Abstract
Aspergillus flavus and its secondary metabolites, aflatoxins (AFs), especially aflatoxin B1 (AFB1), seriously affect agricultural production, food storage, and human health. Succinyl-CoA synthase ADP-forming subunit β (SCS) is involved in the synthesis of succinate from succinyl-CoA in the tricarboxylic acid cycle. In this study, we demonstrated that SCS led to decreased aflatoxin production. Bioassay results showed that deletion of sucB (the gene coding for SCS) led to increased succinyl-CoA accumulation. Catalyzed by succinyl transferase (STA), the increased amount of succinyl-CoA in ΔsucB leads to increased levels of global protein succinylation, which causes upregulation of AFB1 accumulation in ΔsucB. To elucidate the mechanism of increased AFB1 accumulation in ΔsucB, the relevant enzymes and metabolites involved in the aflatoxin biosynthesis pathway were examined through proteome and metabolome analyses. These data illustrate that the deletion of sucB results in an increase in (1'S, 5'S) - averufin catalyzed by AflK, (1'S)-averantin catalyzed by AflD, and aflatoxin G2/O- methylsterigmatocystin catalyzed by AflP. We also found that AflM is not only upregulated but also succinylated in ΔsucB; Ach1 (acetyl-CoA hydrolase, Ach1) is downregulated in ΔsucB and interacts with SCS. Therefore, we deduce a pathway of Ach1/STA-SCS-succinylated AflM for AFB1 biosynthesis, which provides knowledge for the control of A. flavus and AFs.