Oxathiapiprolin-based fungicides provide enhanced control of tomato late blight induced by mefenoxam-insensitive Phytophthora infestans.

Oxathiapiprolin is a new fungicide with extremely high efficacy against oomycete plant pathogens. Solo components oxathiapiprolin (OXPT), chlorothalonil (CHT), azoxystrobin (AZ), mandipropamid (MPD), and mefenoxam (MFX) were compared with each other and with four oxathiapiprolin pre-packed fungicidal mixtures, OXPT+CHT 1+66.7, OXPT+AZ 1+10.3, OXPT+MPD 1+8.3, and OXPT+MFX 1+3 (weight active ingredient ratio), for control efficacy of late blight induced by MFX-insensitive Phytophthora infestans strains in tomato in growth chambers and the field. Mixtures performed better than all partner fungicides alone, except OXPT. Of the four mixtures, OXPT+MFX outperformed, with the highest preventive, curative, translaminar, and systemic efficacies. In the field, OXPT+MFX was superior to other fungicides in controlling late blight epidemics induced by MFX-insensitive isolates. Its deployment in the field will combat the dominating MFX-insensitive isolates, reduce the selection pressure imposed on P. infestans and delay the buildup of subpopulations resistant to oxathiapiprolin.

Pathogenic Fitness of Oosporic Progeny Isolates of Phytophthora infestans on Late-Blight-Resistant Tomato Lines.

Four A1 field isolates and one A2 field isolate of Phytophthora infestans were crossed to produce oospores in tomato leaves. The oospores were extracted and mixed with perlite and water, and healthy tomato leaves were used as bait for oospore-progeny infection. Twenty-nine lesions were obtained from the four crosses and 283 single-sporangium isolates were recovered and tested on four tomato differential lines carrying different major genes (Ph-0, Ph-1, Ph-2, and 3707) for late blight resistance. The pathogenic fitness (number of sporangia per unit leaf area) of parental and progeny isolates was strongly dependent on the host genotype; it decreased in the order Ph-0 > Ph-1 > Ph-2 > 3707. The A2 parent had a higher pathogenic fitness than the A1 parents on Ph-0 and Ph-1 but similar, lower fitness on Ph-2. Different levels of pathogenic fitness were observed across all isolates on Ph-0, although Ph-0 lacks resistance genes. Pathogenic fitness on one tomato genotype was not related to the pathogenic fitness on the other tomato genotypes. Some isolates exhibited reduced pathogenic fitness relative to the respective A1 parent, whereas others demonstrated a higher pathogenic fitness compared with the A2 parent. The tomato genotype Solanum pimpinellifolium L3707/5 was resistant to all five parental isolates of P. infestans. However, 37 of the 283 progeny isolates from 11 different lesions had compatible reactions with this line, producing up to 31 × 103 sporangia/cm2. Overall, reduced fitness was more frequent among the progeny isolates than increased fitness.

Mutagenesis of Phytophthora infestans for Resistance Against Carboxylic Acid Amide and Phenylamide Fungicides.

The carboxylic acid amide (CAA) fungicides mandipropamid, dimethomorph, iprovalicarb, and the phenylamide fungicide mefenoxam (MFX, the active enantiomer of metalaxyl) are anti-oomycete fungicides effective against downy mildews and late blight. Resistance against MFX was reported in nature in several oomycetes including Phytophthora infestans and Plasmopara viticola, whereas resistance against CAAs was reported in P. viticola but not in P. infestans. In this study the mutability of P. infestans for resistance against CAAs and MFX (as a control) was explored under laboratory conditions. UV light or chemical mutagens (e.g., ethyl methan sulfonate [EMS]) were applied to sporangia, and the emergence of mutants resistant to CAAs or MFX, or with altered mating type, was followed. Many mutants resistant to CAAs developed at generation 0 after mutagenesis, but all showed erratic, instable resistance in planta, diminishing after 1 to 8 asexual infection cycles, and failed to grow on CAA-amended medium. In contrast, 19 mutants resistant to MFX were obtained: 6 with UV irradiation (in isolates 28 or 96) and 13 with EMS (in isolates 408, 409, and 410). In three experiments, a shift in mating type, from A1 to A2, was detected. To elucidate whether or not resistance to CAAs is recessive and therefore might emerge only after sexual recombination, A1 and A2 mutants were crossed and the F1 and F2 progeny isolates were tested for resistance. Offspring isolates segregated for resistance to MFX, with resistant isolates maintaining stable resistance in vitro and in planta, whereas all progeny isolates failed to show stable resistance to CAAs in planta or in vitro. The data suggest that P. infestans could be artificially mutated for resistance against MFX, but not against CAAs.