Contribution of peroxisomal docking machinery to mycotoxin biosynthesis, pathogenicity and pexophagy in the plant pathogenic fungus Fusarium graminearum

Abstract

Peroxisomal proliferation is highly stimulated during the biosynthesis of mycotoxins and plant infection by Fusarium graminearum. Currently, the functions of the peroxisome in these cellular processes are poorly understood. In this study, we applied genetic, cell biological and biochemical analyses to investigate the functions of the peroxisomes. We constructed targeted deletion of docking machinery components, including FgPex13, FgPex14 and the filamentous fungal specific peroxin FgPex33. Our results indicated that peroxisome dysfunction resulted in a shortage of acetyl-CoA, the precursor of trichothecene biosynthesis, and subsequently decreased deoxynivalenol (DON) production. Deletion mutants of ΔFgPex13, ΔFgPex14 or ΔFgPex33 showed an increased accumulation of endogenous reactive oxygen species (ROS) and reduced phosphorylation of MAP (Mitogen-Activated Protein) kinase FgMgv1. In addition, mutants of the docking peroxin exhibited increased sensitivity toward host oxidative bursts and cell wall integrity stress agents and reduced virulence on host plants. More importantly, we found for the first time that FgPex14 is required for pexophagy in F. graminearum. Overall, our study suggests that peroxisomes play critical roles in DON biosynthesis and virulence in F. graminearum.

Phospholipid homeostasis plays an important role in fungal development, fungicide resistance and virulence in Fusarium graminearum

“…It is well known that the earliest defense event in response to fungal infection, including in the Fusarium-host interaction, is the production of reactive oxygen species (ROS), such as H 2 O 2, by the plant cell (Lehmann et al 2015). The results of our previous studies also demonstrated that tolerance to H 2 O 2 is important for F. graminearum pathogenicity (Chen et al, 2018a;Tang et al, 2018b). In addition, the reduction in the growth of the mutants may be responsible for their attenuated virulence.…”

The b‐ZIP transcription factor FgTfmI is required for the fungicide phenamacril tolerance and pathogenecity in Fusarium graminearum

“…It is well known that the earliest defense event in response to the fungal infection is the production of reactive oxygen species (ROS) such as H 2 O 2 by the plant cell, including the Fusarium –host interaction . Moreover, oxidative stress response regulation has been shown to be involved in the pathogenecity of F. graminearum . Thus, the increased sensitivity to oxidative stress may also lead to the attenuated virulence of ΔFgTfmI mutant.…”

“…62,63 Moreover, oxidative stress response regulation has been shown to be involved in the pathogenecity of F. graminearum. 18,19,64 Thus, the increased sensitivity to oxidative stress may also lead to the attenuated virulence of ΔFgTfmI mutant. Furthermore, the transcriptome data indicated that FgTfmI also positively regulated the expression of virulence-related genes, including FgCHS8, FgSWD2 and other 20 genes (Supplementary Data 3, Table S2).…”

“…Recently, we found that the class I myosin (also known as myosin‐5) in F. graminearum , FgMyo1, interacts with Tri1 and actin, and participates in DON‐toxisome formation . Environmental and endogenous factors have been shown to dramatically influence DON biosynthesis, such as nitrogen source, pH and reactive oxygen species . Moreover, application of several fungicides including carbendazim and azoles at sub‐lethal concentration can trigger DON biosynthesis .…”

“…9 Environmental and endogenous factors have been shown to dramatically influence DON biosynthesis, such as nitrogen source, 16 pH 17 and reactive oxygen species. 18,19 Moreover, application of several fungicides including carbendazim and azoles at sub-lethal concentration can trigger DON biosynthesis. 9,[20][21][22][23] Therefore, it is urgent to develop new fungicides that can suppress F. graminearum infection and also inhibit mycotoxin biosynthesis simultaneously.…”