Rhizoctonia solani anastomosis group 7 (AG-7) is the major pathogen causing soybean seedling disease in Taiwan, and AG-7 exhibits pencycuron resistance. Pencycuron is one of the few widely registered fungicides with both its mode of action and detoxification mechanism remaining unclear.
M.S. student Yi-Jyun Chen measured the pencycuron sensitivity of AG-7 isolates and found that isolate No.214 was highly sensitive, while isolate No.213 was resistant. Using PacBio Sequel IIe sequencing, the No.213 and No.214 genomes were reassembled. Isolate No.213 was found to have a diploid genome, consistent with previous reports; whereas isolate No.214 exhibited a pentaploid genome with whole-genome duplication. Transcriptome analysis revealed that gene expression in isolate No.214 was deeply affected under pencycuron treatment, which may be attributed to its high genomic complexity. In contrast, only a few genes were upregulated in isolate No.213, including a cytochrome P450 gene (RsCYP-1). Due to the inconvenient transformation in R. solani and the pencycuron resistance in yeast, heterologous expression was performed in the brown rot fungus Monilinia fructicola to demonstrate that RsCYP-1 can enhance pencycuron resistance.
This study provided the first molecular evidence of a fungal detoxification mechanism to pencycuron, and the results have been published in iScience, a journal by Cell Press. link
