Submitted to: Plant Disease
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/1/2003
Publication Date: 10/1/2003
Citation: MALVICK, D.K., CHEN, W., KURLE, J., GRAU, C. CULTIVAR PREFERENCE AND GENOTYPE DISTRIBUTION OF THE BROWN STEM ROT PATHOGEN PHIALOPHORA GREGATA IN THE MIDWESTERN USA. PLANT DISEASE. 2003. v. 87. p. 1250-1255.
Interpretive Summary: Brown stem rot of soybean caused by the fungal pathogen Phialophora gregata is an important disease in the Midwestern United States. Populations of the pathogen is seprarted into two genotypes and the two genotypes are shown to be two pathotypes causing different symptoms. The two genotypes have cultivar preferential infection in preliminary studies, and the distribution of the two genotypes are not known. This study was designed to demonstrate the cultivar preferential infection in the field and to develop a practical methods for determining the genotype distribution. Results showed that the two genotypes of P. gregata infect soybean cultivars differentially. The genotype A preferentially infects susceptible cultivars whereas genotype B preferentially infect resistant soybean cultivars. The research demonstrated that planting the preferred cultivars side by side at various locations as bait plants in combination with specific PCR detection of the genotypes is a practical way to determine genotype distribution. Knowledge of the genotype distribution and the cultivar preference will facilitate developing effective control measures in terms of rotation and cultivar selection for planting at a particular location.
Technical Abstract: Brown stem rot (BSR), caused by Phialophora gregata f. sp. sojae, is an important yield-limiting disease of soybean (Glycine max) in the Midwestern USA. Midwestern populations of P. gregata are separated into two genotypes, A and B, based on intergenic spacer sequences of ribosomal DNA. Genotype A causes both leaf and stem symptoms, and genotype B typically causes internal stem symptoms only. Data is limited on the geographic distribution of genotypes A and B. Furthermore, data is limited on whether soybean genotypes are colonized by each pathogen genotype at different frequencies. Field plots were established at five sites in Illinois, three sites in Wisconsin, and two sites in Minnesota in two different years. Soybean cvs., Bell, BSR101, Dwight, Sturdy, Williams 82, LN92-12033, and LN92-12054 were sown with two to four replications at each field site. Stems (N = 5-10) were harvested arbitrarily per plot at the R8 growth stage and assayed by PCR to detect the A and B genotypes. Both pathogen genotypes were detected at all locations except Urbana where only genotype A detected and St. Paul where only B was detected. Genotype A was the predominant genotype detected in susceptible cultivars Williams 82, and LN92-12054, with 70 and 78% of infected stems positive for A, respectively. The other susceptible cultivar, Sturdy, mainly yielded genotype A at the Illinois and Wisconsin locations where both pathogen genotypes are present, but mainly yielded B at the Minnesota locations where genotype A was absent or undetectable. Genotype B was the predominant type detected in partially resistant cultivars BSR101, LN92-12033 and Bell, with 55, 89 and 99% of the infected stems testing positive for B, respectively. Genotypes A and B were detected approximately equally in Dwight.