Resistance Risk and Resistance‐Related Point Mutation in <i>CtCytb</i> of <i>Colletotrichum truncatum</i> to Florylpicoxamid

ABSTRACT Colletotrichum truncatum is one of the causal pathogens responsible for pepper anthracnose disease. Florylpicoxamid is a new quinone inside inhibitor (QiI) fungicide that can strongly inhibit C. truncatum . The current work investigated the resistance risk of C. truncatum to florylpicoxamid and the potential underlying mechanism. The baseline sensitivity of C. truncatum isolates ( n = 111) to florylpicoxamid was established, yielding an average 50% mycelial growth inhibition concentration (EC 50 ) of 0.1362 ± 0.1144 μg/mL. Four stable florylpicoxamid‐resistant C. truncatum mutants were obtained by fungicide adaptation, each exhibiting resistance factors &gt; 600. Notably, each mutant displayed significantly lower fitness compared with that of the parental isolate. Moreover, it was found that florylpicoxamid does not exhibit cross‐resistance with five fungicides (pyraclostrobin, mefentrifluconazole, prochloraz, carbendazim and fluazinam) that are currently used for the field control of pepper anthracnose. All four highly resistant mutants displayed mutations in the cytochrome b (Cytb) protein, S207L. The amino acid substitution S207L in CtCytb, resulted in decreased binding affinity, as determined by molecular docking, of florylpicoxamid to CtCytb. Overall, there seems to be a moderate risk that C. truncatum develops resistance to florylpicoxamid. The mutation, S207L in CtCytb, indeed confers resistance to C. truncatum against florylpicoxamid.