scholarly journals First Report of Sudden Death Syndrome of Soybean Caused by Fusarium solani f. sp. glycines in Nebraska

Plant Disease ◽  
2006 ◽  
Vol 90 (1) ◽  
pp. 109-109 ◽  
Author(s):  
A. D. Ziems ◽  
L. J. Giesler ◽  
G. Y. Yuen

During August of 2004, soybean (Glycine max (L.) Merr.) plants exhibiting symptoms typical of sudden death syndrome (SDS) caused by Fusarium solani (Mart.) Sacc. f. sp. glycines (= Fusarium virguliforme Akoi, O'Donnell, Homma, & Lattanzi) (1) were observed in Nemaha and Pierce counties in eastern Nebraska. Leaf symptoms ranged from small chlorotic spots to prominent interveinal necrosis on plants at R5-R6 growth stages. Taproots of symptomatic plants were plated on potato dextrose agar (PDA) amended with hymexazol, ampicillin, and rifampicin (HAR). Resulting fungal isolates grew slowly and developed masses of blue macroconidia, characteristic of F. solani f. sp. glycines. Sorghum seed infested with the isolates were placed 1.5 cm below soybean seeds of the susceptible cv. Sloan planted in clay pots (3). Noninfested sorghum seed and sorghum seed infested with F. oxysporum were controls. Plants were maintained for 32 days at 27.5 ± 2.5°C in the greenhouse. Small cholorotic spots were observed on leaves of F. solani f. sp. glycines-inoculated plants within 21 days followed by the development of interveinal chlorosis. Roots of symptomatic plants were plated on PDA with HAR and F. solani f. sp. glycines was recovered. Identification of the fungal cultures was further confirmed as F. solani f. sp. glycines by a real-time quantitative polymerase chain reaction (qPCR) assay described by Gao et al. (2). During 2005, SDS symptoms were also reported in early planted soybeans from Jefferson and Seward counties and the presence of SDS was confirmed by qPCR. The confirmation of SDS at multiple locations suggests that the pathogen is widely distributed in the eastern one-third of Nebraska. SDS could be a serious threat to soybean production in this area since spring weather conditions favor SDS infection and many producers plant soybean early in cool soils. References: (1) T. Akoi et al. Mycologia 95:660, 2003. (2) X. Gao et al. Plant Dis. 88:1372, 2004. (3) K. W. Roy et al. Plant Dis. 81:259, 1997.

Plant Disease ◽  
2003 ◽  
Vol 87 (4) ◽  
pp. 449-449 ◽  
Author(s):  
J. E. Kurle ◽  
S. L. Gould ◽  
S. M. Lewandowski ◽  
S. Li ◽  
X. B. Yang

In August 2002, soybean (Glycine max (L.) Merr.) plants exhibiting foliar and root symptoms typical of sudden death syndrome were observed in Blue Earth and Steele counties in south-central Minnesota. Leaf symptoms ranging from small chlorotic spots to prominent interveinal necrosis were present on soybean plants at the R6 to R7 growth stage. As plants matured, complete defoliation took place with only petioles remaining. Symptomatic plants had necrotic secondary roots, truncated taproots, and discolored cortical tissue at the soil line. Blue sporodochia containing macroconidia were observed on the taproot of affected plants at both locations (3,4). Multiple cultures from both locations were obtained by transferring macroconidia from the sporodochia to potato dextrose agar (PDA) and modified Nash-Snyder Medium (NSM) (3). After 14 days, isolations were made from fungal colonies exhibiting bluish pigmentation and masses of bluish macroconidia (4). The isolates grew slowly, developed a bluish color, and formed sporodochia containing abundant macroconidia on NSM. These isolates were identified as Fusarium solani (Mart.) Sacc. f. sp. glycines based on colony characteristics and morphology of macroconidia (2). Pathogenicity tests were conducted with a single isolate from each location. The isolate from Blue Earth County was inoculated as mycelia in a plug of media onto taproots of plants of susceptible cvs. Williams 82 and Spencer at the V2 growth stage. Chlorotic spots appeared on leaves after 12 days of growth at 22 to 25°C in the greenhouse. Interveinal necrosis appeared after 15 days (4). The isolate from Steele County was used to inoculate the susceptible cv. Great Lakes 3202. Sorghum seed (3 cm3) infested with mycelia of the isolate were placed 2 to 3 cm below soybean seed planted in Cone-Tainers. Noninfested sorghum seed was used as a control. Plants were maintained for 21 days at 22 to 28°C in the greenhouse. Chlorotic spots appeared on leaves of inoculated plants within 21 days after planting followed by the development of interveinal chlorosis and necrosis (1). Molecular analysis further supported the identification of the Steele County isolate as F. solani f. sp. glycines. Polymerase chain reaction with specific primers Fsg1 and Fsg2 of total genomic DNA extracted from the Steele County isolate amplified a 438-bp DNA fragment identical with that extracted from previously identified isolates of F. solani f. sp. glycines (1). In 2002, symptoms of sudden death syndrome were also reported in Olmsted, Freeborn, and Mower counties. Although studies are needed to determine the distribution of sudden death syndrome in the state, the occurrence of the symptoms at multiple locations suggests that F. solani f. sp. glycines is widely distributed in southeast and south-central Minnesota. The counties where sudden death syndrome symptoms were reported are located in the most productive soybean-growing region of Minnesota. Sudden death syndrome could be a serious threat to soybean production in this area since poorly drained, heavy, clay soils are common, and soil temperatures 18°C or less are normal before the end of May. References: (1) S. Li et al. Phytopathology 90:491, 2000. (2) K. W. Roy. Plant Dis. 81:566, 1997. (3) K. W. Roy et al. Plant Dis. 81:1100, 1997. (4) K. W. Roy. Plant Dis. 81:259, 1997.


2018 ◽  
Vol 19 (1) ◽  
pp. 46-53 ◽  
Author(s):  
David A. Marburger ◽  
Jaime F. Willbur ◽  
Maria E. Weber ◽  
Jean-Michel Ané ◽  
Medhi Kabbage ◽  
...  

Lipo-chitooligosaccharides (LCOs) are signal molecules produced by plant root endosymbionts and have been identified, formulated, and marketed as growth-promoting adjuvants for soybean (Glycine max [L.] Merr.). Experiments were conducted under controlled environmental conditions to characterize the effects of foliar LCO applications on early symptom development of sudden death syndrome (SDS), caused by Fusarium virguliforme, and Sclerotinia stem rot (SSR), caused by Sclerotinia sclerotiorum. Treatment factors for the SDS experiment included two soybean cultivars (Sloan and CH2105R2), two inoculation levels (noninoculated control and inoculated), and two LCO applications (control and foliar LCO application), whereas two experimental soybean lines (91-38 and 91-44) and two LCO applications (water control and foliar LCO application) were used in the SSR experiment. The LCO application did not significantly influence SDS root symptom severity or early-season growth characteristics. However, on the susceptible line (P = 0.01) and with LCO application (P = 0.03), significantly larger SSR lesions developed compared with the nontreated control and resistant line. These results suggest foliar-applied LCOs have a limited effect on early root symptom development caused by F. virguliforme but increase stem symptom development caused by S. sclerotiorum.


Plant Disease ◽  
2014 ◽  
Vol 98 (7) ◽  
pp. 1012-1012 ◽  
Author(s):  
C. Tande ◽  
B. Hadi ◽  
R. Chowdhury ◽  
S. Subramanian ◽  
E. Byamukama

During the 2012 soybean growing season, soybean (Glycine max (L.) Merr.) plants submitted to South Dakota State University Plant Diagnostic Clinic exhibited symptoms typical of sudden death syndrome (SDS) caused by Fusarium virguliforme (Aoki, O'Donnell, Homma, & Lattanzi). In the 2013 soybean growing season, a soybean survey targeting SDS-symptomatic plants was carried out in 20 eastern South Dakota counties between July and August when plants were at the beginning seed and beginning seed maturity growth stages. Soybean plants with SDS-like symptoms were found in eight counties at very low incidence (<3%). Approximately 15 plants per field that had symptoms resembling those of SDS were collected and fungal isolations were made. Leaf symptoms included some necrosis and slight interveinal chlorosis. The tap roots also had areas of necrosis and the vascular system was brown. Isolations were made from the symptomatic tap root sections. The tap root sections were surface sterilized using a 10% NaOCl for 1 min and then rinsed once for 1 min with sterile water before being placed on an acidified potato dextrose agar. Slow growing isolates of F. virguliforme with characteristic blue sporodochia were isolated from these symptomatic plant roots. The conidia were banana-shaped with 4 to 5 septae, a typical characteristic for F. virguliforme. Koch's postulates were performed using a modified layer test method (2). Briefly, the conidia from the isolate (PL1200158 from Yankton county, SD) was used to infest sterile sorghum seed. In the greenhouse, three holes were punched in the bottom of 32 oz. Styrofoam cups. The bottom 11 cm of the cup was then filled with vermiculite. A 2-cm layer of fully colonized sorghum seed was placed on top of the vermiculite. This was covered with a 2- to 5-cm layer of vermiculite. Fifteen soybean cv. Sloan seeds were placed on top of this vermiculite layer and covered with approximately 2 cm more vermiculite for each cup for a total of 12 cups. The temperature in the greenhouse was approximately 23°C with 14 h of light and 10 h of darkness for 21 days. Leaves began to show necrosis and the roots had brown, rotted lesions. Symptoms did not develop on non-inoculated controls. After 5 weeks under greenhouse conditions, the roots of infected plants were removed, surface sterilized, and F. virguliforme was re-isolated. SDS was further confirmed by PCR using primers designed from FvTox1 gene. FvTox1, a single-copy gene, has been found to be highly species specific and primers from this region delineate F. virguliforme from other Fusarium species (1). The PCR product size matched that of expected size. The PCR product was sequenced and a BLAST search matched (100%) only the sequences of F. virguliforme FvTox1 gene (GenBank Accession No. JF440964). The confirmation of SDS in eight counties in South Dakota indicates that SDS may be widespread and a concern for soybean production when conditions are conducive for SDS to develop. References: (1) G. C. Y. Mbofung, et al. Plant Dis. 95:1420, 2011. (2) A. F. Schmitthenner and R. G. Bhatt. Useful Methods for Studying Phytophthora in the Laboratory. Special Circular, Ohio Agricultural Research and Development Center, Wooster, OH, 1994.


Plant Disease ◽  
2014 ◽  
Vol 98 (4) ◽  
pp. 569-569 ◽  
Author(s):  
Y. T. Tewoldemedhin ◽  
S. C. Lamprecht ◽  
J. J. Geldenhuys ◽  
F. J. Kloppers

Soybean (Glycine max (L.) Merr.) is an important crop in many countries and production is currently increasing (from 311,450 ha in 2010 to 516,500 ha in 2013) in South Africa. On 27 February 2013 in the Lydenburg/Badfontein area, Mpumalanga Province, on a no-till commercial farm planted to soybean cultivar PAN 737 (Roundup Ready, maturity group 7) under irrigation for a second consecutive season, leaf symptoms typical of soybean sudden death syndrome were observed and reported by a farmer (3). The symptoms developed at the R6 growth stage (near physiological maturity) of the soybean plants. Leaf symptoms were interveinal chlorotic blotches that became necrotic while the veins remained green. These symptoms appeared throughout the plant but were most severe on the top leaves. Some of the severely affected leaflets dropped off with the petioles remaining attached to the plant. The vascular tissue in the upper taproot and lower stem turned gray-brown, but the pith remained white. Roots of the affected plants had decayed lateral roots. Surface disinfested root pieces with rot symptoms and spores directly from blue sporodochia on the rotten root were plated on potato dextrose agar amended with novostreptomycin 0.04 g/L (PDA+). Slow growing Fusarium isolates with blue to purple masses of sporodochia were consistently obtained from diseased plants. Cultures were single-spored and plated on PDA+. Growth rate of cultures on PDA+ was on average 6 to 9 mm after 5 days at 20°C. The morphology of the isolates fit the description of Fusarium virguliforme in Aoki et al. (1). Sequence analyses of the nuclear ribosomal internal transcribed spacer (ITS) and partial translation elongation factor (EF-1a) gene of the recovered eight isolates revealed that these isolates matched 99.6% with F. virguliforme O'Donnell & T. Aoki (Accession Nos. KF648835 to KF648850), one of the soybean sudden death syndrome causing species found in North and South America (1). All isolates are identical in each loci except that three isolates had one nucleotide deletion and two insertions at the EF-1a loci. The isolates are deposited at the national culture collection in Pretoria (PPRI13434 to PPRI13441). A glasshouse bioassay was conducted to test the pathogenicity of eight single-spored isolates by inoculating pasteurized planting medium (1:1:1 ratio of sand, perlite, and soil) with a layer of infested sand-bran medium (2) to each pot (13 cm in diameter) and covered with 2 cm of planting medium (4) after planting 20 seeds of soybean cultivar PAN 737. There were three pots per isolate randomized in a complete block design trial. All the South African F. virguliforme isolates tested induced leaf and root rot symptoms of sudden death syndrome on the soybean seedlings under glasshouse conditions after 4 weeks of inoculation. The fungus was re-isolated on PDA+ from diseased roots of the soybean seedlings to fulfill Koch's postulates. This is the first record of F. virguliforme in South Africa, and as an important component of soilborne diseases of soybean it may pose a major threat to the South African soybean industry. References: (1) T. Aoki et al. Mycoscience 46:162, 2005. (2) S. C. Lamprecht et al. Plant Dis. 95:1153, 2011. (3) J. C. Rupe and G. L. Hartman. Compendium of Soybean Diseases, 4th ed. G. L. Hartman et al., eds. American Phytopathological Society, St. Paul, MN, 1999. (4) M. M. Scandiani et al. Trop. Plant Pathol. 36:133, 2011.


Plant Disease ◽  
1997 ◽  
Vol 81 (3) ◽  
pp. 259-266 ◽  
Author(s):  
K. W. Roy

Two morphological forms of Fusarium solani pathogenic on soybean, forms A and B, were further characterized and distinguished from other fungi. Questions regarding their identity were addressed. Soybean plants grown in the field and in a growth chamber were inoculated with Fusarium solani form A and F. solani f. sp. phaseoli. F. solani form A incited leaf symptoms typical of sudden death syndrome; F. solani f. sp. phaseoli did not. It was concluded that the two fungi are different and distinguishable on the basis of host specialization and the types of symptoms they incite on soybean. F. solani form A, the causal agent of sudden death syndrome, was designated F. solani (Mart.) Sacc. f. sp. glycines form. nov. Cultural and morphological characteristics of F. solani form B, the cause of seedling disease and root rot of soybean, and Plectosphaerella cucumerina were compared to determine the validity of a report indicating that they were conspecific. Results demonstrated that F. solani form B and P. cucumerina are distinctly different and not conspecific. The relevance of identifying and recognizing the two F. solani forms as separate and distinct members of the F. solani pathogen complex on soybean is discussed.


1994 ◽  
Vol 72 (11) ◽  
pp. 1647-1653 ◽  
Author(s):  
J. Melgar ◽  
K. W. Roy ◽  
T. S. Abney

Soybeans were grown in field microplots in sterile, noninfested soil versus soil infested with either Fusarium solani (form A), Heterodera glycines (the soybean cyst nematode), or both. Symptoms of sudden death syndrome occurred on plants in soil containing F. solani or F. solani plus H. glycines. Signs (macroconidia) sometimes occurred on symptomatic roots. Fusarium solani was reisolated from symptomatic plants but not from asymptomatic ones. Histological data further confirmed F. solani as the causal agent and documented the presence of F. solani chlamydospores in infected roots and cysts. Fusarium solani was not isolated from surface-disinfested seeds of infected plants. Irrigation increased disease incidence and severity. Heterodera glycines was not necessary for infection of plants by F. solani; however, when combined with F. solani, leaf symptoms occurred earlier and were more severe. Inoculation with F. solani plus H. glycines increased the incidence of tip dieback of pods, a disorder of uncertain cause. Fusarium solani was isolated in high frequency from roots of symptomatic plants sampled in the South and Midwest. However, F. solani form B was the most common isolate from roots. A significant positive correlation occurred between incidence of the two F. solani forms in roots of symptomatic plants. Key words: Glycine max, Fusarium solani, Heterodera glycines, etiology.


2015 ◽  
Vol 105 (3) ◽  
pp. 378-387 ◽  
Author(s):  
Jie Wang ◽  
Janette L. Jacobs ◽  
Jan M. Byrne ◽  
Martin I. Chilvers

Fusarium virguliforme (syn. F. solani f. sp. glycines) is the primary causal pathogen responsible for soybean sudden death syndrome (SDS) in North America. Diagnosis of SDS is difficult because symptoms can be inconsistent or similar to several soybean diseases and disorders. Additionally, quantification and identification of F. virguliforme by traditional dilution plating of soil or ground plant tissue is problematic due to the slow growth rate and plastic morphology of F. virguliforme. Although several real-time quantitative polymerase chain reaction (qPCR)-based assays have been developed for F. virguliforme, the performance of those assays does not allow for accurate quantification of F. virguliforme due to the reclassification of the F. solani species complex. In this study, we developed a TaqMan qPCR assay based on the ribosomal DNA (rDNA) intergenic spacer (IGS) region of F. virguliforme. Specificity of the assay was demonstrated by challenging it with genomic DNA of closely related Fusarium spp. and commonly encountered soilborne fungal pathogens. The detection limit of this assay was determined to be 100 fg of pure F. virguliforme genomic DNA or 100 macroconidia in 0.5 g of soil. An exogenous control was multiplexed with the assay to evaluate for PCR inhibition. Target locus copy number variation had minimal impact, with a range of rDNA copy number from 138 to 233 copies per haploid genome, resulting in a minor variation of up to 0.76 cycle threshold values between strains. The qPCR assay is transferable across platforms, as validated on the primary real-time PCR platform used in the Northcentral region of the National Plant Diagnostic Network. A conventional PCR assay for F. virguliforme detection was also developed and validated for use in situations where qPCR is not possible.


PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e81832 ◽  
Author(s):  
Subodh K. Srivastava ◽  
Xiaoqiu Huang ◽  
Hargeet K. Brar ◽  
Ahmad M. Fakhoury ◽  
Burton H. Bluhm ◽  
...  

2018 ◽  
pp. 583-591
Author(s):  
Yi Chen Lee ◽  
M Javed Iqbal ◽  
Victor N Njiti ◽  
Stella Kantartzi ◽  
David A. Lightfoot

Soybean (Glycine max (L.) Merr.) cultivars differ in their resistance to sudden death syndrome (SDS), caused by Fusarium virguliforme. Breeding for improving SDS response has been challenging, due to interactions among the 18-42 known resistance loci. Four quantitative trait loci (QTL) for resistance to SDS (cqRfs–cqRfs3) were clustered within 20 cM of the rhg1 locus underlying resistance to soybean cyst nematode (SCN) on Chromosome (Chr.) 18. Another locus on Chr. 20 (cqRfs5) was reported to interact with this cluster. The aims here were to compare the inheritance of resistance to SDS in a near isogenic line (NIL) population that was fixed for resistance to SCN but segregated at two of the four loci (cqRfs1 and cqRfs) for SDS resistance; to examine the interaction with the locus on Chr. 20; and to identify candidate genes underlying QTL. Used were; a NIL population derived from residual heterozygosity in an F5:7 recombinant inbred line EF60 (lines 1-38); SDS response data from two locations and years; four segregating microsatellite and 1,500 SNP markers. Polymorphic regions were found from 2,788 Kbp to 8,938 Kbp on Chr. 18 and 33,100 Kbp to 34,943 Kbp on Chr. 20 that were significantly (0.005 < P > 0.0001) associated with resistance to SDS. The QTL fine maps suggested that the two loci on Chr. 18 were three loci (cqRfs1, cqRfs, and cqRfs19). Candidate genes were inferred.  An epistatic interaction was inferred between Chr. 18 and Chr. 20 loci. Therefore, SDS resistance QTL were both complex and interacting.


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