On the trail of a cereal killer: recent advances in Fusarium graminearum pathogenomics and host resistance

Abstract

The ascomycete fungal pathogen Fusarium graminearum (sexual stage: Gibberella zeae) causes the devastating head blight or scab disease on wheat and barley, and cob or ear rot disease on maize. Fusarium graminearum infection causes significant crop and quality losses. In addition to roles as virulence factors during pathogenesis, trichothecene mycotoxins (e.g. deoxynivalenol) produced by this pathogen constitute a significant threat to human and animal health if consumed in respective food or feed products. In the last few years, significant progress has been made towards a better understanding of the processes involved in F. graminearum pathogenesis, toxin biosynthesis and host resistance mechanisms through the use of high-throughput genomic and phenomic technologies. In this article, we briefly review these new advances and also discuss how future research can contribute to the development of sustainable plant protection strategies against this important plant pathogen.

Figure 1

A simplified model of Fusarium graminearum–wheat interaction. Fusarium graminearum produces effectors, cell wall‐degrading enzymes (see Kikot et al., 2009 for a review) and toxins to colonize wheat. The plant responds to infection by producing defence‐related hormones, pathogenesis‐related (PR) proteins, reactive oxygen and proteins involved in cellular detoxification. Although some of the plant's responses help to restrict infection, others can potentially be exploited by the pathogen to aid pathogenicity. See text for further details. Fg, F. graminearum.

Figure 2

Examples of strategies aimed at the high‐throughput identification of novel compounds that inhibit fungal growth (A) (Schreiber et al., 2011) or induce mycotoxin biosynthesis (B) (Gardiner et al., 2009b). See text for additional details. GFP, green fluorescent protein; Fg, Fusarium graminearum.