Mechanisms underlying the inhibitory effects of linalool on Aspergillus flavus spore germination

Biogenic volatile organic compounds hold remarkable potential for controlling fungal decay in agro- and food products. Recently, we reported that linalool, the major volatile component of the Zanthoxylum schinifolium pericarp, showed great potential as a biofumigant to control Aspergillus flavus growth in postharvest grains. In this study, the inhibitory effects of linalool on A. flavus growth in stored grains and its underlying mechanism were investigated through transcriptomic and biochemical analyses. Linalool vapor at 800 mu L/L can effectively prevent A. flavus growth in 22% moisture wheat grains. Linalool at 2 mu L/mL completely inhibited the germination of A. flavus spores, and 10 mu L/mL caused spore death. Scanning electron microscopy revealed that linalool treatment caused wrinkling and spore breakage. Transcriptomics showed that 3806 genes were significantly differentially expressed in A. flavus spores exposed to 2 mu L/mL linalool, predominantly showing enrichment regarding the ribosome, DNA replication, glutathione metabolism, peroxisome, and MAPK signaling pathways. Flow cytometry showed that linalool treatment caused hyperpolarization of mitochondrial membrane potential. 4,6-Diamidino-2-phenylindole staining indicated that linalool caused DNA fragmentation in A. flavus spores, and monodansylcadaverine staining confirmed that linalool induced autophagy in A. flavus spores. We thus propose that linalool can damage the plasma membrane, cause mitochondrial dysfunction and DNA damage, and induce autophagy in A. flavus spores. These findings considerably improve our understanding of the mechanisms underlying the inhibitory effects of linalool on A. flavus, which is crucial regarding the development of applications to prevent postharvest grain spoilage due to A. flavus infestations.

Automated summary

The study found that linalool can effectively inhibit the growth of Aspergillus flavus in stored grains by damaging the cell membrane, causing mitochondrial dysfunction, DNA damage, and inducing autophagy.