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CROP BREEDING & GENETICS

Irrigation and Inoculation Treatments that Increase the Severity of Soybean Sudden Death Syndrome in the Field

^a EMBRAPA Cerrados, Rodovia BR-020 Km 17, Planaltina, DF, Brazil, 73310-970
^b USDA-ARS and Dep. of Crop Sciences, Univ. of Illinois, Urbana, IL 61801
^c Dep. of Crop Sciences, Univ. of Illinois, Urbana, IL 61801
^d USDA-ARS, Crop Genetics and Production Research Unit, Stoneville, MS 38776

^* Corresponding author (bdiers{at}uiuc.edu)

	ABSTRACT

TOP NOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION REFERENCES

 
The occurrence of sudden death syndrome (SDS), caused by the fungus Fusarium solani (Mart.) Sacc. f. sp. glycines (FSG) (syn. Fusarium virguliforme Akoi, O'Donnell, Homma and Lattanzi), is unpredictable in soybean [Glycine max (L.) Merr.] field trials making it difficult to evaluate soybean for resistance to the pathogen. Our objective was to evaluate the effect of field inoculation, soil compaction, and irrigation on the occurrence and severity of SDS symptoms. Six inoculation treatments were tested which included applications of FSG-infested grain planted in the furrow with the soybean seed, broadcasted and incorporated into the soil before planting, or placed below the soybean seed just before planting. Soil was compacted by driving a tractor across the field once in early spring. Irrigation treatments were applied at combinations of growth stages V3, V7, R3, R4, and/or R5. Significant increases in foliar SDS severity were observed from inoculation and irrigation treatments (P < 0.05), but not from compaction treatments. The inoculation treatments that placed inoculum close to the seed resulted in the greatest foliar severity. Irrigation treatments during mid to late reproductive growth stages resulted in significant increases in SDS foliar symptom development. These results increase our understanding of what environmental conditions increase SDS field symptoms and will be useful to researchers establishing SDS field nurseries.

Abbreviations: CFU, colony-forming unit • DX, disease index • FSG, Fusarium solani (Mart.) Sacc. f. sp. glycines • SCN, soybean cyst nematodes • SDS, sudden death syndrome

	INTRODUCTION

TOP NOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION REFERENCES

 
SUDDEN DEATH syndrome is caused by FSG, which can result in severe seed yield losses to soybean (Gibson et al., 1994; Hartman et al., 1994). The fungus is soilborne and infects plants through the roots resulting in root necrosis and a reduction of root mass (Roy et al., 1997; Rupe and Hartman, 1999). The aboveground symptoms include interveinal chlorosis and necrosis of leaves, premature defoliation, and pod abortion (Hartman et al., 1997). The foliar symptoms develop rapidly usually during the reproductive stage of soybean growth (Gibson et al., 1994; Roy et al., 1997).

The use of resistant cultivars is the most effective method for controlling SDS. Some cultivars and lines with good levels of resistance have been identified (Hartwig et al., 1996; Hartman et al., 1997; Schmidt et al., 1999; Mueller et al., 2002) and this resistance has been shown to be polygenic in field studies (Hnetkovsky et al., 1996; Chang et al., 1996). For example, resistance was conditioned by a minimum of six loci in a population developed from crossing ‘Forrest’ with ‘Essex’ (Iqbal et al., 2001; Njiti et al., 2002; Lightfoot et al., 2005). Resistance to SDS is also partial since all soybean genotypes tested have shown some SDS symptoms under severe disease pressure (Iqbal et al., 2001; Njiti et al., 2002).

Field studies measuring the reaction of cultivars to SDS typically have been conducted in fields with histories of SDS symptoms (Njiti et al., 1996). However, selection for SDS resistance in the field is difficult because of the sensitivity of symptom development to environmental factors (Gibson et al., 1994; Njiti et al., 1996; Scherm and Yang, 1996). The occurrence of SDS in a field is unpredictable and the disease is often too scattered or not severe enough to be useful in evaluating resistance. Inoculation methods have been developed; however, the efficiency of these methods is not clear. Stephens et al. (1993) used microplots to evaluate reactions of 12 soybean cultivars grown in soil infested and inoculated with FSG. Plants were inoculated at the V7 to V9 growth stage (Fehr et al., 1971) by placing 15 infested oat grains next to the taproot 1 cm below the soil surface. They concluded that the inoculation of soil with FSG-infested oats is a reliable alternative to the use of infested soil when soybean cultivars are evaluated for field reactions to FSG. Ringler (1995) compared four field inoculation methods and concluded that FSG-infested sorghum seeds placed next to the taproot at the V2 growth stage was effective for screening cultivars for SDS resistance, but was tedious. The author emphasized the need to identify improved inoculation methods for conducting SDS field studies.

The association of high soil moisture and soil compaction with greater occurrence and severity of SDS is a common field observation (Ringler, 1995; Roy et al., 1997). Melgar et al. (1994) reported that the incidence and severity of SDS was greater in irrigated than nonirrigated plants. Scherm and Yang (1996) reported a positive association between soil moisture and SDS severity, showing that soil moisture plays an important role in the relationship between SDS severity and seed yield loss. In the greenhouse, Roy et al. (1989) also found a positive relationship between soil moisture and SDS incidence. However, information on the optimal timing of irrigation to promote SDS symptom development in the field is not known.

Greater SDS severity has been found in compacted areas of fields when compared to noncompacted areas. This trend may be caused by compacted soils being wetter than noncompacted soils. Deep tillage in poorly drained fields that breaks up compaction can reduce SDS occurrence (Rupe and Hartman, 1999). Vick et al. (2003) compared tilled plots with no-till plots and observed that subsoiling dramatically reduced symptoms of SDS. The authors concluded that in areas where SDS occurs and soil compaction exists, subsoiling can be used to reduce the severity of SDS foliar symptoms.

The development of a reliable field inoculation method as well as greater knowledge about the effect of moisture and soil compaction on SDS symptom development will help researchers identify genotypes with resistance to the disease. The objective of this study was to evaluate the effect of field inoculation treatments, soil compaction, and irrigation timing on the occurrence and development of SDS symptoms.

	MATERIALS AND METHODS

TOP NOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION REFERENCES

 
Inoculation Experiments
The experiments were conducted in Urbana, IL, in 2002 and 2003 in fields with no history of high SDS incidence. Main plots were arranged in a randomized complete block design with four replicates. Main plots were divided in a split-plot, with inoculation treatments applied to main plots and cultivars to subplots. The experiment was sown on 10 June 2002 and 1 May 2003. The soil type of the field during both years was an Elburn silt loam (fine-silty, mixed, superactive, mesic Aquic Argiudoll). Each cultivar in a subplot was sown in a four-row plot that was 5 m long with a 75-cm row spacing, a planting depth of 3 cm, and a seeding rate of 350000 seeds ha^–1. The cultivars were Asgrow AG3302, which is classified as partially resistant to SDS, and Asgrow AG3003, which is classified as SDS susceptible (Monsanto, 2005). Both cultivars are susceptible to soybean cyst nematodes (SCN) (Heterodera glycines Ichinohe). The inoculation treatments evaluated in both 2002 and 2003 were: (1) no inoculum (control), (2) infested sorghum (300 kg ha^–1) broadcasted and incorporated into the soil before planting, (3) infested popcorn (40 kg ha^–1) planted in the furrow with the soybean seed, (4) infested oats (120 kg ha^–1) broadcasted and incorporated into the soil before planting, (5) liquid inoculum placed 5 cm below the seed before planting (500 L ha^–1), and (6) infested sorghum (45 kg ha^–1) placed below the soybean seed just before planting. For inoculation treatments 2 and 4, the infested grain was broadcasted with a fertilizer drop spreader and incorporated with a rear tine rotor tiller to a depth up to 8 cm. For inoculation method 3, the inoculum was mixed with the seed just before planting. For inoculation method 6, the infested sorghum seeds were planted with the plot planter at a depth of 8 cm. The planter was then reset to a normal depth, and the soybean seeds were planted directly on top of the infested sorghum.

The FSG isolate FSG1 (originating from Monticello, IL) was used to produce all the inoculum. FSG1 was isolated by Lynn Gray and was originally named Mont-1. Since 2000, the isolate was inoculated onto soybean and reisolated annually. The grain inoculum was prepared by first soaking seed of white sorghum [Sorghum bicolor (L.) Moench], popcorn (Zea mays L.) or oat (Avena sativa L.) overnight in water. The grain was drained and 4 kg was placed into a clear autoclave bag and autoclaved for 1 h twice. Each bag was then inoculated with 30 plugs (4-mm diameter) of fungal mycelium and incubated at room temperature for 2 wk. For the liquid inoculum, one 100 by 15 mm plate of ground mycelium per liter of water was used. The colony-forming unit (CFU) of the infested sorghum, popcorn, and oat seeds used as inoculum in 2003 was determined as previously reported on hairy roots (Li et al., 2002) with slight modifications. Briefly, 1 g of inoculum was soaked in a 250-mL Erlenmeyer flask containing 100 mL of sterile distilled water. The flasks were shaken at 150 rpm on an orbital shaker for 30 min, and then the mixture was serially diluted 10 fold with sterile distilled water twice. From each dilution, 100 µL of inoculum dilution was spread on an agar plate (100 by 15 mm) containing FSG semiselective medium (Huang and Hartman, 1996). Six plates were used for each inoculum dilution. The plates were incubated at room temperature (25 ± 2°C) for 10 d. Colonies of FSG were identified as described previously (Li et al., 2000). The number of colonies on each plate was used to determine the CFUs per gram of sorghum. The experiment was conducted two times.

To observe the residual effect of the inoculum in the soil, the same cultivars were planted in 2003 in the same positions in the field as the 2002 experiment, without any re-inoculation. This experiment was analyzed as a split-split plot design, with inoculation treatments applied to main plots, cultivars as subplots, and years as sub-subplots. In the inoculation and residual effect experiments, approximately 76 mm of water was applied to the plots at the growth stages V3, V7, and R4 using overhead irrigation to provide sufficient soil moisture to favor disease development.

Irrigation and Compaction Experiments
Experiments were conducted in Urbana in 2002, 2003, and 2004 in fields with no history of high SDS infections. The soil type of the field during all 3 yr was an Elburn silt loam. All plots in these experiments were inoculated with infested sorghum grain by placing the inoculum below the soybean seed according to inoculation method 6. The experimental unit was an eight-row plot, 5 m long with a 75-cm row spacing. The seeding rate was 350000 seeds ha^–1 and the planting depth was 3 cm. In all 3 yr, four replications of a randomized complete block design were used. In 2002, the plots were arranged in a split-split plot design. The compaction treatments were the main plots, irrigation treatments were the sub-plots and cultivars were the sub-subplots. The 2002 experiment was sowed on 16 May, the 2003 experiment was sowed on 1 May, and the 2004 experiment was sowed on 29 April. The compaction treatments were done by driving a Case IH 7220 tractor across the compacted plots once in early spring with the tires edge to edge so the treated areas were compacted uniformly. The tractor weighs approximately 11000 kg and is equipped with 46 by 106 cm radial tires with a tire pressure of 55 kPa. Five compaction measurements were taken in each plot with a Rimik CP20 cone penetrometer (Agridy, Rimik, Toowoomba, QLD) 30° cone tip with a base diameter of 1.27 cm at the growth stage V3.

Irrigation treatments were applied with a trickle irrigation system. The irrigation tapes were placed next to the two center rows of each plot, and the equivalent to 76 mm of rain was applied to the two center rows of the plots at each irrigation application. The 2002 and 2003 irrigation treatments were as follows: (1) rain feed (control), (2) rain with irrigation at V3, (3) rain with irrigation at V7, (4) rain with irrigation at V3 and V7, and (5) rain with irrigation at V3, V7 and R4.

The experiment was repeated in 2003 and 2004 without the compaction treatment. During these years, plots within blocks were arranged in split-plot, using irrigation treatments as main plots and cultivars as subplots. In 2004, the following irrigation treatments were applied: (1) rain feed (control), (2) rain with irrigation at R4, (3) rain with irrigation at V3 and V7, (4) rain with irrigation at V3, V7, and R4, (5) rain with irrigation at V3, V7, R4, and R5, and (6) rain with irrigation at R3, R4, and R5. The treatments were applied to the cultivars AG3003 and AG3302, which also were used in the inoculation experiment.

Soybean Cyst Nematode Egg Counts
For all experiments, soil samples were taken just before harvest to measure the level of SCN infestation. Each sample consisted of 10 subsamples of 20-cm-deep cores. In each replicate from each experiment, a sample was taken from the control plot and from the treatment which showed the most severe SDS symptoms. A 100-cm³ subsample of soil was taken from each sample and processed according to Byrd et al. (1976). Briefly, a 100-cm³ subsample of soil was taken from each sample and processed using a semi-automatic elutriator to extract the cysts from the soil (Univ. of Georgia Science Instrument Shop, Athens, GA). The cysts were ground with a rubber stopper to release the eggs on nested 150 µm over 75 µm over 25 µm wire mesh sieves. The egg suspension was then stained with 3 mL of egg staining solution (0.35 g of acid fuschin, 250 mL lactic acid, 750 mL water) and microwaved on high temperature until the sample had boiled for at least 30 s. The sample was diluted with water by bringing the volume to 100 mL. A 5-mL sample was counted to estimate the number of eggs of H. glycines in each plot.

Collection of Field Data
For all experiments, research plots were rated for maturity date, plant lodging, plant height, seed yield, and SDS foliar symptoms. Maturity date was recorded as the date when 95% of the pods had turned to their mature color. Plant lodging was rated at the growth stage R8 on a scale from 1 = all plants upright to 5 = all plants prostrate, and plant height was measured in centimeters at R8 as the distance from the ground to the uppermost node of an average plant. Seed yields were measured by harvesting the center two rows of plots and were reported as kilograms per hectare on a 130 g kg^–1 moisture basis. The disease incidence (DI) and disease severity (DS) were taken according to Gibson et al. (1994) at the growth stage R6. Disease incidence was taken as a percentage of plants with foliar symptoms. Foliar disease severity was recorded as: 1 = 0 to 10% chlorosis or 1 to 5% necrosis; 2 = 10 to 20% chlorosis or 6 to 10% necrosis; 3 = 20 to 40% chlorosis or 10 to 20% necrosis; 4 = 40 to 60% chlorosis or 20 to 40% necrosis; 5 60% chlorosis or > than 40% necrosis; 6 = up to 33% defoliation; 7 = up to 66% defoliation; 8 66% defoliation; and 9 = premature death of the plant. A disease index (DX; 0–100) was calculated as [(DI)(DS)]/9.

Statistical Analysis
For all experiments, analysis of variance was computed for the field data using the mixed procedure of SAS (SAS Institute, 2000) with standard analysis methods for a split-split plot and split-plot test (Snedcor and Cochran, 1980). Years and blocks were treated as random factors, while all other factors were treated as fixed. The exception was the residual effect experiment, where years were also considered a fixed factor. Means were separated using LSD (5%). Normality and homogeneity of variances of the data were tested and verified. Seed yield was predicted from DX with linear regression in the GLM procedure of SAS (SAS Institute, 2000) using the plot data from the 2002 and 2003 inoculation experiments. To remove the effect of year in this analysis, year was modeled using the MANOVA option in the GLM procedure of SAS (SAS Institute, 2000) and obtained DX and seed yield residuals were fit with the linear regression model.

	RESULTS AND DISCUSSION

TOP NOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION REFERENCES

 
Inoculation Experiments
Low SDS symptoms were observed for noninoculated control plots in 2002 and 2003, indicating that the nurseries had minimal natural infestation of FSG (Table 1). Typical root and foliar symptoms of SDS were observed for some inoculation treatments. Low to moderate end of season egg densities were observed (Table 2), indicating that SCN was not a major factor in these field tests. There were sufficient CFUs from the inoculum used in the 2003 experiment to indicate that all grain were efficient in multiplying the FSG. The CFUs per gram of inoculum were 3.5 x 10³ for the popcorn inoculum, 2.4 x 10⁵ for the sorghum inoculum, and 2.2 x 10⁵ for the oat inoculum.

The SDS DX data obtained in 2002 and 2003 were very consistent with no changes in the ranking among inoculation treatments between years. As expected, more severe SDS symptoms were observed for the susceptible cultivar AG3003 than for the partially resistant cultivar AG3302 (Table 1). When cultivars were analyzed separately, significant differences for DX were observed among the inoculation treatments for AG3003 but not for AG3302. For AG 3003, inoculation treatments 3 and 6 resulted in the highest DX rating and these were significantly greater than the control. Significant differences for DX were observed between the cultivars for treatments 3 and 6 (LSD = 7.6), which show that these treatments were effective in separating the partially resistant from the susceptible cultivar. The inoculum was placed close to the seed for treatments 3 and 6, and this proximity to the roots is the probable reason for the higher DX values for these methods when compared to other inoculation treatments. In contrast, much lower levels of disease were observed for treatments 2 and 4, where the inoculum was broadcast and incorporated into the soil before planting. In addition, the oat seed used in method 4 are bulky and fibrous making it difficult to administer consistent dosage of inoculum (Ringler, 1995). Except for method 6, no significant differences in seed yield from the control were detected for the partially resistant cultivar AG3302 (Table 1). For AG3003, significantly lower seed yields than the control were observed for both treatments 3 and 6. The significantly lower seed yields were probably the result of SDS, as inoculation treatments 3 and 6 caused the greatest symptom expression.

For AG3003, a significant (P < 0.0001) linear relationship was observed between seed yield and DX (Fig. 1 ) across the 2002 and 2003 inoculation test. The seed yield loss was 20.8 kg ha^–1 for each unit increase in DX after the effect of year was removed. This is similar to the loss of 18 to 29 kg ha^–1 reported by Luo et al. (2000). However, in other studies slight seed yield losses due to SDS were reported (Stephens et al., 1993). This lack of association between seed yield and SDS symptoms might be related to the differential resistance of cultivars to the disease. Timing of symptom development is also an important factor in seed yield losses. The effect of SDS on seed yield depends on the growth stage of the host at the onset of symptom development, and whether the disease progresses rapidly and becomes severe (Roy et al., 1997). Stephens et al. (1993) observed that for SDS to affect seed yield, the disease must become severe before the R5 growth stage. In our studies the first symptoms were, in general, observed at the R4 growth stage.

View larger version (11K): [in this window] [in a new window]   Fig. 1. Scatter plot of sudden death syndrome disease index (DX) with seed yield (kg ha–1) for the susceptible cultivar AG3003 using the individual plot data from the 2002 and 2003 inoculation experiments. The slope was calculated by regressing the residuals after the effect of year was removed from the DX and seed yield values.

Inoculation Residual Effect Experiment
The ANOVA of the experiment testing residual effects of inoculation revealed that inoculation treatments, cultivars, and the inoculation method by cultivar interaction were significant for DX. The DX was similar between years for the mean across cultivars and for the susceptible cultivar AG3003 (Table 3). An analysis of inoculation treatments across cultivars showed significant effects of year for inoculation method 2 and inoculation method 6. The significant effect of year for method 2 (sorghum broadcasted) was the result of a greater DX for AG3003 in 2003 than 2002 (Table 3). An explanation for this increase is that the broadcasting and incorporation of sorghum before planting in 2002 may have resulted in the placement of the inoculum too far from the soybean seed resulting in symptom escape in 2002. However, sufficient infection may have occurred in 2002 to result in multiplication of the inoculum causing 2003 infections.

In summary, we found that inoculation treatments 6 (infested sorghum placed below the seed) and 3 (infested popcorn planted in the furrow with the soybean seed) produced the most severe foliar symptoms and can be used for screening genotypes in field experiments. In addition these treatments can be easily applied in large fields, in contrast to other treatments such as described by Stephens et al. (1993) and Ringler (1995). Further experiments should be conducted to identify the optimal inoculum rates.

Irrigation and Compaction Experiment
Typical SDS root and foliar leaf symptoms were observed in the irrigation and compaction experiment during all 3 yr. Low end of season SCN egg densities were observed from egg counts in each year (Table 2). The soil compaction treatments resulted in significant increases in compaction (Table 4). Rainfall was mostly well distributed across the growing seasons each year (Fig. 2 –4 ) with the exception of a dry period from mid June through mid July in 2002 and from mid July through the end of August in 2003.

View larger version (19K): [in this window] [in a new window]   Fig. 2. Precipitation (mm) from May to August 2002. The growth stages when irrigation (75 mm) was applied are denoted by the arrows.

View larger version (19K): [in this window] [in a new window]   Fig. 3. Precipitation (mm) from May to August 2003. The growth stages when irrigation (75 mm) was applied are denoted by the arrows.

View larger version (23K): [in this window] [in a new window]   Fig. 4. Precipitation (mm) from May to August 2004. The growth stages when irrigation (75 mm) was applied are denoted by the arrows.

The analysis of variance across 2002 and 2003 showed no significant effect of irrigation treatments for all traits across the two cultivars. A significant effect of year was observed for maturity and plant height, and a significant cultivar effect was found for lodging. A significant cultivar x year interaction was detected for maturity and a significant irrigation treatment x cultivar interaction was detected for seed yield. Even though the irrigation treatment x cultivar interaction was not significant for the other traits, contrasts for irrigation treatments were calculated by cultivar for all traits because of the high SDS susceptibility for AG3003.

When DX values were analyzed separately by cultivar, no significant differences for any trait were detected among the irrigation treatments for the partially resistant cultivar AG3302 (Table 5). For the susceptible cultivar AG3003, there was a significant effect of irrigation on DX and maturity. Irrigation treatment 5 produced significantly more severe symptoms than treatments 1, 2, and 3.

A significant irrigation treatment effect for DX and maturity was observed only for the susceptible cultivar AG3003 in 2004 (Table 6). This cultivar showed significantly greater DX for three treatments that included irrigation during reproductive stages when compared to the control. One irrigation at the R4 stage (treatment 2) resulted a significant increase in SDS foliar symptoms, while the irrigation applied only at V3 and V7 vegetative stages (treatment 3) was not effective in significantly increasing DX rates compared to the control. However, the greatest DX values were detected for irrigation treatments 4 and 5, showing a tendency of higher DX rates with water application during both vegetative and reproductive stages of the plants.

Our results support previous research which shows that SDS is favored by high soil moisture (Hirrel, 1987; Roy et al., 1989; Melgar et al., 1994; Scherm and Yang, 1996). According to Scherm and Yang (1996), the most severe SDS foliar symptoms would be expected after the appearance of favorable conditions during early stages for root colonization and infection followed by favorable conditions (such as high moisture and intermediate to high temperature) for plant growth. This would lead to high translocation of toxins from the roots to the foliage.

Our results show especially the importance of irrigation during reproductive stages in causing SDS symptoms. The dramatic response to irrigation at R4 suggests that water is important in the translocation of toxins from the roots to the foliage. Another hypothesis is that reduced soil aeration could cause higher toxin production by the fungus. Miller and Burke (1977) implicated reduced soil aeration as a predisposing factor for root rot of bean (Phaseolus vulgaris L.) in wet soils. In contrast, no significant increase in SDS symptoms was observed compared to the control when irrigation treatments were only applied during vegetative stages. Some authors have indicated the importance of high soil moisture at early stages on the development of SDS foliar symptoms in soybeans. Rupe (1988) isolated FSG from soybean roots as early as 3 wk after planting in the field indicating that early season infection may be important for later SDS symptom development. Roy et al. (1989) found that SDS symptoms were more severe in plants irrigated continuously from V3 stage compared with those irrigated continuously from V8 stage, indicating that high soil moisture, probably early in soybean development, is critical for SDS symptom development. The lack of response of the irrigation treatments during vegetative stages in our experiments indicates that natural rainfall provided sufficient soil moisture during these stages to enable good root colonization and infection of FSG on the plant roots.

Although treatment 5 in 2002 and 2003, and treatments 2, 4, and 5 in 2004 resulted in a significantly greater DX than the control for AG3003, the effect of these treatments on seed yield was not significant compared to the control. For these treatments, the expected seed yield reductions resulting from irrigation causing greater disease may have been offset by extra water provided by the irrigation promoting greater pod fill. Due to premature defoliation caused by the disease, those treatments that had significant increases in DX also matured significantly earlier that the control.

In summary, there were no significant effects of soil compaction on SDS foliar symptoms development, but compaction caused a significant seed yield decrease. On the other hand, we observed that moisture, especially during mid to late reproductive growth stages, is an important factor for SDS foliar symptom development. Even in 2002 and 2004 (Fig. 2 and 4), when considerable rainfall occurred during late reproductive stages R4 to R6, the response of SDS symptoms to irrigation was significant. One limitation of our study was that we did not control rainfall by covering the plots when it rained. The lack of significant effects from irrigation treatments during vegetative growth stages may be the result of the rain received during these stages. If less rain occurred, it is possible that irrigation treatments during vegetative growth stages would have had a significant effect.

These results should be useful to researchers testing for resistance to SDS in field trials. Our experience, and the experience of our collaborators, has shown that when SDS field trials are not irrigated or inoculated, there is less that a 50% chance that ratable symptoms will occur. However, our tests show that by placing inoculum close to the seed and irrigating during reproductive growth stages, we were able to obtain sufficient symptoms to separate the SDS resistance level of a partially resistant and susceptible genotype each year we conducted the test. The use of these treatments should help researchers increase the efficiency of field screening for SDS resistance as both the inoculation and irrigation treatments can be applied to fields greater than a hectare without a large commitment of resources.

	NOTES

TOP NOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION REFERENCES

 
This research was supported by grants from the Illinois Soybean Checkoff Board and the United Soybean Board. A.L. Farias Neto was supported by CAPES, Ministry of Education, Brazil and by Embrapa, Ministry of Agriculture, Brazil.

Received for publication February 28, 2006.

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TOP NOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION REFERENCES

 

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