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首页> 外文期刊>Microbiological Research >StSTE12 is required for the pathogenicity of Setosphaeria turcica by regulating appressorium development and penetration
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StSTE12 is required for the pathogenicity of Setosphaeria turcica by regulating appressorium development and penetration

机译:StSTE12是通过调节app的发育和穿透力而使黑斑病菌致病性所必需的

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In filamentous fungi, the pathogenic mitogen-activated protein kinase (PMK) pathway performs an important function in plant infection. STE12-like genes found in higher eukaryotes encode transcription factors and are regulated by the PMK pathway. However, the functions of STE12-like genes in foliar pathogens remain poorly understood. In this study, we cloned StSTE12 from Setosphaeriaturcica and investigated its functions by RNA interference. Transformantsste12-3,ste12-2 and ste12-1, in which the StSTE12 silencing efficiency increased in order, were confirmed by real time PCR. Compared with the wild-type (WT) strain, the transformants showed reduced growth rate, lighter colony color, and obviously decreased conidium production. More importantly, different to WT strain and ste12-3 with lower StSTE12silencing efficiency, ste12-1 and ste12-2 with higher StSTE12 silencing efficiency were nonpathogenic on intact leaves, but pathogenic on wounded leaves. However, the biological activity of HT-toxin from all transformants showed no difference on corn leaves. Furthermore, ste12-1 and ste12-2 did not penetrate artificial cellophane membrane and showed abnormal and delayed development appressoria. Although it could penetrate the cellophane membranes, ste12-3 formed appressoria after 48 h of inoculation more than WT. Therefore, StSTE12 was involved in vegetative growth, conidiation, appressorial development, penetration as well as the pathogenicity, but it was not related to HT-toxin biosynthesis. More interestingly, all the results suggested that StSTE12 was crucial for pathogenicity due to involvement in regulating appressoria development and penetration. (C) 2014 Elsevier GmbH. All rights reserved.
机译:在丝状真菌中,致病性促分裂原激活的蛋白激酶(PMK)途径在植物感染中起重要作用。在高级真核生物中发现的STE12样基因编码转录因子,并受PMK途径调控。然而,STE12样基因在叶病原体中的功能仍然知之甚少。在这项研究中,我们从玉米粉虱中克隆了StSTE12,并通过RNA干扰研究了其功能。实时PCR证实了StSTE12沉默效率依次提高的转化子ste12-3,ste12-2和ste12-1。与野生型(WT)菌株相比,转化子生长速度降低,菌落颜色更浅,分生孢子产生明显减少。更重要的是,与WT菌株和具有较低StSTE12沉默效率的ste12-3不同,具有较高StSTE12沉默效率的ste12-1和ste12-2对完整叶片无致病性,但对受伤叶片具有致病性。然而,来自所有转化体的HT毒素的生物学活性在玉米叶片上没有显示出差异。此外,ste12-1和ste12-2没有穿透人造玻璃纸膜,并显示出异常和延迟的发育期感。尽管它可以穿透玻璃纸膜,但在接种48小时后,ste12-3的附着力比野生型高。因此,StSTE12参与了营养生长,分生,附生发育,穿透以及致病性,但与HT毒素的生物合成无关。更有趣的是,所有结果都表明,由于参与调控食欲的发育和渗透,StSTE12对于致病性至关重要。 (C)2014 Elsevier GmbH。版权所有。

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