Identification of ABC Transporter Genes of Fusarium graminearum with Roles in Azole Tolerance and/or Virulence

Abstract

Fusarium graminearum is a plant pathogen infecting several important cereals, resulting in substantial yield losses and mycotoxin contamination of the grain. Triazole fungicides are used to control diseases caused by this fungus on a worldwide scale. Our previous microarray study indicated that 15 ABC transporter genes were transcriptionally upregulated in response to tebuconazole treatment. Here, we deleted four ABC transporter genes in two genetic backgrounds of F. graminearum representing the DON (deoxynivalenol) and the NIV (nivalenol) trichothecene chemotypes. Deletion of FgABC3 and FgABC4 belonging to group I of ABC-G and to group V of ABC-C subfamilies of ABC transporters, respectively, considerably increased the sensitivity to the class I sterol biosynthesis inhibitors triazoles and fenarimol. Such effects were specific since they did not occur with any other fungicide class tested. Assessing the contribution of the four ABC transporters to virulence of F. graminearum revealed that, irrespective of their chemotypes, deletion mutants of FgABC1 (ABC-C subfamily group V) and FgABC3 were impeded in virulence on wheat, barley and maize. Phylogenetic context and analyses of mycotoxin production suggests that FgABC3 may encode a transporter protecting the fungus from host-derived antifungal molecules. In contrast, FgABC1 may encode a transporter responsible for the secretion of fungal secondary metabolites alleviating defence of the host. Our results show that ABC transporters play important and diverse roles in both fungicide resistance and pathogenesis of F. graminearum.

A Novel Zn2-Cys6 Transcription Factor AtrR Plays a Key Role in an Azole Resistance Mechanism of Aspergillus fumigatus by Co-regulating cyp51A and cdr1B Expressions

“…It has been demonstrated in many fungi, including plant and human pathogens, that certain ABC transporter genes were up-regulated in response to azole treatment, and loss of genes encoding PDR-type ABC transporters resulted in hypersensitivity to azoles [35–37]. According to phylogenetic analysis, the A .…”

The evolutionary origins of pesticide resistance

“…Efflux transporters over‐expressed in azole fungicide‐adapted laboratory strains of Fusarium graminearum contribute to virulence: this may be through the removal of plant‐derived antifungal compounds, or through the secretion of fungal secondary metabolites (Abou Ammar et al, ). ATP‐binding cassette (ABC) and major facilitator superfamily (MFS) transporter proteins confer self‐resistance of the plant pathogen Cercospora nicotianae to cercosporin, a toxin produced by the fungus itself to attack host plants (Beseli et al, ).…”

Two genes in a pathogenicity gene cluster encoding secreted proteins are required for appressorial penetration and infection of the maize anthracnose fungus Colletotrichum graminicola

“…Plants used for inoculation included maize cultivars Mikado (KWS Saat AG, Einbeck, Germany), B73 (ARS-USDA, Ames, Iowa, USA), Farmtop (FarmSaat AG, Everswinkel, Germany) and Golden Jubilee (Territorial Seed Company, Cottage Grove, OR). Plants grew in the greenhouse and in environmentally controlled growth chambers as described (Behr et al, 2010;Abou Ammar et al, 2013).…”

“…Virulence of C. graminicola strains was assayed employing detached maize leaves (Horbach et al, 2009;Oliveira-Garcia and Deising, 2013). In addition, a quantitative stalk infection assay was used (Abou Ammar et al, 2013). For the latter, 10,000 falcate conidia suspended in 10 μl of 0.02% Tween 20 were pipetted into a small cavity made at the first internode of stalks of 6-week-old maize cultivar Mikado plants.…”