The research team led by Professor Jichuan Kang has elucidated the regulatory mechanism of AICAR biosynthesis in endophytic Fusarium solani.
Peer-Reviewed Publication
Updates every hour. Last Updated: 12-Sep-2025 21:11 ET (13-Sep-2025 01:11 GMT/UTC)
Endogenous AICAR (Acadesine) demonstrates significant therapeutic potential as a phase III clinical agent for the treatment of adverse cardiovascular reactions to coronary artery bypass grafting and as a phase I/II clinical agent for chronic lymphocytic leukemia. However, its biosynthetic mechanism remains poorly defined. Previous study demonstrated that AICAR was significantly enriched in the Fusarium solani mutant veAOE14, which overexpressed the global regulator VeA. In May 2025, the research team led by Professor Jichuan Kang from the Engineering and Research Center for Southwest Biopharmaceutical Resource of National Education Ministry of China, Guizhou University, published a research paper titled “MtfA, a C2H2 transcriptional regulator, negatively regulates PRPS2-mediated biosynthesis of the adenosine analogue Acadesine in Fusarium solani” in the journal Mycology.
This study elucidated, at the molecular level, the regulatory mechanism by which VeA overexpression enhances AICAR production in Fusarium solani. The team established a three-tier regulatory network model (VeA-MtfA-PRPS2) (Figure 1), laying an important foundation for the engineering of filamentous fungal strains for AICAR biosynthesis.