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Generation and characterization of a Fusarium graminearum mutant overexpressing the MAPK, Mgv1

Gonzàlez-Peña Fundora D, Eranthodi A, Goyal RK, R. Subramaniam, Rampitsch C, Thakor N, Foroud NA. Generation and characterization of a Fusarium graminearum mutant overexpressing the MAPK, Mgv1. 2017 Joint Meeting of the Canadian Phytopathological Society and the Canadian Society of Agronomy. Winnipeg MB, Canada, June 18-22, 2017. Award Winning Presentation.

Abstract

Fusarium graminearum Schwabe is the causal agent of fusarium head blight (FHB), a devastating disease in wheat (Triticum aestivum L.). Three mitogen-activated protein kinase (MAPK) pathways have been identified in this fungus. MAPKs are ERK (extracellular response kinase) -like proteins that relay cellular signals through phosphorylation of various proteins. The F. graminearum MAPK, Mgv1 (MAPK for growth and virulence 1), plays a role in mycotoxin accumulation and disease development, though the latter may be related to a loss of fitness. Many of the components in the F. graminearum MAPK pathways remain unknown. With the aim of identifying downstream elements in the Mgv1 cascade, we generated F. graminearum mutants for in locus over-expression of Mgv1 under the control of a constitutive promoter. The mutants were characterized for changes in their morphocultural pattern and virulence in the spikes of six week-old Brachypodium distachyon (L) P. Beauv. plants. The growth rate of the mutants measured in potato dextrose agar Petri dishes was slower than the wild type (WT), but no difference was observed in their ability to cause disease. The abundance of phosphorylated (activated) MAPK proteins was assessed by immunoblotting with anti-phosphorylated ERK1/2 antibodies, and showed an increased level of a phosphorylated ERK-like protein (MAPK) in the mutants. Other analyses related to the putative role of Mgv1 in cell wall formation, are underway to further our understanding of Mgv1 signalling pathways. Future directions for this work include the identification of downstream targets of Mgv1 activity.

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