Tian Longyan, Wang Yonglin, Yu Jun, Xiong Dianguang, Zhao Hengjun, Tian Chengming
The Key Laboratory for Silviculture and Conservation of Ministry of Education, College of Forestry, Beijing Forestry University Beijing, China.
Front Microbiol. 2016 Sep 27;7:1532. doi: 10.3389/fmicb.2016.01532. eCollection 2016.
, 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 . 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 . We identified VdPbs2, homologous to the yeast MAPK kinase Pbs2. Similar to the deletion mutant, deletion strains exhibited delayed melanin synthesis and reduced formation of microsclerotia. When exposed to stresses, 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, 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.
一种无处不在的植物病原真菌,会形成休眠结构,即微菌核,其在黄萎病中起着关键作用。VdHog1是一种丝裂原活化蛋白激酶(MAPK),可控制微菌核的形成、致病性以及对压力的反应。在本研究中,我们提供了详细证据表明,VdHog1保守的上游组分VdPbs2是微菌核形成、氧化应激、杀菌剂反应以及植物致病性的关键调节因子。我们鉴定出VdPbs2与酵母MAPK激酶Pbs2同源。与酵母缺失突变体类似,VdPbs2缺失菌株表现出黑色素合成延迟以及微菌核形成减少。当暴露于压力下时,VdPbs2突变体比野生型对渗透剂和过氧化物更敏感,但对细胞壁合成抑制剂和一些杀菌剂更具抗性。最后,VdPbs2缺失突变体在黄栌和烟草幼苗上表现出致病性降低。综合来看,我们认为VdPbs2和VdHog1在一个级联反应中发挥作用,调节微菌核的形成和致病性,但并非所有VdHog1依赖的功能都受VdPbs2调节。因此,本研究为调节该真菌微菌核形成和发病机制的信号转导机制提供了新的见解。