Fig. 6: A proposed model for the molecular mechanism of FgSfp1-deficiency impacts on mycotoxin DON biosynthesis and its accumulation.

The grey circle represents FgSfp1-deficiency condition. At nutrient-sufficient conditions suitable for mycelia growth, FgSfp1 can be activated by FgTOR pathway, binding to the promoter region provoke downstream RiBi gene transcription. Meantime, FgSfp1 controls the pre-rRNA maturation rhythm interacting with a main component for rRNA 2′-O-methylation facilitating ribosomal biogenesis, FgNop1. On the contrary, FgSfp1 deprivation leads to ribosome biogenesis pace slowdown, transcripts of TRI-cluster genes translation process will be impeded. FgSfp1 orchestrates DON biosynthesis activities by coordinating the expression of ribosome assembly factor genes and directly interacting with RNA posttranscriptional 2′-O-methylation modification factor FgNop1, functions as a pivotal executor in Fusarium graminearum.