BcatrB mediates pyrimethanil resistance in Botrytis cinerea revealed by transcriptomics analysis

Gray mold, caused by Botrytis cinerea, poses an escalating threat to ginseng production in China. Excessive application of chemical fungicides has resulted in severe resistance development. To elucidate the resistance mechanism of B. cinerea to pyrimethanil, transcriptomic comparisons were conducted between resistant (HRG21) and sensitive (FSG43) strains following exposure to pyrimethanil for 2 and 6 h. GO and KEGG analyses identified differential expression of genes associated with ABC and MFS transporters as well as methionine biosynthesis. qRT-PCR validation confirmed a marked upregulation of ABC (BcatrA, BcatrB, BcatrD, BcatrO, and Bmr3) and MFS (Bchex1 and BcmfsM2) transporter genes in HRG21, whereas in FSG43, ABC (BcatrA, BcatrB, BcatrD, and BcatrO) and MFS (Bchex1) transporter genes were downregulated. No significant transcriptional changes were observed in Mrr1, a transcription factor gene, following pyrimethanil exposure. Molecular docking analysis identified potential binding sites and interaction targets for five key transporters (BcatrB, BcatrA, BcatrD, Bmr3, and Bchex1). Furthermore, exogenous methionine supplementation partially mitigated pyrimethanil toxicity in FSG43. However, amino acid sequences of enzymes involved in methionine biosynthesis (BcmetC, BcStr2, Bcmet2, Bcmxr1, and Bcmxr2) exhibited no variation between FSG43 and HRG21. The results indicate that BcatrB plays a central role in pyrimethanil resistance, while methionine contributes only marginally to resistance mechanisms.