FgRad50 Regulates Fungal Development, Pathogenicity, Cell Wall Integrity and the DNA Damage Response in Fusarium graminearum.

Chengqi Zhang,Kejian Ding,Qiong Wan,Xuexiang Ren,Xintong Wang,Li Chen

doi:10.3389/fmicb.2019.02970

Abstract

Rad50 is a member of the double strand break repair epistasis group of proteins that play important roles in regulating DNA damage checkpoint signaling, telomere maintenance, homologous recombination and non-homologous end-joining in eukaryotes. However, the function of Rad50 in fungal plant pathogens remains unknown. In this study, we report the functional investigation of FgRad50 in the wheat head blight pathogen Fusarium graminearum. FgRad50 is an ortholog of Saccharomyces cerevisiae Rad50 that could restore the sensitivity of the yeast Rad50 mutant to DNA damage agents. The FgRad50 deletion mutant (ΔFgRad50) exhibited defective vegetative growth, asexual/sexual development and virulence, as well as disrupted deoxynivalenol biosynthesis. Moreover, deletion of FgRad50 resulted in hypersensitivity to DNA damage agents. Unexpectedly, FgRad50 plays a key role in responses to cell wall-damaging agents by negatively regulating phosphorylation of FgMgv1, a MAP kinase in the cell wall integrity (CWI) pathway. Taken together, these results suggest that FgRad50 plays critical roles in fungal development, virulence and secondary metabolism in F. graminearum, as well as CWI and the DNA damage response.

Highlights

Fusarium head blight (FHB) is a destructive disease of wheat and barley caused by Fusarium graminearum species complex that occurs worldwide
These results indicate that FgRad50 and yeast Rad50 share a conserved function associated with DNA damage responses
In order to investigate the possible role of FgRad50 in maintaining cell wall integrity (CWI), we examined the sensitivity of FgRad50 cells to the cell membrane-damaging agent sodium dodecyl sulphate (SDS) and the cell wall-damaging agents congo red (CR) and calcofluor white (CFW)

Summary

Introduction

Fusarium head blight (FHB) is a destructive disease of wheat and barley caused by Fusarium graminearum species complex that occurs worldwide. This pathogen can lead to severe yield losses and produces mycotoxins such as deoxynivalenol (DON) and zearalenones (ZEN) that are harmful to human and animal health (Pestka and Smolinski, 2005; Kimura et al, 2007). The main strategy for controlling FHB remains the application of chemical fungicides, such as carbendazim, tebuconazole, and phenamacril (JS399-19) which has been marketed for controlling FHB in China, Li et al (2008), McMullen et al (2012). Previous studies showed that C14α-methylases encoded by CYP51 genes are the targets of tebuconazole (Becher et al, 2011; Liu et al, 2011).

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