Comparative Transcriptome Analyses Reveal Conserved and Distinct Mechanisms of the SDHI Fungicide Benzovindiflupyr Inhibiting Colletotrichum

Colletotrichum leaf disease (CLD) is an annual production concern for commercial growers worldwide. The succinate dehydrogenase inhibitor (SDHI) fungicide benzovindiflupyr shows higher bioactivity against CLD than other SDHIs. However, the mechanism underlying such difference remains unclear. In this study, benzovindiflupyr exhibits good inhibitory activity against and in vitro and in vivo. To reveal its mechanism for inhibiting , we compared transcriptomes of and under treatment with benzovindiflupyr and boscalid. Benzovindiflupyr exhibited higher inhibitory activity against SDH enzyme than boscalid, resulting in a greater reduction in the ATP content of isolates. Most of the metabolic pathways induced in these fungicide-treated isolates were similar, indicating that benzovindiflupyr exhibited a conserved mechanism of SDHIs inhibiting . At the same level of suppressive SDH activity, benzovindiflupyr activated more than three times greater gene numbers of than boscalid, suggesting that benzovindiflupyr could activate distinct mechanisms against . Membrane-related gene ontology terms, mainly including intrinsic components of membrane, were highly abundant for the benzovindiflupyr-treated isolates rather than boscalid-treated isolates. Only benzovindiflupyr increased the relative conductivities of hyphae, indicating that it could damage the cell membrane and increase mycelial electrolyte leakage. Thus, we proposed that the high bioactivity of benzovindiflupyr against occurred by inhibiting SDH activity and damaging the cell membrane at the same time. The research improves our understanding the mode of action of SDHI fungicides against .