Discovery and biological profile of pyridachlometyl.

Pyridachlometyl is a novel tubulin dynamics modulator fungicide developed by Sumitomo as a new agent designed to tackle fungicide resistance. Pyridachlometyl is being developed as a first-in-class molecule with an anti-tubulin mode of action, the chemical structure of which is characterized by a unique tetrasubstituted pyridazine ring. The first commercial product 'Fuseki flowable' received initial registration in 2023 in Japan. The concepts of the discovery project, optimization of chemical structures, and biological profiles are reviewed herein. © 2024 The Author(s). Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.

Microtiter plate test using liquid medium is an alternative method for monitoring metyltetraprole sensitivity in Cercospora beticola.

BACKGROUND: Metyltetraprole is a new quinone outside inhibitor (QoI) fungicide showing potent activity against QoI-resistant fungi that possess the G143A cytochrome b mutation, which confers resistance to existing QoIs such as trifloxystrobin. For its sustainable use, monitoring of metyltetraprole sensitivity is necessary and the establishment of appropriate methodology is important in each pathogen species. RESULTS: In Cercospora beticola, the causal agent of sugar beet leaf spot, some isolates were less sensitive to metyltetraprole (EC50 > 1 mg L-1 , higher than the saturated concentration) using the common agar plate method, even with 100 mg L-1 salicylhydroxamic acid, an alternative oxidase inhibitor. However, microtiter tests (EC50 < 0.01 mg L-1 ), conidial germination tests (EC50 < 0.01 mg L-1 ) and in planta tests (>80% control at 75 mg L-1 run-off spraying) confirmed that all tested isolates were highly sensitive to metyltetraprole. For trifloxystrobin, G143A mutants were clearly resistant upon microtiter plate tests (median EC50 > 2 mg L-1 ) and distinct from wild-type isolates (median EC50 < 0.01 mg L-1 ). Notably, mycelium fragments were usable for the microtiter plate tests and the test was applicable for isolates that do not form sufficient conidia. Our monitoring study by microtiter plate tests did not indicate the presence of metyltetraprole-resistant C. beticola isolates in populations in Hokkaido, Japan. CONCLUSION: The microtiter tests were revealed to be useful for monitoring the sensitivity of C. beticola to metyltetraprole and trifloxystrobin. © 2020 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.

Fow2, a Zn(II)2Cys6-type transcription regulator, controls plant infection of the vascular wilt fungus Fusarium oxysporum.

The filamentous fungus Fusarium oxysporum is a soil-borne parasite that causes vascular wilts in a wide variety of crops by directly penetrating roots and colonizing the vascular tissue. In previous work, we generated the non-pathogenic mutant B137 of the melon wilt pathogen F. oxysporum f. sp. melonis by using restriction enzyme-mediated integration (REMI) mutagenesis. Molecular characterization of B137 revealed that this mutant has a single-copy plasmid insertion in a gene, designated FOW2, which encodes a putative transcription regulator belonging to the Zn(II)2Cys6 family. The REMI mutant B137 and other FOW2-targeted mutants completely lost pathogenicity, but were not impaired in vegetative growth and conidiation in cultures. Microscopic observation of infection behaviours of green fluorescent protein (GFP)-marked wild-type and mutant strains revealed that the mutants were defective in their abilities to invade roots and colonize plant tissues. FOW2 is conserved in F. oxysporum pathogens that infect different plants. The FOW2-targeted mutants of the tomato wilt pathogen F. oxysporum f. sp. lycopersici also lost pathogenicity. Nuclear localization of Fow2 was verified using strains expressing Fow2-GFP and GFP-Fow2 fusion proteins. These data strongly suggest that FOW2 encodes a transcription regulator controlling the plant infection capability of F. oxysporum pathogens.