Deletion of FgHOG1 Is Suppressive to the mgv1 Mutant by Stimulating Gpmk1 Activation and Avoiding Intracellular Turgor Elevation in Fusarium graminearum
Deletion of FgHOG1 Is Suppressive to the mgv1 Mutant by Stimulating Gpmk1 Activation and Avoiding Intracellular Turgor Elevation in Fusarium graminearum
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DOI：
10.3389/fmicb.2019.01073
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发表时间：
2019-05
影响因子：
5.2
通讯作者：
Jingyi Ren;Chengliang Li;Chengyu Gao;Jin-Rong Xu;Cong Jiang;Guanghui Wang
中科院分区：
文献类型：
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作者：
Jingyi Ren;Chengliang Li;Chengyu Gao;Jin-Rong Xu;Cong Jiang;Guanghui Wang
小麦赤霉病是由禾谷镰刀菌（Fusarium graminearum）引起的小麦和大麦的重要病害。先前的研究表明，所有三个MAP激酶基因，MGV1，FgHOG1和GPMK 1，参与调节菌丝生长，有性生殖，植物感染，以及在该病原体的胁迫反应。为了确定Mgv1和FgHog1途径之间的关系，在这项研究中，我们产生并表征了mgv1 Fghog1双突变体。FgHOG1的缺失部分挽救了mgv1突变体在营养生长和细胞壁完整性方面的缺陷，但对其在植物感染和DON产生方面的缺陷没有影响。mgv1 Fghog1突变体生长速度更快，比mgv1突变体更耐受细胞壁应激。在mgv1突变体中经常观察到swelling隔室和细胞爆发，但在mgv1 Fghog1突变体中很少观察到，当用杀菌剂咯菌腈或细胞壁应激物刚果红处理时。相反，MGV1的缺失也减轻了Fghog1突变体在营养生长中的高渗敏感性。TGY检测表明mgv1突变体中FgHog1的磷酸化增加，TEY检测进一步揭示了mgv1 Fghog1双突变体中Gpmk1的活化升高，特别是在细胞壁应激条件下。总体而言，我们的数据表明，FgHOG 1的缺失部分抑制了mgv1突变体的缺陷，可能是通过影响与细胞壁完整性相关的基因，并通过过度激活Gpmk1 MAP激酶和避免细胞内膨压升高来调节。
Fusarium head blight caused by Fusarium graminearum is an important disease of wheat and barley. Previous studies have showed that all three MAP kinase genes, MGV1, FgHOG1, and GPMK1, are involved in regulating hyphal growth, sexual reproduction, plant infection, and stress responses in this pathogen. To determine the relationship between the Mgv1 and FgHog1 pathways, in this study, we generated and characterized the mgv1 Fghog1 double mutant. Deletion of FgHOG1 partially rescued the defects of the mgv1 mutant in vegetative growth and cell wall integrity but had no effects on its defects in plant infection and DON production. The mgv1 Fghog1 mutant grew faster and was more tolerant to cell wall stressors than the mgv1 mutant. Swollen compartments and cell burst were observed frequently in the mgv1 mutant but rarely in the mgv1 Fghog1 mutant when treated with fungicide fludioxonil or cell wall stressor Congo red. Conversely, the deletion of MGV1 also alleviated the hyperosmotic sensitivity of the Fghog1 mutant in vegetative growth. TGY assays indicated increased phosphorylation of FgHog1 in the mgv1 mutant, and TEY assays further revealed elevated activation of Gpmk1 in the mgv1 Fghog1 double mutant, particularly under cell wall stress conditions. Overall, our data showed that deletion of FgHOG1 partially suppressed the defects of the mgv1 mutant, possibly by affecting genes related to cell wall integrity and osmoregulation via the over-activation of Gpmk1 MAP kinase and avoiding intracellular turgor elevation.