LAUSR

BACKGROUND Rice blast, caused by Magnaporthe grisea, is the most devastating disease in rice. Recently, trifloxystrobin was registered for the control of M. grisea in China. The resistance profile and mechanism of M. grisea to trifloxystrobin were investigated in the present study, providing important data for the recommended use of trifloxystrobin. RESULTS The baseline sensitivity was established at a mean EC50 of 0.024 μg/mL. Nine stable trifloxystrobin-resistant mutants were generated with EC50 values ranging from 12.75 to 171.49 μg/mL. The mutants exhibited strong adaptive traits in sporulation, conidial germination, and pathogenicity. Positive cross-resistance was only observed between trifloxystrobin and azoxystrobin, but not between trifloxystrobin and carbendazim, isoprothiolane, prochloraz, or chlorothalonil. The point mutation G143S in cyt b protein was found in eight high-resistance mutants with resistant factor ranging from 2295.16 to 13 200.00; and the double mutation G137R/M296V only occurred in Mg117-1 with resistance factor ≈ 900. The G143S mutation weakened hydrogen bond interactions, and G137R/M296V changed the conformation of trifloxystrobin in the cyt b binding pocket. A molecular detection method was established for the rapid detection of G143S mutants in M. grisea. CONCLUSION The resistance risk of M. grisea to trifloxystrobin could be moderate to high. Two genotypes with three point-mutations G143S, G137R, and M296V conferred resistance to trifloxystrobin in M. grisea. This article is protected by copyright. All rights reserved.