增加，菌株01-23的HT-毒素在玉米叶片上产生的坏死斑面积减小，抑制程度增加，但不能完全抑制病斑产生，10μmol·L^-1 U0126处理和20μmol·L^-1 U0126处理间差异不显著。【结论】MAPK信号转导途径对玉米大斑病菌HT-毒素的产生和生物学活性具有一定的调控作用，但HT-毒素的产生和活性还受其它因素影响，具有更复杂的调控机制。

英文摘要：

[ Objective ] Elucidation of the effects of MAPK signal pathway on the HT-toxin production and biological activity of Setosphaeria turcica will facilitate the mechanism study of the fungal pathogenicity. [Method] The specific MAPK signal pathway inhibitor, U0126, was used to study the regulation of MAPK pathway on HT-toxin production and activity. [Result] The composition and quantity of HT-toxin fractions extracted from isolate 01-23 were significantly altered after treatment with 1-20 μmol·L^-1 U01262 The production or quantity of some fractions was inhibited and there are some new fractions were induced. The biological activities of HT-toxin on susceptible corn inbred lines, B37 and B37Ht1, were significantly inhibited in isolate 01-23 after treatment with in 1-20 μmol·L^-1 U0126. The inhibition was stronger on B37 than on B37Ht1. The inhibition increased from 1 μmol·L^-1 to 20 μmol·L^-1 U0126 treatments, but there was no significant difference between the 10 μmol·L^-1 and 20 μmol·L^-1 U0126 treatments, indicating that U0126 could not completely inhibit the biological activity of HT-toxin. [ Conclusion ] HT-toxin production and biological activity on susceptible corn leaves are regulated by MAPK signal transduction pathway, but the mechanism of HT-toxin production and biological activity in S. turcica is complex and infected by other unknown factors.