Dysfunction of FadA-cAMP signalling decreases Aspergillus flavus resistance to antimicrobial natural preservative Perillaldehyde and AFB1 biosynthesis.

Aspergillus flavus is an opportunistic fungal pathogen that colonizes agriculture crops with aflatoxin contamination. We found that Perillaldehyde (PAE) effectively inhibited A. flavus viability and aflatoxin production by inducing excess reactive oxygen species (ROS). Transcriptome analysis indicated that the Gα protein FadA was significantly induced by PAE. Functional characterization of FadA showed it is important for asexual development and aflatoxin biosynthesis by regulation of cAMP-PKA signalling. The ΔfadA mutant was more sensitive to PAE, while ΔpdeL and ΔpdeH mutants can tolerate excess PAE compared to wild-type A. flavus. Further RNA-sequence analysis showed that fadA was important for expression of genes involved in oxidation-reduction and cellular metabolism. The flow cytometry and fluorescence microscopy demonstrated that ΔfadA accumulated more concentration of ROS in cells, and the transcriptome data indicated that genes involved in ROS scavenging were downregulated in ΔfadA mutant. We further found that FadA participated in regulating response to extracellular environmental stresses by increasing phosphorylation levels of MAPK Kinase Slt2 and Hog1. Overall, our results indicated that FadA signalling engages in mycotoxin production and A. flavus resistance to antimicrobial PAE, which provide valuable information for controlling this fungus and AF biosynthesis in pre- and postharvest of agricultural crops.