Distinct and combined roles of the MAP kinases of Cochliobolus heterostrophus in virulence and stress responses
Distinct and combined roles of the MAP kinases of Cochliobolus heterostrophus in virulence and stress responses
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DOI：
10.1094/mpmi-21-6-0769
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发表时间：
2008-06-01
影响因子：
3.5
通讯作者：
Horwitz, Benjamin A.
中科院分区：
文献类型：
--
作者：
Igbaria, Aeid;Lev, Sophie;Horwitz, Benjamin A.
与酵母FUS 3/KSS 1相关的致病性丝裂原活化蛋白激酶（MAPK）对于真菌的毒力是必需的，所述真菌包括异柄旋孢菌（Cochliobolus heterostrophus），一种引起南方玉米叶枯病的坏死营养型病原体。我们比较了三个MAPK基因HOG 1，MPS 1和CHK 1突变体的表型。chk 1和mps 1突变体表现出自溶外观，浅色色素沉着，毒力和分生孢子显著降低。mps 1和chk 1突变体的相似性反映在这两个MAPKs对几个基因的共调控上。与chk 1不同，mps 1突变体是雌性可育的，并形成正常外观的附着胞。HOG 1介导对高渗和氧化应激的抵抗，并且在较小程度上介导对甘油-3-磷酸酶、转醛醇酶和单糖转运蛋白的应激上调。Hog 1（而不是Mps 1或Chk 1）因渗透压升高而迅速磷酸化。hog 1突变体具有较小的附着胞，并导致玉米叶片上的病害症状减轻。令人惊讶的是，在野生型或hog 1背景下MPS 1的缺失改善了对一些胁迫的抗性。所有三种MAPK都有助于在正常和应激条件下调节中枢发育功能，如果没有来自所有三种途径的适当输入，就不能实现完全毒力。
Pathogenicity mitogen-activated protein kinases (MAPKs), related to yeast FUS3/KSS1, are essential for virulence in fungi, including Cochliobolus heterostrophus, a necrotrophic pathogen causing Southern corn leaf blight. We compared the phenotypes of mutants in three MAPK genes: HOG1, MPS1, and CHK1. The chk1 and mps1 mutants show autolytic appearance, light pigmentation, and dramatic reduction in virulence and conidiation. Similarity of mps1 and chk1 mutants is reflected by coregulation by these two MAPKs of several genes. Unlike chk1, mps1 mutants are female-fertile and form normal-looking appressoria. HOG1 mediates resistance to hyperosmotic and, to a lesser extent, oxidative stress, and is required for stress upregulation of glycerol-3-phosphate phosphatase, transaldolase, and a monosaccharide transporter. Hog1, but not Mps1 or Chk1, was rapidly phosphorylated in response to increased osmolarity. The hog1 mutants have smaller appressoria and cause decreased disease symptoms on maize leaves. Surprisingly, loss of MPS1 in a wild-type or hog1 background improved resistance to some stresses. All three MAPKs contribute to the regulation of central developmental functions under normal and stress conditions, and full virulence cannot be achieved without appropriate input from all three pathways.