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Tabor, G. M., Tylka, G. L., Behm, J. E., and Bronson, C. R. 2003. Heterodera glycines infection increases incidence and severity of brown stem rot in both resistant and susceptible soybean. Plant Dis. 87:655-661. Growth chamber experiments were conducted to investigate whether parasitism by Heterodera glycines, the soybean cyst nematode, increases incidence and severity of brown stem rot (BSR) of soybean, caused by Phialophora gregata, in both resistant and susceptible soybean cultivars. Soybean genotypes with various combinations of resistance and susceptibility to both pathogens were inoculated with P. gregata alone or P. gregata plus H. glycines. In most tests of H. glycines-susceptible genotypes, incidence and severity of internal stem discoloration, characteristic of BSR, was greater in the presence than in the absence of H. glycines, regardless of susceptibility or resistance to BSR. There was less of an increasing effect of H. glycines on stem symptoms in genotypes resistant to both BSR and H. glycines; however, P. gregata colonization of these genotypes was increased. Stems of both a BSR-resistant and a BSRsusceptible genotype were colonized earlier by P. gregata in the presence than in the absence of H. glycines. Our findings indicate that H. glycines can increase the incidence and severity of BSR in soybean regardless of resistance or susceptibility to either pathogen. Additional keywords: BSR, pathogen interaction, Phialophora gregata, SCN

Growth chamber experiments were conducted to determine if extent of colonization of soybean stems by genotypes A and B of Cadophora gregata (Phialophora gregata), the causal agent of brown stem rot (BSR) of soybean, is similar in soybean plants resistant or susceptible to genotype A. Upon introduction of the two genotypes separately into the base of stems of 2-week-old seedlings, genotype A advanced with the growing tips of susceptible but not resistant genotypes. In contrast, genotype B did not advance with the growing tips of either resistant or susceptible soybean. In similar experiments, 5 weeks after introduction of genotype A, both mean percent stem length colonized by C. gregata and mean percentage of symptomatic trifoliate leaflets were significantly less for resistant than for susceptible genotypes. For genotype B, there was no or a slight difference between resistant and susceptible soybean genotypes in mean percent stem length colonized and no difference in mean percentage of symptomatic trifoliate leaflets 5 weeks after introduction of the pathogen. These results indicate that genotype A and genotype B differ not only in the severity of foliar symptoms they cause on genotype A-susceptible soybean plants, but also in how severely they colonize the stems of these soybean plants. In our experiments, genotype A and genotype B did not differ consistently in their ability to cause internal stem discoloration. The two genotypes of C. gregata can be distinguished based on how severely they colonize stems of genotype A-susceptible soybean. Thus, a BSR resistance screening method, which relies on assessment of stem colonization by C. gregata, works only for screening soybean lines resistance to genotype A. In light of these results, it is important to distinguish soybean resistance to genotype A versus genotype B of C. gregata. Whether genotype B causes yield loss and whether soybean plants can be distinguished as resistant or susceptible to genotype B needs to be investigated.

Greenhouse, growth chamber, and field experiments were conducted to develop a method to assess resistance of soybeans to Cadophora gregata (Phialophora gregata), causal agent of brown stem rot (BSR). In the new method, C. gregata is introduced at the base of the stems of 2-week-old soybeans, and the presence of the fungus is assessed in the tips of the stems 5 weeks later. To test the effectiveness of the method, two populations of soybeans and 10 checks were inoculated at the stem base and then assayed for fungal colonization of the stem tips, percentage of symptomatic leaflets, and percent internal stem length discolored. The lines also were planted in naturally infested fields to assess for percent internal stem length discolored, and were tested for the presence/absence of a BSR-resistant molecular marker. Greenhouse, field, and molecular marker data were compared. Linear regression analysis suggested that percentage of plants with colonized stem tips explained 41 to 64% of the variability (P < 0.0001) in percent stem length discolored in the field and 58 to 85% of the variability (P < 0.0001) in molecular marker data for BSR resistance. Percent stem length discolored assessed in the greenhouse had the lowest correlation with percent stem length discolored in the field and with the molecular marker. Of three incubation temperatures tested, 22°C was the most conducive for distinguishing resistant/susceptible soybeans using the colonization method.

Growth chamber experiments were conducted to determine if resistance to Phialophora gregata, the causal agent of brown stem rot (BSR) of soybean, is expressed in the stems of resistant soybean genotypes. Upon introduction of the pathogen into the base of stems of 2-week-old seedlings, the fungus advanced with the growing tips of plants of susceptible genotypes but lagged behind in resistant genotypes. Five weeks after introduction of the pathogen, both mean percent stem length colonized by P. gregata and mean percentage of symptomatic trifoliate leaflets were significantly less for resistant than for susceptible genotypes. These results indicate that resistance can be expressed in the stems of resistant soybean plants and suggest that stem inoculation methods may be useful for assessing resistance to P. gregata. Also, in our experiments, internal stem discoloration was not as useful as colonization and foliar symptoms in discriminating resistant from susceptible genotypes.

In the north central United States, leaf rust caused by Melampsora medusae is a major disease problem on Populus deltoides. In this study we identified molecular markers linked to a M. medusae resistance locus (Lrd1) that was segregating 1:1 within an intraspecific P. deltoides family (C9425DD). Previous field results were confirmed in the controlled environment of a growth chamber through an excised whole-leaf inoculation method. Using bulked segregant analysis we identified two random amplified polymorphic DNA (RAPD) markers (OPG10340 and OPZ191800) that are linked to Lrd1. Based on segregation in a total of 116 progeny, the genetic distances between OPG10340 and OPZ191800 and the resistance locus were estimated as 2.6 and 7.4 Haldane centimorgans (cM), respectively. Multipoint linkage analyses strongly suggest the most likely order for these loci is Lrd1, OPG10340, and OPZ191800. These markers may prove to be instrumental in the eventual cloning of Lrd1, as well as for marker-assisted selection of leaf-rust resistant genotypes.