Soybean phytophthora resistance gene Rps8 maps closely to the Rps3 region.

Root and stem rot is one of the major diseases of soybean. It is caused by the oomycete pathogen Phytophthora sojae. A series of resistance genes (Rps) have been providing soybean with reasonable protection against this pathogen. Among these genes, Rps8, which confers resistance to most P. sojae isolates, recently has been mapped. However, the most closely linked molecular marker was mapped at about 10 cM from Rps8. In this investigation, we attempted to develop a high-density genetic map of the Rps8 region and identify closely linked SSR markers for marker-assisted selection of this invaluable gene. Bulk segregant analysis was conducted for the identification of SSR markers that are tightly linked to Rps8. Polymorphic SSR markers selected from the Rps8 region failed to show cosegregation with Phytophthora resistance. Subsequently, bulk segregant analysis of the whole soybean genome and mapping experiments revealed that the Rps8 gene maps closely to the disease resistance gene-rich Rps3 region.

Field Response of Glyphosate-Tolerant Soybean to Herbicides and Sudden Death Syndrome.

Three-year field experiments were conducted to assess the development of sudden death syndrome (caused by Fusarium solani f. sp. glycines) in three soybean cultivars, tolerant (P9344 and A3071) and nontolerant (BSR101), to glyphosate following foliar application of four herbicides (acifluorfen, glyphosate, imazethapyr, and lactofen) commonly applied to soybeans in the north-central region of the United States. Cultivar A3071 is resistant to sudden death syndrome, whereas cultivars P9344 and BSR101 are susceptible to this disease. There was no statistically significant cultivar-herbicide interaction with respect to the severity of foliar symptoms of the disease and the frequency of isolation of F. solani f. sp. glycines from roots of soybean plants. Across all herbicide treatments, the level of sudden death syndrome was lower in the disease-resistant cultivar than in the susceptible ones. There was an increase in the disease levels under application of acifluorfen, glyphosate, and imazethapyr compared with nontreated or lactofen-treated plants. The results obtained indicate that the response of glyphosate-tolerant soybeans to sudden death syndrome is not different from the response of conventional soybeans to this disease following application of the selected herbicides, and the resistance of soybean to sudden death syndrome was not changed with application of glyphosate.

Soybean Varietal Response and Yield Loss Caused by Sclerotinia sclerotiorum.

Soybean Sclerotinia stem rot, caused by Sclerotinia sclerotiorum, has recently emerged from being a minor problem in areas where soybeans of maturity groups 0 to I are grown to a significant cause of soybean yield losses in the north-central region, which produces 80% of soybean in the United States. Studies were conducted in Iowa to quantify varietal response to S. sclerotiorum for cultivars of maturity groups I to III in fields that had uniform infestation histories. Over the course of the study, disease incidence was generally high at the northern Iowa sites but low in central Iowa, with disease incidence of susceptible standards >60% and <30%, respectively. Regression analysis showed that maturity class significantly affected disease incidence, with greater effects in environments where susceptible standard cultivars had high disease incidences. Consistency of varietal response among the environments was quantified using Pearson correlation analysis. When disease incidence was high, varietal responses measured by disease ratings and yield were consistent among locations, but the responses were inconsistent when disease incidence was low. Pearson correlation coefficients ranged from 0.80 to 0.94 for disease incidence and 0.58 to 0.81 for yield among the experiments having high disease incidence in susceptible standards. The relationship between disease incidence and yield was well described by linear regression models with coefficients of determination (r2) ranging from 0.59 to 0.83. Based on regression slopes (significant at P < 0.0001), yield losses are estimated to range from 170 to 335 kg/ha for each 10 percentage points of disease incidence. Regression analysis also showed that maturity groups had a linear relationship with disease incidence (r2 = 0.18 to 0.39, P < 0.01).

Soil Variables Associated with Sudden Death Syndrome in Soybean Fields in Iowa.

Sudden death syndrome, caused by Fusarium solani f. sp. glycines, has increased in prevalence in soybean production regions in the North-Central United States. Little is known about soil factors and environmental conditions that influence disease severity in this pathosystem. We studied associations between biological, chemical, and physical soil variables and severity of foliar symptoms of sudden death syndrome in nine commercial soybean fields in Iowa during 1995 and 1996. Disease was patchy in all fields, and soil samples were collected in each field along a transect that ran from a symptomless area through a diseased area. There were 25 sampling stops along each transect, separated by distances of 1.5 to 2.5 m. At each stop, soil samples were collected and soil strength, soil moisture, and foliar disease severity (at plant growth stage R6) were measured. Soil samples were assayed for population densities of F. solani f. sp. glycines, cysts of the soybean cyst nematode (Heterodera glycines), and for chemical variables (soluble salts, pH, organic matter, cation exchange capacity, and concentrations of P, K, Ca, Mg, Mn, and Fe). Cross-correlation analyses were carried out to test for associations between soil variables and disease severity in individual fields, while discriminant analysis was used to assess the effects of soil variables across all fields. Disease severity showed consistent associations with F. solani f. sp. glycines populations (strong effect) and H. glycines cyst counts (minor effect). Available K was identified as a possible disease-enhancing factor, but the magnitude of its effect was dependent on the overall K-concentrations in the fields. For example, as the median K-concentration increased, the correlation between K and disease decreased. None of the other soil variables showed consistent associations with disease. The results suggest that localized presence or absence of F. solani f. sp. glycines is the chief reason for the patchiness of sudden death syndrome in affected fields. Thus, manipulation of soil nutrient status or fertility level appears to have limited potential for reducing disease in the high-yield soybean production environment of Iowa. Instead, producers should focus on preventing the establishment or reducing populations of F. solani f. sp. glycines and H. glycines in their fields.

First Report of Sclerotium Production by Sclerotinia sclerotiorum in Soil on Infected Soybean Seeds.

Stem rot of soybean caused by Sclerotinia sclerotiorum (Lib.) de Bary was not recognized as an important problem in the North Central Region of the United States until severe outbreaks occurred in 1992, 1994, and 1996 (2). Although sclerotia mixed with seeds are known to be important to the spread of this disease, the role of internally infested soybean seed in dissemination of the disease is unknown. Tu (1) demonstrated in dry bean, which differs from soybean in seed size and plant architecture, that internally infected seeds are important to the spread of the disease, by producing sclerotia in the soil after the seeds are planted. Experiments were conducted to determine if sclerotia are formed in soils from internally infected soybean seeds. Soybean seed from a field with 70% disease severity were collected and sorted into three classes: (i) normal quality seed, which included moderate or good seed; (ii) poor quality seed (shriveled and/or whitish); and (iii) seed of regular size with visible mycelial mats (S. sclerotiorum or Peronospora manshurica (Naumov) Syd. in Gäum) on the seed coat. Transfer of surface-disinfested seeds to potato dextrose agar and subsequent production of sclerotia showed that 2, 44, and 6% of the seed from each respective class were infested with S. sclerotiorum. One hundred seeds from each of these classes were planted into sterilized and nonsterilized soil at a rate of 5 seeds per pot. Toothpicks were placed to identify the location of each seed, and seeds were covered with 2 cm of soil. Pots were placed in growth chambers with a 14-h photoperiod under two temperature regimes: (i) at 20°C; and (ii) at 10°C for 10 days and then raised to 20°C. Soil was kept saturated by periodically top watering the pots for the first 10 days and bottom watering after that. Two weeks after planting, seeds were examined for formation of sclerotia and the percentages of seeds from which sclerotia were formed were calculated. The experiments were conducted four times. One to two (occasionally three) sclerotia were found in place of each seed that did not germinate. Sclerotia were mainly found from seeds of poor quality, with an average of 12% seeds that produced sclerotia. The frequency of sclerotia found in normal quality seeds was 0.4%, and no sclerotia were found from seeds with mycelial mats. The sclerotia were 2.36 ± 1.07 mm in width, 3.33 ± 1.11 mm in length, and 6.8 ± 3.7 mg in weight, with an averaged germination rate of 88% 8 months after production. Sclerotia production frequencies were 11.4 and 15.4% for temperature regimes (i) and (ii), respectively. Higher percentages of sclerotium production were found in sterilized soil (15.6%) than nonsterilized soil (7.5%). Our results indicate the possibility of internally infected soybean seeds as a means for field-to-field dissemination of S. sclerotiorum. References: (1) J. C. Tu. J. Phytopathol. 121:40, 1988. (2) X. B. Yang. ICM Newsl. 18, 1997.

Occurrence and Distribution of Soybean Sudden Death Syndrome in Iowa.

Soybean sudden death syndrome (SDS), caused by blue-pigmented, slow-growing strains of Fusarium solani, is a disease recently reported in Iowa. In 1994 and 1995 the geographic distribution and status of the disease was determined at the state, local, and field levels. An east-to-west decreasing trend of SDS prevalence was found at the state level. No SDS was found in the western part of Iowa. The disease was found in commercial production fields in 4 Iowa crop reporting districts - central, north-central, east-central, and southeastern - with the greatest severity and the most frequent occurrence of SDS found in the east-central district. In two counties along the Mississippi River, disease prevalence was high; more than 50% of soybean fields had SDS in locations where surveys were conducted. Intensive surveys on a local scale were conducted in areas around the fields where the disease was first noticed. In areas where disease prevalence was low, all detected infested fields belonged to the same owners. In areas where disease prevalence was high, no such pattern was found. Disease incidence varied from field to field. Information on SDS occurrence at different geographic scales serves as baseline information to monitor the future development of the disease in Iowa.

An approach to locating a family practice office in a metropolitan area.

A simple, economically feasible approach to locating a family practice office within a metropolitan area is presented. The Grand Rapids area serves as the population base for this investigation. An Office Location-Population Profile is determined from census tract population data and known physician office distrubution. Based on this information, a subsegment of the total area is delineated as a possible neighborhood for an office location and a physician-opulation ratio for this subsegment is determined. This is compared with recommended ratios. A statistical profile of the population, within the area considered as a possible site location, is developed using information available through census bureau statistics. Finally, a direct survey of a random sample of households within the selected area is performed. This format provides an objective approach to facilitate rational decision making in locating a family practice office in a metropolitan area.