J. P. Bond

Response of Soybean Sudden Death Syndrome to Subsoil Tillage

The soilborne pathogen Fusarium solani f. sp. glycines causes sudden death syndrome (SDS) of soybean. Previous research indicated that soil compaction related directly to disease foliar symptoms. Therefore, we hypothesized that decreasing soil compaction would increase soil porosity and provide a more aerated root zone that would hinder root infection by the fungus and decrease SDS foliar symptom severity. Two experimental areas (110 by 120 m) were established to evaluate the relationship between soil variables and SDS. Across the experimental area, strips (9.14 m wide) were subsoiled perpendicular to soybean rows to a depth of 40 to 45 cm, which alternated with strips that were not tilled. In both 1999 and 2000, subsoiling dramatically reduced foliar symptoms of SDS. Compared with no-till plots, subsoiled plots had lower soil bulk density, greater soil porosity, and less soil moisture. In areas where SDS occurs and soil compaction exists, the use of subsoiling can be used to reduce severity of foliar symptoms of SDS.

A Coordinated Effort to Manage Soybean Rust in North America: A Success Story in Soybean Disease Monitoring

Existing crop monitoring programs determine the incidence and distribution of plant diseases and pathogens and assess the damage caused within a crop production region. These programs have traditionally used observed or predicted disease and pathogen data and environmental information to prescribe management practices that minimize crop loss. Monitoring programs are especially important for crops with broad geographic distribution or for diseases that can cause rapid and great economic losses. Successful monitoring programs have been developed for several plant diseases, including downy mildew of cucurbits, Fusarium head blight of wheat, potato late blight, and rusts of cereal crops. A recent example of a successful disease-monitoring program for an economically important crop is the soybean rust (SBR) monitoring effort within North America. SBR, caused by the fungus Phakopsora pachyrhizi, was first identified in the continental United States in November 2004. SBR causes moderate to severe yield losses globally. The fungus produces foliar lesions on soybean (Glycine max) and other legume hosts. P. pachyrhizi diverts nutrients from the host to its own growth and reproduction. The lesions also reduce photosynthetic area. Uredinia rupture the host epidermis and diminish stomatal regulation of transpiration to cause tissue desiccation and premature defoliation. Severe soybean yield losses can occur if plants defoliate during the mid-reproductive growth stages. The rapid response to the threat of SBR in North America resulted in an unprecedented amount of information dissemination and the development of a real-time, publicly available monitoring and prediction system known as the Soybean Rust-Pest Information Platform for Extension and Education (SBR-PIPE). The objectives of this article are (i) to highlight the successful response effort to SBR in North America, and (ii) to introduce researchers to the quantity and type of data generated by SBR-PIPE. Data from this system may now be used to answer questions about the biology, ecology, and epidemiology of an important pathogen and disease of soybean.

Development of Soybean Cyst Nematode on Henbit (Lamium amplexicaule) and Purple Deadnettle (Lamium Purpureum)

A survey of seven production fields in Indiana, Illinois, and Ohio was conducted to assess henbit and purple deadnettle growth and soybean cyst nematode (SCN) development and reproduction on these weeds. Autumn and spring growth of purple deadnettle and henbit was influenced by location within each state. In general, winter annual weeds were larger in size and reached maturity earlier in the spring at the southern sample sites than those in the north. All growth stages of SCN were found to be associated with henbit and purple deadnettle at both autumn and spring sample timings. SCN juveniles were generally found infecting roots at highest abundance in the spring. SCN cyst and egg production also were widespread and occurred to a much higher degree during the autumn than the spring developmental period. The results of this survey indicate that management tactics designed to minimize the potential for SCN reproduction on winter annual weeds would probably be most effective if conducted in the autumn, when the majority of SCN reproduction occurred. However, spring populations of winter annual weeds that harbor SCN juveniles might facilitate additional SCN reproduction and population increase if the weeds are not controlled in a timely manner prior to planting. Nomenclature: Henbit, Lamium amplexicaule L. LAMAM; purple deadnettle, Lamium purpureum L. LAMPU; soybean, Glycine max (L.) Merr; soybean cyst nematode, Heterodera glycines Ichinohe.

Response of soybean sudden death syndrome to tillage and cultivar

Sudden death syndrome (SDS), caused by Fusarium solani f. sp. glycines, is a season-long root disease of soybean (Glycine max) with foliar symptoms beginning in late vegetative and early reproductive stages of plant growth. The disease has been reported in most soybean-growing regions of the United States of America and the world. Previous research found that SDS was less severe in areas that were subsoiled when compared with those with no-till. The objectives of the current study were to determine (i) if cost-effective tillage practices, i.e., chisel plowing and disk tillage, can be efficient in reducing SDS and (ii) if cultivars with a range of SDS resistance or susceptibility respond differently in SDS expression across various tillage practices. In the fall of 2000 and 2001, plots were established in a field with a history of severe SDS and with a soil type consisting of an Armiesburg silty clay loam. The experiment was organized in a split-plot design with four replications. Main plots were tillage (chisel tillage, disk tillage, and no tillage), and subplots were cultivars randomized in main plots. Twelve cultivars were selected based on resistance or susceptibility to SDS. In 2000, chisel tillage reduced the area under the foliar disease progress curve (AUFDPC) when compared with no-till or disk tillage. In 2001, both chisel and disk tillage reduced AUFDPC similarly when compared with no-till. In 2000, the rate of root infection by the fungus, that is, the area under the root colonization progress curve (AURCPC), was higher in both disk- and chisel-tillage treatments than in no-tillage treatments. In 2001, higher rates of root infection occurred with chisel tillage compared with disk tillage and no-till. Among the cultivars, foliar disease ratings, AUFDPC, and soybean yield differed, but there were no differences in the AURCPC.

Characterization of Quinone Outside Inhibitor Fungicide Resistance in Cercospora sojina and Development of Diagnostic Tools for its Identification

Frogeye leaf spot of soybean, caused by the fungus Cercospora sojina, reduces soybean yields in most of the top-producing countries around the world. Control strategies for frogeye leaf spot can rely heavily on quinone outside inhibitor (QoI) fungicides. In 2010, QoI fungicide-resistant C. sojina isolates were identified in Tennessee for the first time. As the target of QoI fungicides, the cytochrome b gene present in fungal mitochondria has played a key role in the development of resistance to this fungicide class. The cytochrome b genes from three QoI-sensitive and three QoI-resistant C. sojina isolates were cloned and sequenced. The complete coding sequence of the cytochrome b gene was identified and found to encode 396 amino acids. The QoI-resistant C. sojina isolates contained the G143A mutation in the cytochrome b gene, a guanidine to cytosine transversion at the second position in codon 143 that causes an amino acid substitution of alanine for glycine. C. sojina-specific polymerase chain reaction primer sets and TaqMan probes were developed to efficiently discriminate QoI-resistant and -sensitive isolates. The molecular basis of QoI fungicide resistance in field isolates of C. sojina was identified as the G143A mutation, and specific molecular approaches were developed to discriminate and to track QoI-resistant and -sensitive isolates of C. sojina.

Effect of fungicide seed treatments on Fusarium virguliforme infection of soybean and development of sudden death syndrome

Abstract Sudden death syndrome (SDS), caused by Fusarium virguliforme (Fv), is a major yield-limiting disease of soybean in North America. Infection of soybean seedling roots by Fv results in severe root damage; therefore, fungicide seed treatments could potentially reduce these early-season infections and reduce severity of foliar symptoms that typically occur later in the season. Multiple fungicide seed treatment combinations were evaluated for their effects on Fv infection, DNA concentrations in roots, soybean root development, and SDS development in the field, greenhouse and laboratory trials. Several seed treatments decreased root disease symptoms compared with the non-treated inoculated control in the laboratory assay, and the biological seed treatment, Bacillus pumilus, significantly decreased seedling development and increased SDS root disease compared with the non-treated inoculated control. In the greenhouse, Fv DNA concentrations in roots were reduced by a treatment combining mefenoxam + thiophanate-methyl + azoxystrobin + Bacillus pumilus + prothioconazole + fludioxonil compared with the non-treated control; however, the reduction in Fv DNA did not improve root growth or decrease SDS symptoms compared with the non-treated control. Field trials were conducted in Valmeyer, IL in 2008 and in Urbana, IL in 2008 and 2009. Seed treatments had no effect on the concentration of Fv DNA in soybean roots and had very little effect on root morphology. At the Valmeyer location, most seed treatments significantly decreased SDS symptoms compared with the control. In summary, no consistent, significant effects of the seed treatments evaluated in this study on SDS or Fv root infection were observed. Therefore, soybean growers should continue to utilize other practices for SDS management until new seed treatments with consistent efficacy in controlling SDS are available.

Quantitative Trait Loci (QTL) that Underlie SCN Resistance in Soybean (Glycine max (L.) Merr.) PI438489B by 'Hamilton' Re- combinant Inbred Line (RIL) Population

1 Plant Genomics & Biotechnology Lab, Department of Biological Sciences, Fayetteville State University, Fayetteville, NC, USA; 2 Department of Plant, Soil, and Agricultural Systems, Southern Illinois University, Carbondale, IL, USA; 3 Soybean Genomics and Improvement Lab, 10300 Baltimore Ave, Bldg. 006, Rm. 201, Beltsville, MD 20705; 4 Unite de Recherche En Genomique Vegetale, INRA, Ivry, France; 5 USDA-ARS Midsouth Area, Jackson, TN, USA; 6 Department of Agriculture, Alcorn State University, Alcorn State, MS, USA; 7 Plant Pathology Department and Agronomy Department, Iowa State University, Ames, IA 50011-1010.

FvSNF1 , the sucrose non-fermenting protein kinase gene of Fusarium virguliforme , is required for cell-wall-degrading enzymes expression and sudden death syndrome development in soybean

Fusarium virguliforme is a soil-borne pathogenic fungus that causes sudden death syndrome (SDS) in soybean. Its pathogenicity is believed to require the activity of cell-wall-degrading enzymes (CWDEs). The sucrose non-fermenting protein kinase 1 gene (SNF1) is a key component of the glucose de-repression pathway in yeast, and a regulator of gene expression for CWDEs in some plant pathogenic fungi. To elucidate the functional role of the SNF1 homolog in F. virguliforme, FvSNF1 was disrupted using a split-marker strategy. Disruption of FvSNF1 in F. virguliforme abolishes galactose utilization and causes poor growth on xylose, arabinose and sucrose. However, the resulting Fvsnf1 mutant grew similar to wild-type and ectopic transformants on glucose, fructose, maltose, or pectin as the main source of carbon. The Fvsnf1 mutant displayed no expression of the gene-encoding galactose oxidase (GAO), a secretory enzyme that catalyzes oxidation of D-galactose. It also exhibited a significant reduction in the expression of several CWDE-coding genes in contrast to the wild-type strain. Greenhouse pathogenicity assays revealed that the Fvsnf1 mutant was severely impaired in its ability to cause SDS on challenged soybean plants. Microscopy and microtome studies on infected roots showed that the Fvsnf1 mutant was defective in colonizing vascular tissue of infected plants. Cross and longitudinal sections of infected roots stained with fluorescein-labeled wheat germ agglutinin and Congo red showed that the Fvsnf1 mutant failed to colonize the xylem vessels and phloem tissue at later stages of infection. Quantification of the fungal biomass in inoculated roots further confirmed a reduced colonization of roots by the Fvsnf1 mutant when compared to the wild type. These findings suggest that FvSNF1 regulates the expression of CWDEs in F. virguliforme, thus affecting the virulence of the fungus on soybean.

Benefits and profitability of fluopyram-amended seed treatments for suppressing sudden death syndrome and protecting soybean yield: A meta-analysis

A meta-analytic approach was used to summarize data on the effects of fluopyram-amended seed treatment on sudden death syndrome (SDS) and yield of soybean (Glycine max L.) in over 200 field trials conducted in 12 U.S. states and Ontario, Canada from 2013 to 2015. In those trials, two treatments-the commercial base (CB), and CB plus fluopyram (CBF)-were tested, and all disease and yield data were combined to conduct a random-effects and mixed-effects meta-analysis (test of moderators) to estimate percent control and yield response relative to CB. Overall, a 35% reduction in foliar disease and 295 kg/ha (7.6%) increase in yield were estimated for CBF relative to CB. Sowing date and geographic region affected both estimates. The variation in yield response was explained partially by disease severity (19%), geographic region (8%), and sowing date (10%) but not by the resistance level of the cultivar. The probability of not offsetting the cost of fluopyram was estimated on a range of grain prices and treatment cost combinations. There was a high probability (>80%) of yield gains when disease level was high in any cost-price combinations tested but very low when the foliar symptoms of the disease were absent.

Unraveling Microbial and Edaphic Factors Affecting the Development of Sudden Death Syndrome in Soybean

Sudden death syndrome (SDS) caused by Fusarium virguliforme is a widespread and economically important disease of soybean. SDS is typically distributed unevenly in patches across soybean fields. While certain spots in fields are highly conducive to the development of severe SDS, other areas appear to be naturally healthy or suppressive to the disease. The role of soil microbial communities and soil physical and chemical properties in SDS development was investigated in 45 soybean fields in Illinois, Iowa, and Minnesota. Soil samples were collected from symptomatic patches in fields and from adjacent areas where SDS foliar symptoms did not develop. Multiple edaphic factors were measured, and markers specific to bacteria, fungi, archaea, oomycete, and nematodes, coupled with Illumina MiSeq sequencing, were used to identify key taxa likely associated with SDS development. A total of 14,200,000 reads were mapped against the National Center for Biotechnology Information nucleotide database and taxonomically co...