Transcriptomics of cereal–Fusarium graminearum interactions: what we have learned so far

Abstract

The ascomycete fungal pathogen Fusarium graminearum causes the globally important Fusarium head blight (FHB) disease on cereal hosts, such as wheat and barley. In addition to reducing grain yield, infection by this pathogen causes major quality losses. In particular, the contamination of food and feed with the F. graminearum trichothecene toxin deoxynivalenol (DON) can have many adverse short- and long-term effects on human and animal health. During the last decade, the interaction between F. graminearum and both cereal and model hosts has been extensively studied through transcriptomic analyses. In this review, we present an overview of how such analyses have advanced our understanding of this economically important plant-microbe interaction. From a host point of view, the transcriptomes of FHB-resistant and FHB-susceptible cereal genotypes, including near-isogenic lines (NILs) that differ by the presence or absence of quantitative trait loci (QTLs), have been studied to understand the mechanisms of disease resistance afforded by such QTLs. Transcriptomic analyses employed to dissect host responses to DON have facilitated the identification of the genes involved in toxin detoxification and disease resistance. From the pathogen point of view, the transcriptome of F. graminearum during pathogenic vs. saprophytic growth, or when infecting different cereal hosts or different tissues of the same host, have been studied. In addition, comparative transcriptomic analyses of F. graminearum knock-out mutants with altered virulence have provided new insights into pathogenicity-related processes. The F. graminearum transcriptomic data generated over the years are now being exploited to build a systems level understanding of the biology of this pathogen, with an ultimate aim of developing effective and sustainable disease prevention strategies.

Fusarium crown rot caused by Fusarium pseudograminearum in cereal crops: recent progress and future prospects

“…In this study, several metabolites associated with host defence were also induced. Many responses observed in wheat during F. pseudograminearum infection show similarities to those induced by related Fusarium pathogens, such as F. graminearum and F. culmorum (Kazan and Gardiner, ; Tufan et al ., ), suggesting that these related pathogens employ a common set of weaponry to colonize wheat. To the best of our knowledge, no transcription profiling of durum wheats and barley during FCR has been reported.…”

Bakery yeasts, a new model for studies in ecology and evolution

“…Strains isolated from soil, bark, fruits, fermented beverages, and vectors, such as Drosophila, bees, wasps, or humans, have been studied at the genetic level (Goddard & Greig, 2015;Jouhten, Ponomarova, Gonzalez, & Patil, 2016). Recently, whole genome studies comparing tens, hundreds, and now thousands of strains from natural and man-made environments have emerged and provided insights into yeast domestication (Almeida et al, 2015;Fay & Benavides, 2005;Gallone et al, 2016;Gonçalves et al, 2016;Legras et al, 2018;Libkind et al, 2011;Liti et al, 2009;Ludlow et al, 2016;Peter et al, 2018;Schacherer, Shapiro, Ruderfer, & Kruglyak, 2009). Yeasts from wine, sake, cocoa, coffee, and beer have undergone various domestication events.…”

Fusarium diseases: biology and management perspectives

“…The interaction between Fusarium species and cereals is one of the most studied and important pathosystems in plant pathology (Dean et al 2012). Full transcriptome analysis in the interactions between F. graminearum with cereals has been reviewed in depth recently by Kazan and Gardiner (2017). The fungal infection dynamics appear to be somewhat similar for both FHB and FCR.…”

“…Most of them appear to confer Type II resistance and in some cases by combining several mechanisms. For example, QTLs QFhb1 and QFhb2 have been associated with increased defence metabolites from the phenylpropanoid pathway, as well as activation of the JA pathway and detoxification of DON to less toxic compounds (Kazan and Gardiner 2017). QTL Qfhs.ifa5a conferred Type I resistance by enhanced lipid transfer protein, although the mechanism is unclear (Schweiger et al 2013).…”