中文摘要：

激活 mitogen 的蛋白激酶(MAPK ) 的效果上的全身的研究在 Setosphaeria turcica 的生长和开发上表明转导小径不仅在理解病原体的分子的机制招待相互作用而且在 S 引起的疾病的有效控制是有用的。turcica。U0126，特定的 MEK 禁止者，被用来对待 S。在病原体的无性孢子的萌芽， appressorium 生产，和致病力的观察前的 turcica。没有殖民地形态学和病原体的菌丝体生长上的 U0126 的重要效果。在有 U0126 的处理以后，菌丝体和 conidia 的生长是正常，而是无性孢子的萌芽， S 的 appressorium 生产，和致病力。在易受影响的玉米叶子的 turcica 显著地被禁止。在明确的集中范围下面， U0126 集中的增加增加无性孢子的萌芽和 appressorium 生产的抑制度，但是抑制度与处理时间的延伸减少。S 的无性孢子的萌芽， appressorium 生产，和致病力。在易受影响的玉米叶子的 turcica 被 U0126 禁止的 MAPK 小径调整。

英文摘要：

Systemic studies on the effects of mitogen-activated protein kinase （MAPK） signal transduction pathway on the growth and development of Setosphaeria turcica is helpful not only in understanding the molecular mechanism of pathogenhost interaction but also in the effective control of the diseases caused by S. turcica. U0126, the specific MEK inhibitor, is used to treat S. turcica before the observation of the conidial germination, appressorium production, and pathogenicity of the pathogen. There is no significant effect of U0126 on the colony morphology and mycelium growth of the pathogen. After treatment with U0126, the growth of mycelium and conidia are normal, but the conidial germination, appressorium production, and pathogenicity of S. turcica on susceptible corn leaves are significantly inhibited. Under the definite concentration scope, an increase in U0126 concentration increases the inhibition degree of conidial germination and appressorium production, but the inhibition degree decreases with elongation of treatment time. The conidial germination, appressorium production, and pathogenicity of S. turcica on susceptible corn leaves are regulated by the MAPK pathway inhibited by U0126.