The Sensor Proteins BcSho1 and BcSln1 Are Involved in, Though Not Essential to, Vegetative Differentiation, Pathogenicity and Osmotic Stress Tolerance in Botrytis cinerea

The Sensor Proteins BcSho1 and BcSln1 Are Involved in, Though Not Essential to, Vegetative Differentiation, Pathogenicity and Osmotic Stress Tolerance in Botrytis cinerea
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DOI:
10.3389/fmicb.2019.00328
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发表时间:
2019-02
影响因子:
5.2
通讯作者:
Weichao Ren;Na Liu;Yalan Yang;Qianqian Yang;Changjun Chen;Qingli Gao
Weichao Ren;Na Liu;Yalan Yang;Qianqian Yang;Changjun Chen;Qingli Gao
中科院分区:
生物学2区
文献类型:
--
作者:
Weichao Ren;Na Liu;Yalan Yang;Qianqian Yang;Changjun Chen;Qingli Gao

文献摘要

相似文献

高渗透甘油(HOG)信号通路属于丝裂原激活蛋白激酶(MAPK)级联,调节生物体对多种细胞外刺激的反应。跨膜蛋白 Sho1 和 Sln1 在酿酒酵母中充当 HOG 途径的生物传感器。在本研究中,我们研究了 BcSHO1 和 BcSLN1 在灰霉病菌 Botrytis cinerea 中的生物学功能。靶基因删除表明 BcSHO1 和 BcSLN1 对于菌丝生长、分生孢子和菌核形成都很重要。 BcSHO1和BcSLN1双缺失突变体ΔBcSln1-Sho1比ΔBcSho1和野生型(WT)菌株产生更多但更小的菌核,而ΔBcSln1在所有测试的培养基上均未能形成菌核,而是形成大量分生孢子。感染试验显示,ΔBcSln1-Sho1的毒力显着下降,但ΔBcSho1或ΔBcSln1与WT株无差异。此外,ΔBcSln1-Sho1 通过负向调节 BcSak1(酵母 Hog1)的磷酸化来表现出对渗透胁迫的抵抗力。突变体的所有表型缺陷均通过靶基因互补得到恢复。这些结果表明,BcSHO1 和 BcSLN1 在灰霉病菌真菌发育、发病机制和渗透胁迫反应的调节方面具有一些功能冗余。
High-osmolarity glycerol (HOG) signaling pathway belongs to mitogen-activated protein kinase (MAPK) cascades that regulate responses of organism to diverse extracellular stimuli. The membrane spanning proteins Sho1 and Sln1 serve as biosensors of HOG pathway in Saccharomyces cerevisiae. In this study, we investigated the biological functions of BcSHO1 and BcSLN1 in the gray mold fungus Botrytis cinerea. Target gene deletion demonstrated that both BcSHO1 and BcSLN1 are important for mycelial growth, conidiation and sclerotial formation. The BcSHO1 and BcSLN1 double deletion mutant ΔBcSln1-Sho1 produced much more, but smaller sclerotia than ΔBcSho1 and the wild-type (WT) strain, while ΔBcSln1 failed to develop sclerotia on all tested media, instead, formed a large number of conidia. Infection tests revealed that the virulence of ΔBcSln1-Sho1 decreased significantly, however, ΔBcSho1 or ΔBcSln1 showed no difference with the WT strain. In addition, ΔBcSln1-Sho1 exhibited resistance to osmotic stress by negatively regulating the phosphorylation of BcSak1 (yeast Hog1). All the phenotypic defects of mutants were recovered by target gene complementation. These results suggest that BcSHO1 and BcSLN1 share some functional redundancy in the regulation of fungal development, pathogenesis and osmotic stress response in B. cinerea.