No abstract

The antagonistic activity of volatile compounds from Streptomyces alboflavus TD‐1 against Aspergillus ochraceus were investigated in this study. Conidial germination and mycelial growth of A. ochraceus were completely suppressed after exposure to 40 and 80 g/L of wheat bran cultures of S. alboflavus TD‐1. A total of 35 compounds (relative peak area [RA] >0.10) were identified from wheat bran cultures of S. alboflavus TD‐1. Five standard compounds were purchased for the antifungal activity assay: anisole, dimethyl trisulfide, β‐pinene, benzenamine and 1,5‐cyclooctadiene. Among these, dimethyl trisulfide and benzenamine showed strong inhibitory effects on the mycelial growth of A. ochraceus. In addition, conidial and hyphal morphological abnormalities were observed in treated A. ochraceus. Scanning electron microscopy (SEM) and OD‐260 nm absorption analysis demonstrated that disruption of membrane integrity may be a possible mechanism of action for volatiles from S. alboflavus TD‐1. This study indicates that volatiles of S. alboflavus TD‐1 have tremendous potential to act as a strategy for the biocontrol of postharvest diseases in food during storage.

The acquisition of susceptibility to necrotrophy over the course of ripening is one of the critical factors limiting shelf life. In this study, phytopathology and molecular biology were employed to explore the roles of pectinase in fruit susceptibility and ripening. Solanum lycopersicum fruit softened dramatically from entirely green to 50% red, which was accompanied by a continuously high expressed SlPG2 gene. The necrotrophic fungus Botrytis cinerea further activated the expression of SlPGs and SlPMEs to accelerate cell wall disassembly, while most of the polygalacturonase inhibitor proteins encoding genes expression were postponed in ripe fruit following the pathogen attack. Pectin induced the antagonistic yeast to secrete pectinolytic enzymes to increase fruit resistance against gray mold. The activities of pathogenic pectinase of B. cinerea were correspondingly depressed in the pectin-inducible yeast enzyme elicited ripe fruit. These data suggest that pectinase is a molecular target for regulation of disease resistance during fruit ripening.

Blue light, as an important environmental factor, can regulate the production of various secondary metabolites of Monascus purpureus M9, including mycotoxin-citrinin, pigments, and monacolin K. The analysis of citrinin in Monascus M9 exposed to blue light for 0 min./d, 15 min./d, and 60 min./d showed that 15 min./d of blue light illumination could significantly increase citrinin production, while 60 min./d of blue light illumination decreased citrinin production. Analysis of long non-coding RNA (LncRNA) was performed on the transcripts of Monascus M9 under three culture conditions, and this analysis identified an lncRNA named AOANCR that can negatively regulate the mraox gene. Fermentation studies suggested that alternate respiratory pathways could be among the pathways that are involved in the regulation of the synthesis of citrinin by environmental factors. Aminophylline and citric acid were added to the culture medium to simulate the process of generating cyclic adenosine monophosphate (cAMP) in cells under illumination conditions. The results of the fermentation showed that aminophylline and citric acid could increase the expression of the mraox gene, decrease the expression of lncRNA AOANCR, and reduce the yield of citrinin. This result also indicates a reverse regulation relationship between lncRNA AOANCR and the mraox gene. A blue light signal might regulate the mraox gene at least partially through lncRNA AOANCR, thereby regulating citrinin production. Citrinin has severe nephrotoxicity in mammals, and it is important to control the residual amout of citrinin in red yeast products during fermentation. LncRNA AOANCR and mraox can potentially be used as new targets for the control of citrinin production.

Aspergillus flavus is a soilborne pathogenic fungus that poses a serious public health threat due to it contamination of food with carcinogenic aflatoxins. Our previous studies have demonstrated that benzenamine displayed strong inhibitory effects on the mycelial growth of A. flavus. In this study, we systematically investigated the inhibitory effects of benzenamine on the development, aflatoxin biosynthesis, and virulence in A. flavus, as well as the underlying mechanism. The results indicated that benzenamine exhibited great capacity to combat A. flavus at a concentration of 100 µL/L, leading to significantly decreased aflatoxin accumulation and colonization capacity in maize. The transcriptional profile revealed that 3589 genes show altered mRNA levels in the A. flavus after treatment with benzenamine, including 1890 down-regulated and 1699 up-regulated genes. Most of the differentially expressed genes participated in the biosynthesis and metabolism of amino acid, purine metabolism, and protein processing in endoplasmic reticulum. Additionally, the results brought us to a suggestion that benzenamine affects the development, aflatoxin biosynthesis, and pathogenicity of A. flavus via down-regulating related genes by depressing the expression of the global regulatory factor leaA. Overall, this study indicates that benzenamine have tremendous potential to act as a fumigant against pathogenic A. flavus. Furthermore, this work offers valuable information regarding the underlying antifungal mechanism of benzenamine against A. flavus at the level of transcription, and these potential targets may be conducive in developing new strategies for preventing aflatoxin contamination.