Abstract

Wheat scab caused by Fusarium graminearum is an important disease. In a previous study, the FGK3 glycogen synthase kinase gene orthologous to mammalian GSK3 was identified as an important virulence factor. Although GSK3 orthologs are well-conserved, none of them have been functionally characterized in fungal pathogens. In this study, we further characterized the roles of FGK3 gene. The Δfgk3 mutant had pleiotropic defects in growth rate, conidium morphology, germination, and perithecium formation. It was non-pathogenic in infection assays and blocked in DON production. Glycogen accumulation was increased in the Δfgk3 mutant, confirming the inhibitory role of Fgk3 on glycogen synthase. In FGK3-GFP transformants, GFP signals mainly localized to the cytoplasm in conidia but to the cytoplasm and nucleus in hyphae. Moreover, the expression level of FGK3 increased in response to cold, H2O2, and SDS stresses. In the Δfgk3 mutant, cold, heat, and salt stresses failed to induce the expression of the stress response-related genes FgGRE2, FgGPD1, FgCTT1, and FgMSN2. In the presence of 80 mM LiCl, a GSK3 kinase inhibitor, the wild type displayed similar defects to the Δfgk3 mutant. Overall, our results indicate that FGK3 is important for growth, conidiogenesis, DON production, pathogenicity, and stress responses in F. graminearum.

Highlights

  • IntroductionThe FGK3 glycogen synthase kinase gene orthologous to mammalian GSK3 was identified as an important virulence factor

  • Wheat scab caused by Fusarium graminearum is an important disease

  • One of the mycotoxins produced by F. graminearum is trichothecene mycotoxin deoxynivalenol (DON), which is a potent inhibitor of eukaryotic protein synthesis and an important virulence factor[3]

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Summary

Introduction

The FGK3 glycogen synthase kinase gene orthologous to mammalian GSK3 was identified as an important virulence factor. In addition to components of the well-conserved cAMP signaling and MAP kinase pathways, we found 31 protein kinase genes that had not been previously characterized as important pathogenicity factors. GSK3 kinases function in hormonal signaling networks that involve brassinosteroids, abscisic acid, and auxin during growth and development[12] They play roles in floral organ development and cell expansion, as well as in responses to biotic and abiotic stresses[13]. The expression of RIM11 increases in response to DNA replication stress[18] Both YGK3 and MRK1 play roles in protein degradation and Msn2-dependent transcription[14,19]. YGK3 is required for optimal growth under zinc-limiting conditions but the MRK1 deletion mutant had no obvious defects in growth, colony morphology, and glycogen accumulation[20]

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