Sedaxane is a new broad-spectrum seed treatment fungicide developed by Syngenta Crop Protection for control of seed- and soil-borne diseases in a broad range of crops. Its physicochemical properties and activity spectrum have been optimised for use as a seed treatment providing both local and systemic protection of the seed and roots of target crops.
Sedaxane inhibits respiration by binding to the succinate dehydrogenase complex in the fungal mitochondrium. Its activity spectrum covers seed-borne fungi such as Ustilago nuda, Tilletia caries, Monographella nivalis and Pyrenophora graminea, as well as the soil-borne fungi Rhizoctonia solani, R. cerealis and Typhula incarnata. Under greenhouse conditions, sedaxane showed high levels and consistent protection against U. nuda, P. graminea and Rhizoctonia spp. Under field conditions, efficacy against Rhizoctonia spp. resulted in increased yield compared with the untreated check. Efficacy against snow mould has been shown under very high disease pressure conditions. The combination of sedaxane plus fludioxonil against snow mould can provide resistance management for sustainable use.
Seed- and soil-borne diseases caused by fungi impact upon almost all crop species and can have a significant effect on the early development of the seedlings as well as on the final yield. Seed-borne diseases such as loose smut of barley, caused by Ustilago nuda, and common bunt of wheat, caused by Tilletia caries, have been known for centuries and can cause significant yield reductions. Rhizoctonia spp. are among the most important soil-borne pathogens, in that they attack a broad range of crops and occur throughout the world in most soils and climates. Disease symptoms can vary, depending on the crop, e.g. damping-off in cotton and soybean, root rot in sugar beet, stalk rot in cereals and corn and black scurf in potatoes. Rhizoctonia solani Kühn (teleomorph: Thanatephorus cucumeris AB Frank) is divided into several anastomosis groups which are based on the ability of the hyphae of different cultures to fuse. Each anastomosis group specialises on a certain host range, e.g. AG2-2IIIB attacks corn, sugar beet and soybean. Besides R. solani, cereals can also be infected by R. cerealis van der Hoeven (teleomorph: Ceratobasidium cereale DIL Murray and LL Burpee), which is the cause of sharp eyespot in wheat and rye.
Seed treatments are a convenient way to protect valuable seeds against both seed- and soil-borne diseases. By improving stand establishment and seedling health, seed treatments help to ensure that the crop will be able to reach its yield potential. Use of seed treatments is common in almost all developed agricultural areas and on almost all crops where seeds are used to raise the plants. Fungicides from many different chemical classes are in use as seed treatments, e.g. triazoles (DMI), phenylpyrroles (PP), phenylamides (PA), benzimidazoles (MBC) and strobilurines (QoI).
Sedaxane is a new, unique, broad-spectrum seed treatment fungicide with focus on control of seed- and soil-borne diseases in a broad range of crops. Its activity spectrum covers seed-borne fungi such as Ustilago nuda, Tilletia caries, Monographella nivalis (causal agent of snow mould) and Pyrenophora graminea (causal agent of stripe disease of barley), as well as the soil-borne fungi Rhizoctonia solani, R. cerealis and Typhula incarnata. Sedaxane discovery was the result of an intense chemical synthesis and biological screening programme that included hundreds of carboxamide analogues, a chemical class that has recently achieved much attention as lead structure for agricultural fungicides.[3, 4] Sedaxane was selected for seed treatment use only, because it combines optimal physicochemical properties, a broad spectrum of activity and excellent crop tolerance for this specific use. Sedaxane specifically inhibits the succinate dehydrogenase enzyme (SDH, EC 126.96.36.199) which catalyses a crucial step in the TCA cycle and the respiration chain.[5, 6] The activity of sedaxane against various soil- and seed-borne diseases is presented.
Materials And Methods
The structure and physicochemical properties of sedaxane are shown in Fig. 1 and Table 1. Sedaxane is a mixture of the trans- and cis-isomers of N-[2-(1,1′-bicyclopropyl)-2-ylphenyl]-3-(difluoromethyl)-1-methyl-1H-pyrazole-4-carboxamide in a ratio of 6:1.
Table 1. Physicochemical properties of sedaxane
Physicochemical properties of sedaxane
log P (o/w)
3.3 at 25 °C
14 mg L−1
Stable at pH 3–10
For all lab and greenhouse trials, sedaxane formulated either as FS100 (100 g AI L−1) or as FS500 (500 g AI L−1) was used. For seed treatments, a slurry of sedaxane was prepared by mixing the FS formulation with tap water, the slurry was transferred to a glass flask, seeds were put into the flask and applications were done by rotating the flask twice for 30 s each time in a Turbola device (Maschinenfabrik, Basel, Switzerland).
Except for isopyrazam and sedaxane, which were supplied by Syngenta Crop Protection, the chemicals used for the enzyme assay (bixafen, boscalid carboxin, fluopyram and penthiopyrad) were purchased from Sigma-Aldrich.
For field trials, the following formulated ingredients were used: fludioxonil 5 g ai dt−1 (Celest FS025 at 200 mL dt−1), fludioxonil 5 g dt−1 + difenoconazole 5 g dt−1 (Celest Extra FS050 at 200 mL dt−1), 10 g sedaxane dt−1 (Vibrance FS500 at 20 mL dt−1) and 10 g sedaxane dt−1 + 5 g fludioxonil dt−1 and 5 g difenoconazole dt−1 (Vibrance Gold FS100 at 200 mL dt−1). Treatments were applied in a Hege 11 seed treater at 8 mL slurry kg−1 seed prior to planting.
Isolation ofR. solani mitochondria
Mycelium from ten-day-old R. solani cultures growing in Sabouraud maltose broth (SMB) was harvested by vacuum filtration and disrupted in liquid nitrogen using a mortar and pestle. The resultant powder was resuspended to 10% w/v in mitochondrial extraction buffer (10 mM of KHPO4 pH 7.2, 10 mM of KCl, 10 mM of MgCl2, 0.5 M of sucrose, 0.2 mM of EDTA, 2 mM of PMSF). The extract was clarified by centrifugation (5000 × g, 4 °C for 10 min, 2 times), and intact mitochondria were then pelleted at 10 000 g for 20 min at 4 °C and resuspended in the same buffer. Mitochondrial suspensions were brought to a concentration of 10 mg mL−1 and stored at −80 °C until use. SDH activity was found to remain stable for months.
Succinate:ubiquinone/DCPIP activity inhibition
Mitochondrial suspensions were diluted 1/20 in extraction buffer and preactivated at 30 °C for 30 min in the presence of 10 mM of succinate. Succinate:ubiquinone/DCPIP activity inhibition measurements were performed by adding 10 μL of preactivated mitochondria to 200 μL of assay buffer (50 mM of phosphate-Na pH 7.2, 250 mM of sucrose, 3 mM of NaN3, 10 mM of succinate) supplemented with 140 μM of dichlorophenolindophenol (DCIP) and 1 mM of 2,3-dimethoxy-5-methyl-1,4-benzoquinone (Q0). Inhibitor concentrations ranged between 0.5 mM and 0.084 nM, with uniform 3× dilution factor steps (11 inhibitor concentrations + DMSO control). A total of 96 well plates were pre-equilibrated at reaction temperature (30 °C) for 10 min before the reactions were started by the addition of 10 μL of preactivated R. solani mitochondrial suspension. DCPIP reduction was conducted at 30 °C and monitored at 595 nm using a HTS7000 microtitre plate reader (PerkinElmer). Calculated absorbance slopes (OD h−1) were used for half-inhibitory concentration (IC50) calculations using Graphpad Prism 5.0 software.
Laboratory in vitro assay
PDA medium was prepared by adding 26 g of potato dextrose agar (PDA) to 900 mL of double-distilled water. The medium was autoclaved at 121 °C for 20 min, and then cooled to 55 °C. The fungicides were diluted in sterile double-distilled water, mixed with the medium to a final concentration of 100, 10,1, 0.1 and 0.01 g L−1 and poured into petri dishes (9 cm diameter). An untreated check was included as reference, and four replicates per treatment were done. Each petri dish was inoculated with a mycelial disc (6 mm diameter) cut from the margin of freshly prepared source colonies of the respective fungus growing on PDA medium. All fungal isolates were taken from the Syngenta strain collection, and details are listed in Table 2. After an incubation period of 2–14 days, at 20 °C in the dark, for all four replicates the diameter of the mycelium was measured, including the agar disc, the average was calculated and the data were converted to percentage activity. Dose–response curves were drawn by plotting percentage growth activity against fungicide concentration on a log-probit scale, and EC50 values (dosage causing 50% growth inhibition) were determined.
Table 2. Overview of the fungal isolates used for the in vitro assay
Switzerland, isolated from potato
DSM1957, isolated from leather
ATCC38602, isolated from cucumber
ATCC MYA724, isolated from maize
ATCC16402, isolated from squash
Switzerland, isolated from wheat
CBS169.33, isolated from wheat
Switzerland, isolated from oats
Germany, isolated from maize
IACR, UK, isolated from wheat
UK, isolated from oil seed rape
Switzerland, isolated from wheat
Japan, isolated from rice
DSM63481, isolated from barley
Netherlands, isolated from citrus
ATCC44725, isolated from potato
Ireland, isolated from barley
Switzerland, isolated from wheat
Switzerland, isolated from cucumber
CBS559.77, isolated from wheat
Rhizoctonia solani AG1
Japan, isolated from sudan grass
R. solani AG2-2IIIB
Germany, isolated from maize
R. solani AG3
Japan, isolated from potato
R. solani AG4
Switzerland, isolated from bean
R. solani AG5
Germany, isolated from oil seed rape
Switzerland, isolated from carrot
CBS572.81, isolated from grass seed
Soybean seeds (cv. Toliman) were sown in plastic trays (30 × 20 × 7 cm) filled with a mixture of 45% sand, 45% vermiculite and 10% sterilised silty loam. Each tray consisted of 50 seeds, and for each treatment three replicates (= trays) were done in a randomised complete block design. The fungal inoculum was produced by first growing R. solani AG2-2IIIB (for isolate information, see Table 2) for 7 days on potato carrot agar at 22 °C in the dark. Three agar discs (6 mm diameter) overgrown with R. solani were then placed into 500 mL flasks containing 40 g of millet seeds and 100 mL of water, which had been autoclaved twice prior to the inoculation. After an incubation period of 14 days at 22 °C in the dark, the inoculum was ready to use. Artificial inoculation of the soil was done by mixing 2 g of dried, ground millet seeds infested with R. solani AG2-2IIIB uniformly with 100 L of soil, using the same soil mixture as described above. After an incubation period of 7 days, this mixture was then added to the topsoil layer at 10%. Trays were kept in a growth chamber at 20 °C and 80% relative humidity in darkness. After germination had occurred, a 14:10 h day:night cycle was provided. Plants were transferred to the greenhouse at 12 days after planting (DAP) and kept there at 21–24 °C and 60–70% relative humidity. Overhead irrigation was applied 3 times per day to keep the soil at constant moisture level. Assessment was carried out by taking plants out of the soil at 38 DAP, roots were washed with tap water and disease ratings were done according to a scheme used and described by Faessel. According to this scheme, an index for each disease rating from 0 to 5 was used, for each treatment the number of plants per disease rating was multiplied by the respective index and the products were added to give a final disease index.
The fungal inoculum was produced as described above. A quantity of 0.6 g of dried R. solani millet inoculum was mixed with 10 L of soil (soil mixture as for soybean) and incubated for 7 days at 23 °C. Trays (18 × 10 × 5 cm) were filled with the inoculated soil, and corn seeds (cv. PR39G12) were placed on top of the soil and covered with a layer of 1.5 cm infected soil. Four replicates consisting of 10 seeds each were done in a randomised complete block design. The trials were placed in a growth chamber at 23 °C, 80% relative humidity and a 12 h light period. Trays were incubated for 10 days under plastic hoods providing high relative humidity. After the hoods had been removed, the trays were kept in the growth chamber until assessment took place. Assessments were done at 22 DAP by taking plants out of the soil, washing the roots with tap water and assessing the infected root area visually by rating the percentage of brown and black roots.
Cotton seeds (cv. Sure Grow 747) were sown in plastic trays (30 × 20 × 7 cm) filled with a mixture of 45% sand, 45% vermiculite and 10% silty loam. Each tray consisted of 50 seeds, and for each treatment three replicates (= trays) were done in a randomised complete block design. The fungal inoculum was produced as described for soybean, but instead of AG2-2IIIB an isolate of R. solani AG4 was used. Artificial inoculation of the soil was done by mixing 1.5 g of dried, ground millet seeds infected with R. solani AG4 (for isolate information, see Table 2) uniformly with 100 L of soil. After an incubation period of 10 days, this mixture was then added to the top soil layer at 10%. Trays were kept in a growth chamber at 20 °C and 90% relative humidity in darkness. After germination had occurred, a 14:10 h day:night cycle was provided. Plants were transferred to the greenhouse at 13 DAP and kept there at 21–24 °C and 60–70% relative humidity. Overhead irrigation was applied 3 times a day to keep the soil at constant moisture level. Assessments were done by counting plant stand.
Winter barley seeds (cv. Baretta) naturally infected with U. nuda were sown at 2 cm depth in plastic trays (44 × 33 × 9 cm) filled with steam-sterilised field soil. After applying 3 mm of water, the trays were kept for 2 days at 15 °C to initiate germination and then placed at 4 °C in a growth chamber in the dark. After a vernalisation period of 2 weeks, plants were moved to a greenhouse at a temperature of 10–14 °C during a period of 5 weeks to allow tillering. Then, the temperature in the greenhouse was increased to 21 °C until flowering. During the greenhouse phase of the experiment, day length was adjusted to 14 h by supplying artificial light, and relative humidity was kept at 70%. Each treatment consisted of two replicates with 100 seeds each in a randomised complete block design. The experiment was repeated twice with two different seed lots, the first one having a U. nuda seed infection level of 15% and the second one an infection level of 20%. Both seed lots orginated from Syngenta nursery fields, and seed infection levels were determined by the Scotish Agricultural Science Agency (SASA) according to their standard procedures. Assessments were done 4 times per experiment by counting the loose-smut-affected barley heads to determine disease incidence.
Winter barley seeds (cv. Baretta) naturally infected with P. graminea were sown in plastic trays as described for Ustilago nuda. The seed lot orginated from Syngenta nursery fields, and seed infection levels were determined by the SASA to be 70%. After applying 3 mm of water, the trays were kept for 3 weeks at 4 °C in a growth chamber in the dark. Plants were then moved to a greenhouse at a temperature of 10–12 °C until the end of the experiment. During the greenhouse phase of the experiment, day length and relative humidity were adjusted as described for Ustilago nuda. Each treatment consisted of two replicates with 100 seeds each, and a randomised complete block design was used. The experiment was repeated 3 times. Assessments were done at 57 DAP (experiments 1 and 2) or at 64 DAP (experiment 3) by counting seedlings with symptomatic leaves to determine disease incidence. Symptomatic leaves showed typical yellow to brown stripes which occur in parallel to the leave veins.
Efficacy against snow mould (caused by Monographella nivalis) was tested on trial sites in Germany (Börnichen and Grünhain), Switzerland (La Baune) and the United Kingdom (Barton) that were naturally infested with snow mould. Winter wheat cv. Titlis (La Baune) and cv. Robigus (Barton) and winter barley cv. Fidericus (Börnichen and Grünhain) were planted between 30 September and 2 November 2009. The seeds were trated as follows: untreated; sedaxane 10 g dt−1 seeds; fludioxonil 5 g + difenoconazole 5 g dt−1 seeds; sedaxane 10 g + fludioxonil 5 g + difenoconazole 5 g dt−1. Each treatment was planted in four replicates in 3 m plots in a randomised complete block design. Disease assessment was done by counting the surviving plants between 12 February and 22 March 2010.
Efficacy against R. cerealis was tested on trial sites in Switzerland (Stein), in the Czech Republic (Kluky, Komeriz and Zubri) and in Poland (Chrzastowo). The sites were artificially infested using R. cerealis isolate 196 from the Syngenta strain collection. The inoculum was produced in sterile plastic bags filled with 2 kg of millet grains. These were inoculated with a starter culture of R. cerealis. After 14 days, the bags were opened and dried at room temperature. The dried inoculum was distributed into the row prior to planting at a rate of 30 g m−2 using a Hege Plotspider PLS fertiliser applicator or equivalent equipment. Winter wheat (cv. Arina) was planted in Stein on 15 October 2008. In the 2009/2010 season, trials were planted between 5 October and 14 October. Winter wheat varieties used were Banquet (Kluky), Chevalier (Komeriz), Akteur (Zubri) and Nutka (Chrzastowo). The seeds were treated as follows: untreated; sedaxane at 10 g dt−1, fludioxonil 5 g + difenoconazole 5 g dt−1 seeds; 10 g sedaxane + 5 g fludioxonil + 5 g difenoconazole dt−1. Each treatment was planted in four replicates in 15 m plots in a randomised complete block design. Plots were harvested with a Wintersteiger Nurserymaster Elite small-plot harvester or equivalent equipment to determine grain yield.
Calculation of activity and statistics
Activity for all greenhouse trials was calculated by the following formula:
Data were subjected to analysis of variance using the software SAS 9.2 (SAS Institute, Cary, NC). All references to significant effects or differences among means relate to significance at P ≤ 0.05 by the LSD test.
Intrinsic potency at the enzyme level
The potency of the different SDHI compounds to the SDH enzyme from Rhizoctonia solani was compared by measuring the concentration-dependent inhibition of the SDH activity with purified R. solani mitochondria (see Section 2). Although potency differed greatly across the compounds tested, they all displayed specific inhibition of the succinate dehydrogenase activity in vitro (Fig. 2). Lowest half-inhibitory concentrations were obtained with isopyrazam (0.13 nM) and with sedaxane (0.7 nM), whereas fluopyram required the highest concentration of 4533 nM (Fig. 2).
In vitro activity
Sedaxane provides a broad-spectrum activity across all fungal classes except oomycetes. It is particularly active against the two most important Rhizoctonia species and all anastomosis groups of R. solani that have been tested. Further, a high-level activity against Typhula incarnata, Sclerotinia sclerotiorum and Monographella nivalis was observed. An overview of the in vitro activity of sedaxane is given in Table 3.
Table 3. In vitro activity spectrum of sedaxane
Growth inhibition (EC50, mg AI L−1)
Rhizoctonia solani AG1 (rice)
R. solani AG2-2IIIB (sugar beet)
R. solani AG3 (potato)
R. solani AG4 (cotton)
R. solani AG5 (cereals)
Rhizoctonia solani – soybean, corn and cotton
Sedaxane was highly active against Rhizoctonia solani on several crops. Table 4 summarises the results of three greenhouse experiments on soybean, corn and cotton. In the inoculated checks, high disease incidence of 85% (soybean), 87.5% (corn) and 100% (cotton) were observed. Sedaxane provided consistent and significant levels of Rhizoctonia root rot and damping-off control. For example, in corn, sedaxane at 50 g dt−1 provided 98% activity against R. solani, with a disease level of 87.5% in the untreated control. At the tested rates, no signs of phytotoxicity were observed on soybean, cotton or corn (no data shown).
Table 4. Activity of sedaxane against Rhizoctonia solani in greenhouse experiments
* indicates significant difference at P ≤ 0.05 from the UTC.
Ustilago nuda – barley
Sedaxane seed treatments at the recommended field rate of 10 g dt−1 provided very efficient control of barley loose smut in two independent trials (Table 5). In trial 1, up to disease levels of 13% in the untreated control, sedaxane completely controlled Ustilago nuda, and only when the disease pressure in the control reached 18% did the control by sedaxane drop to 97%. In a second trial where a different seed lot of the same barley cultivar was used, disease levels in the untreated control increased from 5% (at 89 DAP) to 29% (at 112 DAP). Sedaxane provided 100% control of loose smut throughout the experiment.
Table 5. Activity of sedaxane against Ustilago nuda on barley in greenhouse experiments with two different U. nuda-infected seed lots
* indicates significant difference at P ≤ 0.05 from the UTC.
Pyrenophora graminea – barley
In three independent greenhouse trials, sedaxane seed treatments at the recommended field rate of 10 g dt−1 provided excellent control of leaf stripe disease (Table 6). Depending on the disease level observed in the untreated control (47, 54 and 69% respectively), sedaxane showed control levels of 95.7–100%.
Table 6. Activity of sedaxane against Pyrenophora graminea on barley in greenhouse experiments
* indicates significant difference at P ≤ 0.05 from the UTC.
Monographella nivalis – wheat and barley
The disease pressure was high in all trials, varying from 29% of the plants infected in one experiment in Barton (United Kingdom) to 61% of the plants infected in a second trial in Barton. The trials in Germany and Switzerland had infection levels of 48–59% in the untreated control. The efficacy of the standard Celest ExtraTM varied strongly between the trials. The efficacy of sedaxane solo (10 g dt−1) varied across the trials as well, but was higher than the efficacy of Celest ExtraTM on average across all trials. The three-way mixture of sedaxane (10 g dt−1) with fludioxonil (5 g dt−1) and difenoconazole (5 g dt−1) gave the lowest disease rating and consequently the highest level of efficacy. The results of the disease rating in spring are summarised in Table 7.
Table 7. Activity of seed treatments against Monographella nivalis in field trials 2009/2010
Different lower-case letters indicate statistical differences in activity (P ≤ 0.05).
SE = standard error.
FDL + DFZ (5 + 5)
SDX + FDL + DFZ (10 + 5 + 5)
Rhizoctonia cerealis – wheat
Rhizoctonia damage could be observed during the trials as reduced growth and delayed development of the crop, but the number of plants was not strongly affected.
Although not statistically significant, the yield results (Table 8) indicate numerically that the crop was damaged by the pathogen by comparison with the non-infested check treatment in the 2008/2009 season. In the 2009/2010 season, three out of four trials showed significant yield increases for all treatments compared with the untreated inoculated check. The treatments containing sedaxane resulted in the highest yields, higher than the yields in the non-infested check.
Table 8. Wheat grain yields in field trials with Rhizoctonia cerealis
Different letters indicate statistical differences in yield (P ≤ 0.05).
SE = standard error.
FDL + DFZ (5 + 5)
SDX + FDL + DFZ (10 + 5 + 5)
Using an enzymatic test on purified Rhizoctonia solani mitochondria, it was shown that sedaxane is a highly potent inhibitor of the fungal succinate dehydrogenase enzyme. The compound displays a broad spectrum of activity against phytopathogenic fungi, as shown by the in vitro efficacy trials. Sedaxane provided particularly high intrinsic activity against soil-borne fungi such as Monographella nivalis, Typhula incarnata and Rhizoctonia spp., making it well suited for use as a seed treatment. The potential as seed treatment is further underlined by the high activity against major seed-borne diseases such as Pyrenophora graminea and Ustilago nuda.
Rhizoctonia spp. are pathogens of many crops.[8, 9] The activity of sedaxane against all anastomosis groups tested suggests the possibility of wide use. This is supported by the results of the greenhouse tests, showing activity against R. solani in corn, soybeans and cotton. In cereals, R. solani is an important disease, especially under reduced-tillage regimes in Australia and the United States.[10-12] Significant yield losses in wheat caused by R. cerealis have been reported from China, and a worldwide increase in importance of R. cerealis is expected according to recent reviews of this disease.[13, 14] In Europe, yield impact is believed to be smaller; results presented here indicate that a yield reduction of 5% is possible. Increase in reduced-tillage cropping systems in Europe will most likely increase the importance of this disease in Europe as well. Sugar beet and corn are attacked by the same anastomosis group of R. solani, and rotations with these crops will increase disease pressure in sugar beet, which is highly susceptible to R. solani damage.[15, 16] In some areas of the United States, soybean production has increased dramatically, resulting in shorter crop rotations or continuous soybean production, and an increase in the importance of soil-borne diseases, including Rhizoctonia spp., has been observed. Similarly, R. solani is known to be an important pathogen in Brazilian soybean,[18, 19] and yield losses of up to 60% were reported, underlying the importance of having new chemistries available to control Rhizoctonia spp. and in order to provide best antiresistance strategies.
Management of Rhizoctonia spp. by rotation is difficult, and current shifts in rotation patterns are believed to be increasing its significance.[20-22] As carbon sequestration in soil is becoming more important, a renewed trend to no-till practices is expected. This will result in higher Rhizoctonia inoculum levels in agricultural soils and pose a higher risk of crop losses caused by this pathogen.
In cereals in particular, a broad spectrum of disease is controlled by sedaxane. Not only soil-borne diseases such as Rhizoctonia spp. and Typhula spp. but also seed-borne diseases such as Ustilago spp., T. caries and P. graminea are controlled. This makes sedaxane mixture products very well suited for cereal seed treatments.
Snow mould caused by M. nivalis is a key disease in European rye and wheat, but also in barley. Fludioxonil is the current market standard for control of snow mould, providing excellent activity, and so far no cases of fludioxonil-resistant M. nivalis have been reported. However, the recent occurrence of QoI-resistant M. nivalis isolates shows that a sound resistance management for this pathogen will become more important. The mixture of two highly active snow mould compounds with a different mode of action, such as sedaxane and fludioxonil, will provide a long-term protection of wheat against this disease, but also ensure sustainable usage owing to an active resistance management.
Owing to its broad-spectrum activity against numerous soil- and seed-borne diseases, the SDHI inhibitor sedaxane fits well as a seed treatment in a broad range of crops.
It provides excellent control of Rhizoctonia spp., a key soil-borne disease of all crops that damages seedlings and results in a reduced root system that is less capable of absorbing nutrients and water from the soil, leading to reduced yields in all crops. Important seed-borne diseases of cereals such as Ustilago spp., Tilletia caries and Pyrenophora graminea will be controlled by seed applied sedaxane.
Besides its activity, sedaxane adds sound resistance management to snow mould control schemes by seed treatment. The compound will be introduced not only in cereals but also in soybean and numerous other crops.
The authors would like to thank all colleagues within Syngenta who have contributed to the results presented in this article with their valuable work, especially Urban Anderau, Franz Brandl, Daniel Dollinger, Walter Leimgruber, Elfriede Mueller, Harald Walter and Jan Werthmueller.