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Brown Stem Rot (BSR), caused by the soil borne fungal pathogen Phialophora gregata , can reduce soybean yields by as much as 38%. Previous allelism studies identified three Resistant to brown stem Rot genes ( Rbs1, Rbs2 , and Rbs3 ), all mapping to large, overlapping regions on soybean chromosome 16. However, recent fine-mapping and genome wide association studies (GWAS) suggest Rbs1, Rbs2 , and Rbs3 are alleles of a single Rbs locus. To address this conflict, we characterized the Rbs locus using the Williams82 reference genome (Wm82.a4.v1). We identified 120 Receptor-Like Proteins (RLPs), with hallmarks of disease resistance receptor-like proteins (RLPs), which formed five distinct clusters. We developed virus induced gene silencing (VIGS) constructs to target each of the clusters, hypothesizing that silencing the correct RLP cluster would result in a loss of resistance phenotype. The VIGS constructs were tested against P. gregata resistant genotypes L78-4094 ( Rbs1 ), PI 437833 ( Rbs2 ), or PI 437970 ( Rbs3) , infected with P. gregata or mock infected. No loss of resistance phenotype was observed. We then developed VIGS constructs targeting two RLP clusters with a single construct. Construct B1a/B2 silenced P. gregata resistance in L78-4094, confirming at least two genes confer Rbs1 -mediated resistance to P. gregata . Failure of B1a/B2 to silence resistance in PI 437833 and PI 437970 suggests additional genes confer BSR resistance in these lines. To identify differentially expressed genes (DEGs) responding to silencing, we conducted RNA-seq of leaf, stem and root samples from B1a/B2 and empty vector control plants infected with P. gregata or mock infected. B1a/B2 silencing induced DEGs associated with cell wall biogenesis, lipid oxidation, the unfolded protein response and iron homeostasis and repressed numerous DEGs involved in defense and defense signaling. These findings will improve integration of Rbs resistance into elite germplasm and provide novel insights into fungal disease resistance.

Genetic variation and variation in aggressiveness in Phialophora gregata f. sp. sojae, the cause of brown stem rot of soybean, was characterized in a sample of 209 isolates from the north-central region. The isolates were collected from soybean plants without regard to symptoms from randomly selected soybean fields. Seven genotypes (A1, A2, A4, A5, A6, M1, and M2) were distinguished based on DNA fingerprinting with microsatellite probes (CAT) 5 and (CAC) 5 , with only minor genetic variation within the A or M genotypes. Only the A1, A2, and M1 genotypes were represented by more than one isolate. The A genotypes dominated in the eastern Iowa, Illinois, and Ohio samples, whereas the M genotypes were dominant in samples from western Iowa, Minnesota, and Missouri. In growth chamber experiments, isolates segregated into two pathogenicity groups based on their aggressiveness toward soybean cvs. Kenwood and BSR101, which are relatively susceptible and resistant, respectively, to brown stem rot. In both root dip inoculation and inoculation by injecting spores into the stem near the ground line (stab inoculations), isolates of the A genotypes caused greater foliar symptoms and more vascular discoloration than isolates of the M genotypes on both cultivars of soybean. All isolates caused foliar symptoms in both cultivars and in three additional cultivars of soybean with resistance to brown stem rot. Greater differences between the A and M genotypes were seen in foliar symptoms than in the linear extent of xylem discoloration, and greater differences were seen in Kenwood than in BSR101. Inoculation of these genotypes into five cultivars of soybean with different resistance genes to brown stem rot showed a genotype × cultivar interaction. A similar distinction was found in an earlier study of the adzuki bean pathogen, P. gregata f. sp. adzukicola, and consistent with the nomenclature of that pathogen, the soybean pathogens are named the aggressive race (race A) and the mild race (race M) of P. gregata f. sp. sojae.

The soybean cyst nematode (SCN) and Phialophora gregata f. sp. sojae, the causal agent of brown stem rot (BSR), are two pathogens of soybean commonly found in the same field throughout the north-central United States. Field experiments designed to study the role of SCN-resistant germ plasm in soybean production have led to data suggesting that some sources of SCN resistance also may provide resistance to BSR. Soybean germ plasm with resistance to SCN was evaluated in greenhouse and field environments for resistance to BSR development based on the percentage of host tissue symptomatic of BSR. Comparison of SCN-resistant cultivars and plant introductions (PI) to standard BSR-resistant and -susceptible checks were conducted in two greenhouse experiments using a root-dip inoculation with a single isolate of P. gregata. For both greenhouse experiments, PI 209332 was the only source of SCN resistance with resistance to BSR similar to standard BSR-resistant checks. Nine other sources of SCN resistance, including PI 88788 and Peking, expressed BSR symptom severity similar to BSR-susceptible checks. Cultivars derived from most SCN-resistant sources, including PI 209332, also were susceptible to BSR development, while four of the five cultivars derived from PI 88788 were highly resistant to BSR development. SCN-resistant cultivars derived from PI 88788, Peking, and PI 209332 were planted along with standard BSR-resistant and -susceptible checks at two field locations naturally infested with P. gregata and SCN or P. gregata alone. As in greenhouse experiments, four of the five cultivars derived from PI 88788 expressed resistance to BSR development equal to or better than standard BSR-resistant checks at both locations. In contrast, cultivars derived from PI 209332 and Peking expressed varying levels of disease development depending on field environment. Yields observed for PI 88788-derived cultivars were higher than BSR-resistant checks regardless of the presence of SCN. Data from both greenhouse and field experiments suggest that cvs. Williams and Williams 82 may contain a gene or genes for BSR resistance that require one or more modifier genes, possibly located in the genome of PI 88788, for complete expression.

Phialophora gregata elicits different symptoms of brown stem rot (BSR) of soybean depending on the genotype of the pathogen and host. Genotype A of the pathogen causes leaf and internal stem browning, whereas genotype B typically causes internal stem browning only. A species-specific TaqMan primer and probe set for quantitative, real-time PCR (QPCR) analysis was developed and used to determine if genotypes A and B differentially grow in soybean cultivars that are resistant (R) or susceptible (S) to BSR. One R and one S cultivar were inoculated with each genotype in greenhouse experiments by injection at the root-stem interface. The top 2 cm (apex) of stems of two plants per treatment were sampled weekly for 7 weeks after inoculation, and the quantity of pathogen DNA present was determined with QPCR. Only genotype A was detected in the apex of the S cultivar, and fungal DNA increased over the sampling period. Genotype A was not detected in the R cultivar, but low levels of genotype B were detected on weeks 2 and 3. More DNA of genotype A was detected (P < 0.01) in the S cultivar than the R cultivar from weeks 4 to 7. Preliminary results suggest that genotypes A and B of P. gregata differentially colonized the apex of resistant and susceptible soybean stems, and some cultivars may limit growth of both pathogen genotypes in the apex.

Two genotypes of Phialophora gregata cause brown stem rot (BSR) of soybean. Typically, genotype A causes leaf symptoms and internal stem browning, whereas genotype B causes internal stem browning only. This study was conducted to determine the effects of each genotype on soybean growth and yield in replicated greenhouse and field experiments. Four to six cultivars with different levels of BSR resistance were inoculated by stem injection with genotypes A and B in replicated greenhouse and field experiments. Internal stem browning developed in all inoculated plots. In greenhouse experiments, both genotypes reduced fresh biomass and number of pods per plant 5%-50% relative to controls at the R7 stage. In field experiments in 2002, both genotypes reduced yields of four cultivars tested, although the only significant (P = 0.05) yield reduction (12%) occurred in one cultivar inoculated with the B genotype. Field inoculations in 2003 had no consistent effect on yields of the five cultivars tested. Preliminary results suggest both genotypes of P. gregata can reduce growth and yield of soybeans in greenhouse and field studies.

This review covers the biosynthesis of glyceollin and its biological activities including antiproliferative/antitumor action (toward B16 melanoma cells, LNCaP prostate cancer cells, and BG-1 ovarian cancer cells), anti-estrogenic action (through estrogen receptors α- and β-), antibacterial action (toward Erwinia carotovora, Escherichia coli, Bradyrhizobium japonicum, Sinorhizobium fredii ), antinematode activity, and antifungal activity (toward Fusarium solani, Phakospora pachyrhizi, Diaporthe phaseolorum, Macrophomina phaseolina, Sclerotina sclerotiorum, Phytophthora sojae, Cercospora sojina, Phialophora gregata, and Rhizoctonia solani). Other activities include insulinotropic action and attenuation of vascular contractions in rat aorta. [PUBLICATION ABSTRACT]

Dark-septate endophytic (DSE) fungi are ubiquitous in the roots of Arctic and alpine plants, yet very little is known about their phylogenetic identities or effects on their host plants. Several such fungi were isolated from the alpine snowbed plant Ranunculus adoneus in the Front Range of Colorado, USA; one isolate was chosen for detailed study. The ability of this isolate to re-colonize plant roots in pot cultures was assessed, and phylogenetic analyses were performed using small-subunit (SSU), 5.8S and internal transcribed spacer (ITS) 2 ribosomal DNA sequences. This isolate had the ability to produce root endophytic structures in pot cultures similar to those reported from other sources and observed in R. adoneus roots. SSU phylogenetic analyses showed this isolate to be related to a clade within the Euascomycetes containing the Leotiales and Erysiphales. In addition, SSU and 5.8S-ITS2 sequences showed high phylogenetic similarity to a variety of isolates reported from other plants of diverse geographical origins. Although most of these isolates remain unidentified, one closely related isolate was the anamorphic taxon Phialophora gregata. The results suggest that this DSE isolate might belong to the fairly closely related group of plant endophytes that have varied effects on the plants that they inhabit.

Brown stem rot (BSR) of soybean [Glycine max (L.) Merr.], caused by Phialophora gregata (Allington & D.W. Chamb.) W. Gams 1971, is an economically important disease prevalent in soybean producing regions of the north-central United States and Canada. To date, all BSR resistant genes identified are located on chromosome 16 (formerly molecular linkage group J). The objective of this study was to determine if four plant introductions from south-central China identified as BSR resistant have resistance genes mapping to the same location on chromosome 16 as previously mapped BSR resistance genes. The four plant introductions, PI 594637, PI 594638B, PI 594650A, and PI 594858B, were crossed to the BSR-susceptible cultivar ‘Century 84’ to develop four F2 populations. Each segregating population and the parental lines were screened for BSR resistance in growth chamber conditions. The F2:3 individual plants of each population were tested with the simple sequence repeat (SSR) markers Satt431 or Satt547, which map closely to BSR resistance quantitative trait loci (QTL) on chromosome 16. Associations between molecular data and phenotypic data used to validate QTL were analyzed using single factor ANOVA. Three of the four populations had markers on chromosome 16 significantly associated with BSR resistance with R 2 values from 24 to 48%. However, when marker Satt547 was regressed on BSR resistance in population PI 594637 × Century 84, no significant association was observed. This result suggests that PI 594637 could have a new BSR resistance gene. Transgressive segregation also was observed in this population, and highly BSR resistant progeny could be used in the development of BSR resistant cultivars. Additional research and testing in this population will be conducted to identify resistance QTL(s) from this source.

Many soybean [Glycine max (L.) Merr.] genotypes that carry resistance to soybean cyst nematode (Heterodera glycines Ichinohe) (SCN) from plant introduction (PI) 88788 also carry resistance to brown stem rot (BSR) caused by the soilborne fungus Phialophora gregata (Allington & Chamberlain) W. Gams f. sp. sojae Kobayashi, Yamamoto, Negishi, and Ogoshi. The objectives of our research were to map and localize BSR resistance quantitative trait loci (QTL) from Bell, a BSR resistant cultivar with SCN resistance from PI 88788. Initial mapping was done with a population of 93 F4-derived lines developed from a cross between Bell and the SCN and BSR susceptible cultivar, Colfax. Lines were evaluated for BSR resistance in two field environments, a greenhouse, and with genetic markers from linkage group (LG) J. To confirm and further localize a resistance QTL, three near isogenic line (NIL) populations were created using an F4-derived line from the Bell x Colfax population. In the F4 population, markers on LG J were significantly (P < 0.001) associated with BSR resistance in both the field (R2 = 45%) and greenhouse (R2 = 51%). Data from the NIL populations indicates the QTL is near the closely linked markers 21E22.sp1, 21E22.sp2, and 35E22.sp1, which is the same genetic region where Rbs1, Rbs2, and Rbs3, the three named BSR resistance genes, were previously mapped. In addition, the genetic region is tightly linked to a previously identified SCN resistance QTL from PI 88788. These results explain why many SCN resistant cultivars also carry BSR resistance and should assist breeders when selecting for resistance to both diseases.

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 BSR-susceptible 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.