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

Weichao Ren,Changjun Chen,Na Liu,Qianqian Yang,Yalan Yang,Qingli Gao

doi:10.3389/fmicb.2019.00328

Abstract

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.

Highlights

IntroductionBotrytis cinerea (teleomorph: Botryotinia fuckeliana) is a devastating fungal pathogen that causes gray mold on over 500 plant species worldwide (Fillinger and Elad, 2016)
Botrytis cinerea is a devastating fungal pathogen that causes gray mold on over 500 plant species worldwide (Fillinger and Elad, 2016)
The sclerotial germination of BcSho1 and BcSln1-Sho1 was severely delayed compared with that of B05.10 (Figure 4D). These results indicate that BcSLN1 is essential for sclerotial development in B. cinerea, while BcSHO1 is less important, and there exists cooperative regulation between them

Summary

Introduction

Botrytis cinerea (teleomorph: Botryotinia fuckeliana) is a devastating fungal pathogen that causes gray mold on over 500 plant species worldwide (Fillinger and Elad, 2016). The Roles of BcSho and BcSln in Botrytis cinerea the most effective strategy for controlling gray mold, many kinds of fungicides have lost effectiveness due to resistance development (Hu et al, 2016; Weber and Hahn, 2019). Signals from the Sho and Sln branches are independently transduced by unique components and converge to activate the MAPK kinase (MAPKK) Pbs. The Sln branch activates two partially redundant MAPKKs, Ssk, and Ssk through Ypd and Ssk to Reiser et al (2003), Pbs could be activated by any of the three osmoresponsive MAPKKKs (Ste, Ssk, or Ssk22), the activated Pbs phosphorylates the MAPK Hog, resulting in the translocation of Hog to nucleus and regulates the expression of responsible genes (Figure 1A; O’Rourke and Herskowitz, 2003)

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