Search

Glycine max root cells developing into syncytia through the parasitic activities of the pathogenic nematode Heterodera glycines underwent isolation by laser microdissection (LM). Microarray analyses have identified the expression of a G. max DOESN'T MAKE INFECTIONS3 (DMI3) homolog in syncytia undergoing parasitism but during a defense response. DMI3 encodes part of the common symbiosis pathway (CSP) involving DMI1, DMI2 , and other CSP genes. The identified DMI gene expression, and symbiosis role, suggests the possible existence of commonalities between symbiosis and defense. G. max has 3 DMI1 , 12 DMI2 , and 2 DMI3 paralogs. LM-assisted gene expression experiments of isolated syncytia under further examination here show G. max DMI1-3, DMI2-7 , and DMI3-2 expression occurring during the defense response in the H. glycines -resistant genotypes G. max [Peking/PI548402] and G. max [PI88788] indicating a broad and consistent level of expression of the genes. Transgenic overexpression (OE) of G. max DMI1-3, DMI2-7 , and DMI3-2 impairs H. glycines parasitism. RNA interference (RNAi) of G. max DMI1-3, DMI2-7 , and DMI3-2 increases H. glycines parasitism. The combined opposite outcomes reveal a defense function for these genes. Prior functional transgenic analyses of the 32-member G. max mitogen activated protein kinase (MAPK) gene family has determined that 9 of them act in the defense response to H. glycines parasitism, referred to as defense MAPK s. RNA-seq analyses of root RNA isolated from the 9 G. max defense MAPK s undergoing OE or RNAi reveal they alter the relative transcript abundances (RTAs) of specific DMI1, DMI2 , and DMI3 paralogs. In contrast, transgenically-manipulated DMI1-3, DMI2-7 , and DMI3-2 expression influences MAPK3-1 and MAPK3-2 RTAs under certain circumstances. The results show G. max homologs of the CSP, and defense pathway are linked, apparently involving co-regulated gene expression. [ABSTRACT FROM AUTHOR]

The conserved oligomeric Golgi (COG) complex maintains correct Golgi structure and function during retrograde trafficking. Glycine max has 2 paralogs of each COG gene, with one paralog of each gene family having a defense function to the parasitic nematode Heterodera glycines. Experiments presented here show G. max COG paralogs functioning in defense are expressed specifically in the root cells (syncytia) undergoing the defense response. The expressed defense COG gene COG7-2-b is an alternate splice variant, indicating specific COG variants are important to defense. Transcriptomic experiments examining RNA isolated from COG overexpressing and RNAi roots show some COG genes co-regulate the expression of other COG complex genes. Examining signaling events responsible for COG expression, transcriptomic experiments probing MAPK overexpressing roots show their expression influences the relative transcript abundance of COG genes as compared to controls. COG complex paralogs are shown to be found in plants that are agriculturally relevant on a world-wide scale including Manihot esculenta, Zea mays, Oryza sativa, Triticum aestivum, Hordeum vulgare, Sorghum bicolor, Brassica rapa, Elaes guineensis and Saccharum officinalis and in additional crops significant to U.S. agriculture including Beta vulgaris, Solanum tuberosum, Solanum lycopersicum and Gossypium hirsutum. The analyses provide basic information on COG complex biology, including the coregulation of some COG genes and that MAPKs functioning in defense influence their expression. Furthermore, it appears in G. max and likely other crops that some level of neofunctionalization of the duplicated genes is occurring. The analysis has identified important avenues for future research broadly in plants. [ABSTRACT FROM AUTHOR]

The Glycine max xyloglucan endotransglycosylase/hydrolase (EC 2.4.1.207), GmXTH43, has been identified through RNA sequencing of RNA isolated through laser microdissection of Heterodera glycines-parasitized root cells (syncytia) undergoing the process of defense. Experiments reveal that genetically increasing XTH43 transcript abundance in the H. glycines-susceptible genotype G. max[Williams 82/PI 518671] decreases parasitism. Experiments presented here show decreasing XTH43 transcript abundance through RNA interference (RNAi) in the H. glycines-resistant G. max[Peking/PI 548402] increases susceptibility, but it is unclear what role XTH43 performs. The experiments presented here show XTH43 overexpression decreases the relative length of xyloglucan (XyG) chains, however, there is an increase in the amount of those shorter chains. In contrast, XTH43 RNAi increases XyG chain length. The experiments show that XTH43 has the capability to function, when increased in its expression, to limit XyG chain extension. This outcome would likely impair the ability of the cell wall to expand. Consequently, XTH43 could provide an enzymatically-driven capability to the cell that would allow it to limit the ability of parasitic nematodes like H. glycines to develop a feeding structure that, otherwise, would facilitate parasitism. The experiments presented here provide experimentally-based proof that XTHs can function in ways that could be viewed as being able to limit the expansion of the cell wall. [ABSTRACT FROM AUTHOR]

The conserved oligomeric Golgi (COG) complex, functioning in retrograde trafficking, is a universal structure present among eukaryotes that maintains the correct Golgi structure and function. The COG complex is composed of eight subunits coalescing into two sub-complexes. COGs1–4 compose Sub-complex A. COGs5–8 compose Sub-complex B. The observation that COG interacts with the syntaxins, suppressors of the erd2-deletion 5 (Sed5p), is noteworthy because Sed5p also interacts with Sec17p [alpha soluble NSF attachment protein (α-SNAP)]. The α-SNAP gene is located within the major Heterodera glycines [soybean cyst nematode (SCN)] resistance locus (rhg1) and functions in resistance. The study presented here provides a functional analysis of the Glycine max COG complex. The analysis has identified two paralogs of each COG gene. Functional transgenic studies demonstrate at least one paralog of each COG gene family functions in G. max during H. glycines resistance. Furthermore, treatment of G. max with the bacterial effector harpin, known to function in effector triggered immunity (ETI), leads to the induced transcription of at least one member of each COG gene family that has a role in H. glycines resistance. In some instances, altered COG gene expression changes the relative transcript abundance of syntaxin 31. These results indicate that the G. max COG complex functions through processes involving ETI leading to H. glycines resistance. [ABSTRACT FROM AUTHOR]

Glycine max has 32 mitogen activated protein kinases (MAPKs), nine of them exhibiting defense functions (defense MAPKs) to the plant parasitic nematode Heterodera glycines. RNA seq analyses of transgenic G. max lines overexpressing (OE) each defense MAPK has led to the identification of 309 genes that are increased in their relative transcript abundance by all 9 defense MAPKs. Here, 71 of those genes are shown to also have measurable amounts of transcript in H. glycines-induced nurse cells (syncytia) produced in the root that are undergoing a defense response. The 71 genes have been grouped into 7 types, based on their expression profile. Among the 71 genes are 8 putatively-secreted proteins that include a galactose mutarotase-like protein, pollen Ole e 1 allergen and extensin protein, endomembrane protein 70 protein, O-glycosyl hydrolase 17 protein, glycosyl hydrolase 32 protein, FASCICLIN-like arabinogalactan protein 17 precursor, secreted peroxidase and a pathogenesis-related thaumatin protein. Functional transgenic analyses of all 8 of these candidate defense genes that employ their overexpression and RNA interference (RNAi) demonstrate they have a role in defense. Overexpression experiments that increase the relative transcript abundance of the candidate defense gene reduces the ability that the plant parasitic nematode Heterodera glycines has in completing its life cycle while, in contrast, RNAi of these genes leads to an increase in parasitism. The results provide a genomic analysis of the importance of MAPK signaling in relation to the secretion apparatus during the defense process defense in the G. max-H. glycines pathosystem and identify additional targets for future studies. [ABSTRACT FROM AUTHOR]

A Glycine max (soybean) hemicellulose modifying gene, xyloglucan endotransglycoslase/hydrolase (XTH43), has been identified as being expressed within a nurse cell known as a syncytium developing within the soybean root undergoing the process of defense to infection by the parasitic nematode, Heterodera glycines. The highly effective nature of XTH43 overexpression in suppressing H. glycines parasitism in soybean has led to experiments examining whether the heterologous expression of XTH43 in Gossypium hirsutum (upland cotton) could impair the parasitism of Meloidogyne incognita, that form a different type of nurse cell called a giant cell that is enclosed within a swollen root structure called a gall. The heterologous transgenic expression of XTH43 in cotton resulted in an 18% decrease in the number of galls, 70% decrease in egg masses, 64% decrease in egg production and a 97% decrease in second stage juvenile (J2) production as compared to transgenic controls. The heterologous XTH43 expression does not significantly affect root mass. The results demonstrate XTH43 expression functions effectively in impairing the development of M. incognita at numerous life cycle stages occurring within the cotton root. The experiments reveal that there are highly conserved aspects of the defense response of G. max that can function effectively in G. hirsutum to impair M. incognita having a different method of parasitism. [ABSTRACT FROM AUTHOR]

The defense regulon has been defined genetically in Arabidopsis thaliana to involve the syntaxin PENETRATION1 (PEN1), the secreted glucosidase (PEN2) and an ATP-binding cassette (ABC) transporter (PEN3). Experiments in Glycine max (soybean) have identified homologous genes being expressed in root cells undergoing defense processes to Heterodera glycines parasitism. These experiments have not examined proteins involved in cargo delivery to the infection site. A good candidate fulfilling this role would be myosin XI. In related studies, prior microscopic analyses have shown the accumulation of callose at these defense sites. Experiments presented here show that callose synthase expression impairs H. glycines parasitism. The experiments presented here have expanded on prior results demonstrating the central defense role of the plant vesicular trafficking apparatus and callose synthase to the defense process that G. max has toward H. glycines parasitism. [ABSTRACT FROM AUTHOR]

A quantitative PCR procedure targeting the Heterodera glycines ortholog of the Caenorhabditis elegans uncoordinated-78 gene was developed. The procedure estimated the quantity of H. glycines from metagenomic DNA samples isolated directly from field soil under agronomic production. The estimation of H. glycines quantity was determined in soil samples having other soil dwelling plant parasitic nematodes including Hoplolaimus, predatory nematodes including Mononchus, free-living nematodes and biomass. The methodology provides a framework for molecular diagnostics of nematodes from metagenomic DNA isolated directly from field soil. [ABSTRACT FROM AUTHOR]

Abstract: The plant parasitic nematode, Heterodera glycines is the major pathogen of Glycine max (soybean). H. glycines accomplish parasitism by creating a nurse cell known as the syncytium from which it feeds. The syncytium undergoes two developmental phases. The first is a parasitism phase where feeding sites are selected, initiating the development of the syncytium. During this earlier phase (1–4 days post infection), syncytia undergoing resistant and susceptible reactions appear the same. The second phase is when the resistance response becomes evident (between 4 and 6dpi) and is completed by 9dpi. Analysis of the resistant reaction of G. max genotype PI 88788 (G. max [PI 88788]) to H. glycines population NL1-RHg/HG-type 7 (H. glycines [NL1-RHg/HG-type 7]) is accomplished by laser microdissection of syncytia at 3, 6 and 9dpi. Comparative analyses are made to pericycle and their neighboring cells isolated from mock-inoculated roots. These analyses reveal induced levels of the jasmonic acid biosynthesis and 13-lipoxygenase pathways. Direct comparative analyses were also made of syncytia at 6 days post infection to those at 3dpi (base line). The comparative analyses were done to identify localized gene expression that characterizes the resistance phase of the resistant reaction. The most highly induced pathways include components of jasmonic acid biosynthesis, 13-lipoxygenase pathway, S-adenosyl methionine pathway, phenylpropanoid biosynthesis, suberin biosynthesis, adenosylmethionine biosynthesis, ethylene biosynthesis from methionine, flavonoid biosynthesis and the methionine salvage pathway. In comparative analyses of 9dpi to 6dpi (base line), these pathways, along with coumarin biosynthesis, cellulose biosynthesis and homogalacturonan degradation are induced. The experiments presented here strongly implicate the jasmonic acid defense pathway as a factor involved in the localized resistant reaction of G. max [PI 88788] to H. glycines [NL1-RHg/HG-type 7]. [Copyright &y& Elsevier]

Background. A comparative microarray investigation was done using detection call methodology (DCM) and differential expression analyses. The goal was to identify genes found in specific cell populations that were eliminated by differential expression analysis due to the nature of differential expression methods. Laser capture microdissection (LCM) was used to isolate nearly homogeneous populations of plant root cells. Results. The analyses identified the presence of 13,291 transcripts between the 4 different sample types. The transcripts filtered down into a total of 6,267 that were detected as being present in one or more sample types. A comparative analysis of DCM and differential expression methods showed a group of genes that were not differentially expressed, but were expressed at detectable amounts within specific cell types. Conclusion. The DCM has identified patterns of gene expression not shown by differential expression analyses. DCM has identified genes that are possibly cell-type specific and/or involved in important aspects of plant nematode interactions during the resistance response, revealing the uniqueness of a particular cell population at a particular point during its differentiation process. [ABSTRACT FROM AUTHOR]

The article presents a study that discusses research on gene expression when soybean interacts with soybean cyst nematode (SCN). It mentions that SCN is the major pest that affect soybean. It discusses the application of this information to identify genes involved in soybean and SCN involved in resistance and susceptibility. It concludes that soybean and SCN interactions were revealed using genome sequencing and development of microarrays with soybean and SCN genes.

Background: A single Glycine max (soybean) genotype (Peking) reacts differently to two different populations of Heterodera glycines (soybean cyst nematode) within the first twelve hours of infection during resistant (R) and susceptible (S) reactions. This suggested that H. glycines has population-specific gene expression signatures. A microarray analysis of 7539 probe sets representing 7431 transcripts on the Affymetrix® soybean GeneChip® were used to identify population-specific gene expression signatures in pre-infective second stage larva (pi-L2) prior to their infection of Peking. Other analyses focused on the infective L2 at 12hours post infection (i-L212h), and the infective sedentary stages at 3days post infection (i-L23d) and 8days post infection (i-L2/L38d). Results: Differential expression and false discovery rate (FDR) analyses comparing populations of pi-L2 (i.e., incompatible population, NL1-RHg to compatible population, TN8) identified 71 genes that were induced in NL1-RHg as compared to TN8. These genes included putative gland protein G23G12, putative esophageal gland protein Hgg-20 and arginine kinase. The comparative analysis of pi-L2 identified 44 genes that were suppressed in NL1-RHg as compared to TN8. These genes included a different Hgg-20 gene, an EXPB1 protein and a cuticular collagen. By 12 h, there were 7 induced genes and 0 suppressed genes in NL1-RHg. By 3d, there were 9 induced and 10 suppressed genes in NL1-RHg. Substantial changes in gene expression became evident subsequently. At 8d there were 13 induced genes in NL1-RHg. This included putative gland protein G20E03, ubiquitin extension protein, putative gland protein G30C02 and β-1,4 endoglucanase. However, 1668 genes were found to be suppressed in NL1-RHg. These genes included steroid alpha reductase, serine proteinase and a collagen protein. Conclusion: These analyses identify a genetic expression signature for these two populations both prior to and subsequently as they undergo an R or S reaction. The identification of genes like steroid alpha reductase and serine proteinase that are involved in feeding and nutritional uptake as being highly suppressed during the R response at 8d may indicate genes that the plant is targeting. The analyses also identified numerous putative parasitism genes that are differentially expressed. The 1668 genes that are suppressed in NL1-RHg, and hence induced in TN8 may represent genes that are important during the parasitic stages of H. glycines development. The potential for different arrays of putative parasitism genes to be expressed in different nematode populations may indicate how H. glycines evolve mechanisms to overcome resistance. [ABSTRACT FROM AUTHOR]

The development of an infection in soybean [ Glycine max L. cultivar (cv.) Peking] roots by incompatible (I) and compatible (C) populations of soybean cyst nematode (SCN) ( Heterodera glycines) was assayed using an Affymetrix® soybean GeneChip®. This time-course microarray analysis, using 37,744 probe sets, measured transcript abundance during I and C. These analyses reveal that infection by individual I and C H. glycines populations influence the transcription of G. max genes differently. A substantial difference in gene expression is present between I and C at 12 h post infection. Thus, G. max can differentiate between I and C nematode populations even before they have begun to select their feeding sites. The microarray analysis identified genes induced earlier in infection during I than C. MA also identified amplitude differences in transcript abundance between I and C reactions. Some of the probe sets measuring increased transcript levels during I represented no apical meristem (NAM) and WRKY transcription factors as well as NBS-LRR kinases. Later during I, heat shock protein (HSPs) probe sets (i.e. HSP90, HSP70, ClpB/HSP101) measured increased transcript abundance. These results demonstrate that G. max roots respond very differently to the different H. glycines races even before their feeding site selection has occurred. The ability of G. max to engage an I reaction, thus, appears to be dependent on the ability of root cells to recognize the different races of H. glycines because these experiments were conducted in the identical G. max genetic background. [ABSTRACT FROM AUTHOR]

Vesicle and target membrane fusion involves tethering, docking and fusion. The GTPase SECRETORY4 (SEC4) positions the exocyst complex during vesicle membrane tethering, facilitating docking and fusion. Glycine max (soybean) Sec4 functions in the root during its defense against the parasitic nematode Heterodera glycines as it attempts to develop a multinucleate nurse cell (syncytium) serving to nourish the nematode over its 30-day life cycle. Results indicate that other tethering proteins are also important for defense. The G. max exocyst is encoded by 61 genes: 5 EXOC1 (Sec3), 2 EXOC2 (Sec5), 5 EXOC3 (Sec6), 2 EXOC4 (Sec8), 2 EXOC5 (Sec10) 6 EXOC6 (Sec15), 31 EXOC7 (Exo70) and 8 EXOC8 (Exo84) genes. At least one member of each gene family is expressed within the syncytium during the defense response. Syncytium-expressed exocyst genes function in defense while some are under transcriptional regulation by mitogen-activated protein kinases (MAPKs). The exocyst component EXOC7-H4-1 is not expressed within the syncytium but functions in defense and is under MAPK regulation. The tethering stage of vesicle transport has been demonstrated to play an important role in defense in the G. max-H. glycines pathosystem, with some of the spatially and temporally regulated exocyst components under transcriptional control by MAPKs. [ABSTRACT FROM AUTHOR]

Expression of the central circadian oscillator components CIRCADIAN CLOCK ASSOCIATED 1 (CCA1), TIMING OF CAB1 (TOC1), GIGANTEA (GI), and CONSTANS (CO) occurs in Glycine max root cells (syncytia) parasitized by the nematode Heterodera glycines while undergoing resistance, indicating a defense role. GmCCA1-1 relative transcript abundance (RTA) in roots experiencing overexpression (OE) or RNA interference (RNAi) is characterized by rhythmic oscillations, compared to a ribosomal protein gene (GmRPS21) control. A GmCCA1-1 RTA change, advancing by 12 h, exists in H. glycines -infected as compared to uninfected controls in wild-type, H. glycines -resistant, G. max [Peking/PI 548402]. The G. max [Peking/PI 548402] transgenic controls exhibit the RTA change by 4 h post infection (hpi), not consistently occurring in the H. glycines -susceptible G. max [Williams 82/PI 518671] until 56 hpi. GmCCA1-1 expression is observed to be reduced in H. glycines -infected GmCCA1-1 -OE roots as compared to non-infected transgenic roots with no significant change observed among RNAi roots. The GmCCA1-1 expression in transgenic GmCCA1-1 -OE roots remains higher than control and RNAi roots. Decreased GmCCA1-1 mRNA among infected roots shows the altered expression is targeted by H. glycines. Gene expression of proven defense genes including 9 different mitogen activated protein kinases (GmMAPK s), NON-RACE SPECIFIC DISEASE RESISTANCE 1 (GmNDR1-1), RPM1-INTERACTING PROTEIN 4 (GmRIN4-4), and the secreted xyloglucan endotransglycosylase/hydrolase 43 (GmXTH43) in GmCCA1- 1-OE and GmCCA1-1 -RNAi roots, compared to controls, reveal a significant role of GmCCA1-1 expression in roots undergoing defense to H. glycines parasitism. The observation that GmCCA1-1 regulates GmXTH43 expression links the central circadian oscillator to the functionality of the secretion system. • Central circadian oscillator genes are expressed in nematode-parasitized root cells undergoing defense. • The overexpression of the central circadian oscillator genes suppresses parasitism. • The central circadian oscillator gene CCA1-1 regulates the expression of proven defense genes. [ABSTRACT FROM AUTHOR]

Pathogen-secreted polygalacturonases (PGs) alter plant cell wall structure by cleaving the α-(1 → 4) linkages between D-galacturonic acid residues in homogalacturonan (HG), macerating the cell wall, facilitating infection. Plant PG inhibiting proteins (PGIPs) disengage pathogen PGs, impairing infection. The soybean cyst nematode, Heterodera glycines , obligate root parasite produces secretions, generating a multinucleate nurse cell called a syncytium, a byproduct of the merged cytoplasm of 200–250 root cells, occurring through cell wall maceration. The common cytoplasmic pool, surrounded by an intact plasma membrane, provides a source from which H. glycines derives nourishment but without killing the parasitized cell during a susceptible reaction. The syncytium is also the site of a naturally-occurring defense response that happens in specific G. max genotypes. Transcriptomic analyses of RNA isolated from the syncytium undergoing the process of defense have identified that one of the 11 G. max PGIP s, GmPGIP11 , is expressed during defense. Functional transgenic analyses show roots undergoing GmPGIP11 overexpression (OE) experience an increase in its relative transcript abundance (RTA) as compared to the ribosomal protein 21 (GmRPS21) control, leading to a decrease in H. glycines parasitism as compared to the overexpression control. The GmPGIP11 undergoing RNAi experiences a decrease in its RTA as compared to the GmRPS21 control with transgenic roots experiencing an increase in H. glycines parasitism as compared to the RNAi control. Pathogen associated molecular pattern (PAMP) triggered immunity (PTI) and effector triggered immunity (ETI) components are shown to influence GmPGIP11 expression while numerous agricultural crops are shown to have homologs. [Display omitted] • The complete Glycine max (soybean) polygalacturonase inhibiting protein (PGIP) protein family is identified. • The expression of soybean PGIP gene family members are investigated. • A PGIP that is expressed in a pathogen infection site during defense functions in defense. [ABSTRACT FROM AUTHOR]

Abstract Mitogen activated protein kinases (MAPKs) play important signal transduction roles. However, little is known regarding how they influence the gene expression of other family members and the relationship to a biological process, including the Glycine max defense response to Heterodera glycines. Transcriptomics have identified MAPK gene expression occurring within root cells undergoing a defense response to a pathogenic event initiated by H. glycines in the allotetraploid Glycine max. Functional analyses are presented for its 32 MAPKs revealing 9 have a defense role, including homologs of Arabidopsis thaliana MAPK (MPK) MPK2, MPK3, MPK4, MPK5, MPK6, MPK13, MPK16 and MPK20. Defense signaling occurring through pathogen activated molecular pattern (PAMP) triggered immunity (PTI) and effector triggered immunity (ETI) have been determined in relation to these MAPKs. Five different types of gene expression relate to MAPK expression, influencing PTI and ETI gene expression and proven defense genes including an ABC-G transporter, 20S membrane fusion particle components, glycoside biosynthesis, carbon metabolism, hemicellulose modification, transcription and secretion. The experiments show MAPKs broadly influence defense MAPK gene expression, including the co-regulation of parologous MAPKs and reveal its relationship to proven defense genes. The experiments reveal each defense MAPK induces the expression of a G. max homolog of a PATHOGENESIS RELATED1 (PR1), itself shown to function in defense in the studied pathosystem. Highlights • The entire MAPK gene family has been examined functionally. • The results have identified the MAPK gene family functions as a cohort during the defense response. • The results reveal levels of co-regulated gene expression that underlie the defense response. [ABSTRACT FROM AUTHOR]

Soybean ( Glycine max ) infection by the charcoal rot (CR) ascomycete Macrophomina phaseolina is enhanced by the soybean cyst nematode (SCN) Heterodera glycines . We hypothesized that G. max genetic lines impairing infection by M. phaseolina would also limit H. glycines parasitism, leading to resistance. As a part of this M. phaseolina resistance process, the genetic line would express defense genes already proven to impair nematode parasitism. Using G. max [DT97-4290/PI 642055] , exhibiting partial resistance to M. phaseolina , experiments show the genetic line also impairs H. glycines parasitism. Furthermore, comparative studies show G. max [DT97-4290/PI 642055] exhibits induced expression of the effector triggered immunity (ETI) gene NON-RACE SPECIFIC DISEASE RESISTANCE 1/HARPIN INDUCED1 (NDR1/HIN1) that functions in defense to H. glycines as compared to the H. glycines and M. phaseolina susceptible line G. max [Williams 82/PI 518671] . Other defense genes that are induced in G. max [DT97-4290/PI 642055] include the pathogen associated molecular pattern (PAMP) triggered immunity (PTI) genes ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1), NONEXPRESSOR OF PR1 (NPR1) and TGA2. These observations link G. max defense processes that impede H. glycines parasitism to also potentially function toward impairing M. phaseolina pathogenicity. Testing this hypothesis, G. max [Williams 82/PI 518671] genetically engineered to experimentally induce GmNDR1-1, EDS1-2, NPR1-2 and TGA2-1 expression leads to impaired M. phaseolina pathogenicity. In contrast, G. max [DT97-4290/PI 642055] engineered to experimentally suppress the expression of GmNDR1-1, EDS1-2, NPR1-2 and TGA2-1 by RNA interference (RNAi) enhances M. phaseolina pathogenicity. The results show components of PTI and ETI impair both nematode and M. phaseolina pathogenicity. [ABSTRACT FROM AUTHOR]