The Mitogen-Activated Protein Kinase Kinase VdPbs2 of Verticillium dahliae Regulates Microsclerotia Formation, Stress Response, and Plant Infection.

The Mitogen-Activated Protein Kinase Kinase VdPbs2 of Verticillium dahliae Regulates Microsclerotia Formation, Stress Response, and Plant Infection.
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大丽黄萎病的丝裂原激活蛋白激酶激酶 VdPbs2 调节微菌核形成、应激反应和植物感染

DOI:
10.3389/fmicb.2016.01532
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发表时间:
2016
影响因子:
5.2
通讯作者:
Tian C
Tian C
中科院分区:
生物学2区
文献类型:
--
作者:
Tian L;Wang Y;Yu J;Xiong D;Zhao H;Tian C

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大丽轮枝菌(Verticillium dahliae)是一种普遍存在的植物病原真菌,它形成的休眠结构称为微菌核,在黄萎病中起着至关重要的作用。VdHog1是一种丝裂原活化蛋白激酶(MAPK),控制大丽轮枝菌的微菌核形成、毒力和胁迫反应。在这项研究中,我们提出了详细的证据表明,VdHog1,VdPbs2,保守的上游组件,是一个关键的调节微菌核形成,氧化胁迫和杀菌剂的反应和植物毒力大丽轮枝菌。我们确定VdPbs2,同源的酵母MAPK激酶Pbs2。与VdHog1缺失突变体相似,VdPbs2缺失菌株表现出黑色素合成延迟和微菌核形成减少。当暴露于应力,VdPbs2突变体比野生型更敏感的渗透剂和过氧化物,但更耐细胞壁合成抑制剂和一些杀菌剂。最后,VdPbs2缺失突变体表现出降低烟树和烟草幼苗的毒力。当两者结合在一起时,我们暗示VdPbs2和VdHog1在调节微菌核形成和毒力的级联中起作用,但并非所有VdHog1依赖性功能都受VdPbs2调节。因此,这项研究提供了新的见解信号转导机制,调节微菌核的形成和发病机制,在这种真菌。
Verticillium dahliae, a ubiquitous phytopathogenic fungus, forms resting structures, known as microsclerotia that play crucial roles in Verticillium wilt diseases. VdHog1, a mitogen-activated protein kinase (MAPK), controls microsclerotia formation, virulence, and stress response in V. dahliae. In this study, we present detailed evidence that the conserved upstream component of VdHog1, VdPbs2, is a key regulator of microsclerotia formation, oxidative stress and fungicide response and plant virulence in V. dahliae. We identified VdPbs2, homologous to the yeast MAPK kinase Pbs2. Similar to the VdHog1 deletion mutant, VdPbs2 deletion strains exhibited delayed melanin synthesis and reduced formation of microsclerotia. When exposed to stresses, VdPbs2 mutants were more sensitive than the wild type to osmotic agents and peroxide, but more resistant to inhibitors of cell wall synthesis and some fungicides. Finally, VdPbs2 deletion mutants exhibited reduced virulence on smoke tree and tobacco seedlings. When taken together, we implicate that VdPbs2 and VdHog1 function in a cascade that regulates microsclerotia formation and virulence, but not all VdHog1 dependent functions are VdPbs2 regulated. This study thus provides novel insights into the signal transduction mechanisms that regulate microsclerotia formation and pathogenesis in this fungus.
DOI: 10.1007/bf00408881
发表时间: 1970-01-01
期刊: ARCHIV FUR MIKROBIOLOGIE
影响因子: --
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