Effects of the dinitroaniline fungicide fluazinam on Fusarium fujikuroi and rice.

Fusarium fujikuroi is the primary causal agent of rice bakanae disease. Fluazinam is a protective dinitroaniline fungicide which could interrupt the fungal cell's energy production. Little is known about the effects of fluazinam on F. fujikuroi. In this study, baseline sensitivity of F. fujikuroi to fluazinam was determined using 103 isolates collected from diseased young rice of different fields in Shaoxing of Zhejiang Province and Huaian of Jiangsu Province of China in 2016. The EC50 values of fluazinam on inhibiting mycelial growth against 103 isolates of F. fujikuroi ranged from 0.0621 to 0.5446 µg/mL with the average value of 0.2038 ±â€¯0.0099 µg/mL (mean ±â€¯standard error). The EC50 values of fluazinam on suppressing conidium germination against 103 isolates of F. fujikuroi ranged from 0.1006 to 0.9763 µg/mL with the mean value of 0.3552 ±â€¯0.0181 µg/mL. Treated with fluazinam, hyphae of F. fujikuroi were contorted, offshoot of top mycelia increased, conidial production descreased significantly and exopolysaccharide (EPS) content did not change significantly while peroxidase (POD) activity significantly decreased. Meanwhile, cell membrane permeability increased after treated with fluazinam. The analysis of cell ultrastructure indicated that fluazinam could damage the membrane structure of F. fujikuroi and cause a large number of vacuoles formed. In addition, fluazinam did not affect germination rate, plant height and fresh weight of rice, which indicated that fluazinam was safe to rice. All the results indicated that fluazinam had strong antifungal activity against F. fujikuroi and a potential application in controlling rice bakanae disease. These results will provide useful information for management of rice bakanae disease caused by F. fujikuroi and further increase our understanding about the mode of action of fluazinam against F. fujikuroi and other phytopathogens.

PSMB8 regulates glioma cell migration, proliferation, and apoptosis through modulating ERK1/2 and PI3K/AKT signaling pathways.

Glioma has been considered as one of the most aggressive and popular brain tumors of patients. It is essential to explore the mechanism of glioma. In this study, we established PSMB8 as a therapeutic target for glioma treatment. Expression of PSMB8 as well as Ki-67 was higher in glioma tissues demonstrated by western blot and immunohistochemistry. Then, the role of PSMB8 in migration and proliferation of glioma cells was investigated by conducting wound-healing, trans-well assay, cell counting kit (CCK)-8, flow cytometry assay and colony formation analysis. The data showed that interfering PSMB8 may inhibit the migration and proliferation of glioma cells by reducing expression of cyclin A, cyclin B1, cyclin D1, Vimentin, and N-cadherin, and by increasing expression of E-cadherin. Additionally, interfering PSMB8 may induce apoptosis of glioma cells by upregulating caspase-3 expression. Furthermore, these in vitro findings were validated in vivo and the ERK1/2 and PI3k/AKT signaling pathways were involved in PSMB8-triggered migration and proliferation of glioma cells. In an in vivo model, downregulation of PSMB8 suppressed tumor growth. In conclusion, PSMB8 is closely associated with migration, proliferation, and apoptosis of glioma cells, and might be considered as a novel prognostic indicator in patients with gliomas.