Qian Xiu

Fusarium graminearum, causal agent of Fusarium head blight (FHB), causes a huge economic loss. No information is available on the activity of quinofumelin, a novel quinoline fungicide, against F. graminearum or other phytopathogens. In this study, we used mycelial growth and spore germination inhibition methods to determine the inhibitory effect of quinofumelin against F. graminearum in vitro. The results indicated that quinofumelin excellently inhibited mycelial growth and spore germination of F. graminearum, with the average EC₅₀ values of 0.019 ± 0.007 μg/mL and 0.087 ± 0.024 μg/mL, respectively. In addition, we found that quinofumelin could significantly decrease deoxynivalenol (DON) production and inhibit the expression of DON-related gene TRI5 in F. graminearum. Furthermore, we found that quinofumelin could disrupt the formation of Fusarium toxisome, a structure for producing DON. Western blot analysis demonstrated that the translation level of TRI1, a marker gene for Fusarium toxisome, was suppressed by quinofumelin. The protective and curative assays indicated that quinofumelin had an excellent control efficiency against F. graminearum on wheat coleoptiles. Taken together, quinofumelin exhibits not only an excellent antifungal activity on mycelial growth and spore germination, but also could inhibit DON biosynthesis in F. graminearum. The findings provide a novel candidate for controlling FHB caused by F. graminearum.

The high osmolarity glycerol (HOG) pathway, comprising a two-component system and the Hog1 mitogen-activated protein kinase (MAPK) cascade, plays a pivotal role in eukaryotic organisms. Previous studies suggested that the biological functions of some key genes in the HOG pathway varied in filamentous fungi. In this study, we characterized a putative MAPK kinase kinase gene, Ssos4, in Sclerotinia sclerotiorum, which encoded a phosphotransferase in the MAPK cascade. Compared with the wild-type progenitor HA61, the deletion mutant ∆Ssos4-63 exhibited impaired mycelial growth, sclerotia formation, increased hyphal branches, and decreased virulence. The deficiencies of the deletion mutant ∆Ssos4-63 were recovered when the full-length Ssos4 gene was complemented. Deletion of Ssos4 increased the sensitivity to osmotic stresses and cell wall agents and the resistance to fludioxonil and dimethachlon. Intracellular glycerol accumulation was not induced in the deletion mutant ∆Ssos4-63 when treated with fludioxonil and NaCl and the phosphorylation of SsHog1 was also cancelled by the deletion of Ssos4. Consistent with the glycerol accumulation and increased expression levels of SsglpA and Ssfps1, controlling glycerol synthesis and close of glycerol channel under hyperosmotic stress, respectively, were detected in the wild-type strain HA61 but not in the deletion mutant ∆Ssos4-63. Moreover, the relative expression level of Sshog1 significantly decreased, whereas the expression level of Ssos5 increased in the deletion mutant ∆Ssos4-63. These results indicated that Ssos4 played important roles in mycelial growth and differentiation, sclerotia formation, virulence, hyperosmotic adaptation, fungicide sensitivity, and the phosphorylation of SsHog1 in S. sclerotiorum.

Cucumber target spot, caused by Corynespora cassiicola, is a devastating fungal disease in greenhouses in China. Lack of resistant cultivars and unscientific use of fungicides aggravated the difficulty to manage this disease. In recent years, resistance of C. cassiicola to benzimidazoles, quinone outside inhibitors, and succinate dehydrogenase inhibitors has occurred in China. Here, we tested the fluazinam sensitivity distribution of 79 C. cassiicola isolates from different provinces in China based on mycelial growth inhibition. The EC₅₀values of fluazinam ranged from 0.1002 to 0.3129 µg/ml with a mean of 0.2136 ± 0.0495 µg/ml, and the sensitivity frequency was normally distributed (P = 0.2083, Shapiro–Wilk test). Meanwhile, the EC₅₀values for spore germination inhibition ranged from 0.0992 to 0.2278 µg/ml with a mean of 0.1499 ± 0.0504 µg/ml. This indicated that fluazinam exhibited an excellent in vitro fungicidal activity on both mycelial growth and spore germination. In addition, fluazinam also exhibited a good in planta control efficacy on detached cucumber leaves in the protective and curative assays. Moreover, the biological and physiological characteristics of C. cassiicola as affected by fluazinam were determined. Fluazinam not only significantly inhibited respiration and adenosine triphosphate production but also caused the increase of cell membrane permeability and the dysfunctions of cellular homeostasis. Interestingly, we found that fluazinam especially damaged vacuole structures, causing the redistribution of vacuole substances. Taken together, our findings provide not only essential references for resistance management of C. cassiicola but also interesting insights for further revealing the action mode of fluazinam against plant pathogens.