Download or read book Characterization of Host Responses in Compatible and Incompatible Interactions Between Soybean Glycine Max L Merr and Soybean Cyst Nematode Heterodera Glycines I written by Ramamurthy Mahalingam and published by . This book was released on 1998 with total page 238 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Biology and Management of the Soybean Cyst Nematode written by Robert D. Riggs and published by American Phytopathological Society. This book was released on 1992 with total page 200 pages. Available in PDF, EPUB and Kindle. Book excerpt: 1 History, distribution, and economics. 2 Systematics and morphology. 3 Epiphytology and life cycle. 4 Cellular responses to infection. 5 Population dynamics. 6 Genetics. 7 The race concept. 8 Nematode race identification, A look to the future. 9 Interactions with other organisms. 10 Host range. 11 Chemical control. 12 Management by cultural practices. 13 Biological control. 14 Breeding for resistance to soybean cyst nematode. 15 Cytopathological reactions of resistant soybean plants to nematode invasion. 16 Tolerance in soybean.

Download or read book The Defense Response of I Glycine Max I to Its Major Parasitic Nematode Pathogen I Heterodera Glycines I written by and published by . This book was released on 2016 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Heterodera glycines , soybean cyst nematode (SCN) causes more than one billion dollars soyben production loss in the U.S. annually. SCN is an obligate parasite of specialized feeding cells within the host root known as syncytium. The SCN resistance genes and signaling pathways in soybean have not been fully characterized. Gene expression analysis in syncytium from compatible and incompatible interactions identified candidate genes that might involve conferring resistance to SCN. This dissertation aimed to investigate the biological functions of the candidate resistance genes to confirm the roles of these genes in resistance to SCN. The study demonstrated a role of syntaxin 31-like genes (Gm-SYP38) in resistance to SCN. Overexpression of Gm-SYP38 induced the transcriptional activity of the cytoplasmic receptor-like kinase BOTRYTIS INDUCED KINASE 1 (Gm-BIK1-6). Overexpression of Gm-BIK1-6 rescued the resistant phenotype. In contrast, Gm-BIK1-6 RNAi increased parasitism. In another experiment, the expression of a Glycine max homolog of LESION SIMULATING DISEASE1 (LSD1) resulted in the transcriptional activation of ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) and NONEXPRESSOR OF PR1 (NPR1), that function in salicylic acid (SA) signaling, implicating the involvement of the antiapoptotic, environmental response gene LESION SIMULATING DISEASE1 (LSD1) in defense that is demonstrated here. The study also investigated the role of SNARE components (genes functioning in membrane fusion) in resistance to SCN. Experiments showed that SNARE functions in concert with a beta-glucosidase having homology to PEN2 and an ATP binding cassette transporter having homology to PEN3 . This study provides novel information for the genetic improvement of soybean for enhanced disease resistance.

Download or read book The Defense Response of Glycine Max to Its Major Parasitic Nematode Pathogen Heterodera Glycines written by Shankar R. Pant and published by . This book was released on 2016 with total page 162 pages. Available in PDF, EPUB and Kindle. Book excerpt: Heterodera glycines, soybean cyst nematode (SCN) causes more than one billion dollars soyben production loss in the U.S. annually. SCN is an obligate parasite of specialized feeding cells within the host root known as syncytium. The SCN resistance genes and signaling pathways in soybean have not been fully characterized. Gene expression analysis in syncytium from compatible and incompatible interactions identified candidate genes that might involve conferring resistance to SCN. This dissertation aimed to investigate the biological functions of the candidate resistance genes to confirm the roles of these genes in resistance to SCN. The study demonstrated a role of syntaxin 31-like genes (Gm-SYP38) in resistance to SCN. Overexpression of Gm-SYP38 induced the transcriptional activity of the cytoplasmic receptor-like kinase BOTRYTIS INDUCED KINASE 1 (Gm-BIK1-6). Overexpression of Gm-BIK1-6 rescued the resistant phenotype. In contrast, Gm-BIK1-6 RNAi increased parasitism. In another experiment, the expression of a Glycine max homolog of LESION SIMULATING DISEASE1 (LSD1) resulted in the transcriptional activation of ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) and NONEXPRESSOR OF PR1 (NPR1), that function in salicylic acid (SA) signaling, implicating the involvement of the antiapoptotic, environmental response gene LESION SIMULATING DISEASE1 (LSD1) in defense that is demonstrated here. The study also investigated the role of SNARE components (genes functioning in membrane fusion) in resistance to SCN. Experiments showed that SNARE functions in concert with a beta-glucosidase having homology to PEN2 and an ATP binding cassette transporter having homology to PEN3. This study provides novel information for the genetic improvement of soybean for enhanced disease resistance.

Download or read book Global DNA Methylation Changes in Soybean as a Response to Soybean Cyst Nematode SCN Infection written by Aditi Rambani and published by . This book was released on 2018 with total page 182 pages. Available in PDF, EPUB and Kindle. Book excerpt: Soybean cyst nematode (SCN, Heterodera glycines) is the most damaging pest in soybean production worldwide. The compatible interaction of SCN with susceptible soybean plants is mediated by differential expression of thousands of genes in the infected root cells, leading to the formation of a functional feeding site, the syncytium. During an incompatible interaction of SCN with resistant soybean, the developing syncytium degenerates leading to nematode death. The resistance to SCN in soybean is derived from two major loci, Rhg1 and Rhg4. In this study, the role of genome-wide DNA methylation in regulating gene expression during the compatible interaction was examined using susceptible soybean cultivar 'Williams 82'. The analysis revealed that SCN induces both hyper- and hypomethylation in thousands of genomic regions overlapping with genes. The level and pattern of DNA methylation in various genic regions were found to impact gene transcription. A significant number of the differentially methylated genes was found to overlap with genes known to be significantly differentially expressed in syncytium, providing the first experimental evidence that syncytium transcriptome is epigentically controlled. In addition, the levels and patterns of DNA methylation were compared between the compatible and incompatible interactions using a pair of near-isogenic lines differing in Rhg4 allele. The methylomes of two near isogenic lines, susceptible (TN09-16) and the resistant (TN09-29) were substantially different both under SCN-infected and non-infected conditions. Stably heritable as well as novel non-parental differentially methylated regions in genes with functions related to SCN parasitism of soybean were discovered. Furthermore, differential DNA methylation in microRNA genes was also examined in the susceptible and resistant lines in response to SCN infection. A number of differentially methylated microRNAs were identified specifically in the susceptible lines, Williams 82 and TN09-16, indicating that various components of epigenetic mechanisms are mutually linked. Taken together, profiling DNA methylation at single nucleotide resolution during the susceptible and resistant interactions provided unprecedented insights into the role of this epigenetic mark in determining the compatibility of the interaction between soybean and SCN by impacting the expression of protein-coding and microRNA genes as well as transposable elements located nearby genes.

Download or read book Investigating Root knot and Soybean Cyst Nematode Parasitic Interactions Through Transcriptomic Analyses of the Host and Parasite written by Ellie Walsh and published by . This book was released on 2016 with total page 188 pages. Available in PDF, EPUB and Kindle. Book excerpt: Plant-parasitic nematodes are a major threat to global agricultural production. Root-knot nematodes (RKN, Meloidogyne spp.) are arguably the biggest threat, capable of parasitizing virtually every crop. Soybean cyst nematode (SCN; Heterodera glycines) has a narrow host range, but is the most destructive pathogen of a particularly important crop, soybean (Glycine max). RKN’s wide host range makes crop rotation often inadequate for management, and host resistance is unavailable in many crops. Effective resistance is available against SCN however populations have adapted to the most frequently used sources of resistance. RKN and SCN both induce elaborate feeding sites. In addition to being the sole source of nutrition, the feeding sites are the primary targets of nematode secretions to manipulate host cellular functions; consequently, they are very important interfaces of the interaction. The general aim of this research was to elucidate changes in the transcriptome underlying the successful interaction between these nematodes and their hosts. Although the use of RNA interference (RNAi) to knockdown nematode genes is actively being pursued as a new strategy for nematode control, little is known about the effects of general RNAi mechanisms during parasitism. As the suppression of RNAi has been characterized in other pathosystems, I hypothesized that parasitic nematodes may also be influencing these pathways. Tanscriptomic analysis of genes associated with RNAi machinery and target genes indicates that RNAi-regulated pathways are altered during the parasitic interaction. Using a silenced reporter gene, I found the disturbance to be specific to the nematode feeding site. Furthermore, disrupting these pathways with viral suppressors of RNAi renders the host more susceptible to nematode parasitism. Transcriptomic analysis indicates that this effect extends into later stages in parasitism, making the adult female stage of particular interest for further analyses. I performed a transcriptomic analysis of adult female RKN to address the hypothesis that transcriptional patterns in this later stage of parasitism will reveal new candidate genes encoding proteins that regulate the parasitic process, such as proteins that interact with RNAi among other plant pathways. Results from RNA-Seq analysis and reverse transcriptase PCR indicate that cell wall modifiers likely continue to play an important role in the parasitic interaction. Results from transcriptomic analysis including the putative secretome have highlighted new candidates for functional analysis to determine their role in the interaction. The later stage in parasitism is similarly of interest in SCN. SCN populations are adapting to the most commonly planted host resistance available in soybean, derived from Plant Introduction (PI) 88788 and “Peking.” The resistance response in PI 88788 appears to be longer-lasting than that in Peking, which impacts nematodes’ early development. Due to my focus on the adult female stage, I chose to investigate parasitism on PI 88788. I hypothesize that transcriptional differences between females from populations avirulent and virulent on PI 88788 may play a role in their adaptation to resistance. Results from this study indicate that the expression of an effector-like gene may have been lost in virulent populations, presumably allowing them to evade host detection and subsequent defense responses.

Download or read book Response of Soybean Glycine Max to Glyphosate and Soybean Cyst Nematode Heterodera Glycines written by Xiaoyu Yang and published by . This book was released on 2000 with total page 318 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Dissertation Abstracts International written by and published by . This book was released on 1999 with total page 856 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Evaluation of Soybean Glycine Max L Merr Source of Resistance to Soybean Cyst Nematode Heterodera Glycines Ichinohe written by Beth Holmes and published by . This book was released on 1996 with total page 222 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Structural Modifications Associated with Resistance and Susceptibility of Selected Plants Infected with Heterodera Glycines Ichinohe written by Young Ho Kim and published by . This book was released on 1985 with total page 302 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book American Doctoral Dissertations written by and published by . This book was released on 1998 with total page 784 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Functional Analysis Identifies Glycine Max Genes Involved in Defense to Heterodera Glycines written by Prachi D. Matsye and published by . This book was released on 2013 with total page 241 pages. Available in PDF, EPUB and Kindle. Book excerpt: The infection of plants by Heterodera glycines, commonly known as soybean cyst nematode (SCN), is a serious agricultural problem of worldwide extent. Meanwhile, it provides an excellent experimental model to study basic aspects of how cells function, in particular, during biotic challenge. Heterodera glycines challenges plant cells by initiating, developing and sustaining an interaction that results in the formation of a nurse cell from which the nematode derives nourishment. The presented experiments examine (1) how a cell can be de-differentiated and reprogrammed to perform a much different biological role and (2) how a cell’s immune responses can be engaged or suppressed to accomplish that goal. The observation of alpha soluble N-ethylmaleimide-sensitive factor attachment protein (alpha-SNAP) expression, its location within the rhg1 locus and known involvement in the vesicular transport machinery relating to defense made it a strong candidate for further functional analysis. Functional studies demonstrated that overexpression of alpha-SNAP in the susceptible G. max[Williams 82/PI 518671] genotype that lacks its expression results in the partial suppression of H. glycines infection. This indicated that the vesicles could be delivering cargo to the site of infection to engage a defense response. High levels of expression of a cell wall modifying gene called xyloglucan endotransglycosylase also occur during defense. XTHs associate with vesicles, act in the apoplast outside of the cell, and have a well-known function in cell wall restructuring. These observations indicated that alterations in the cell wall composition of nurse cells could be important for the successful defense response. Overexpression of a G. max xyloglucan endotransglycosylase (Gm-XTH) in the susceptible G. max[Williams 82/PI 518671] genotype resulted in a significant negative effect on H. glycines as well as R. reniformis parasitism. The results, including preliminary experiments on components of the vesicle transport system, identify a potent mechanism employed by plants to defend themselves from two types of plant-parasitic nematodes.

Download or read book Distribution and Characterization of the Soybean Cyst Nematode Heterodera Glycines HG Types in South Dakota written by Krishna Acharya and published by . This book was released on 2016 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Soybean Cyst Nematode Heterodera Glycines Resistance Genes in PI 8972 and PI 209332 Soybean written by M. da S. ASSUNCAO and published by . This book was released on 2000 with total page 52 pages. Available in PDF, EPUB and Kindle. Book excerpt: Soybean cyst nematode(SCN), Heterodera glycines Ichinohe, is the most serious disease of soybean glycine max(L.) Merr., in the United States and also is a serious pest of soybean on a world-wide basis. The nematode was first found in the United States in North Carolina in 1954 and now occurs in 30 states. Crop rotation plays an important role in controlling the nematode. Control also utilizes different cropping systems and resistant soybean cultivars to supress yield loss caused by H. glycines. A racetest was developed in early 1970's to classify variability in the nematode and was expanded in late 1980's to include 16 races. Eight races have been identified in the United States and in the North Central United States race 3 is the prevalent. Several plants introductions have been found with resistance to the most important races that occur in the soybean production areas in Asia, North America, and South America. The number of resistance genes in PI 89772 and PI 209332 conferring resistance to H.glycines race 3 is not well defined. Crosses of PI 89772 x 'Lee 68', PI 88788 x PI 89772, and Lee 68 x PI 209332 were made in the field and greenhouse. To verify that F1 plants resulted from the cross rather than selfing, simple sequence repeat molecular marker analysis was used to characterize F1 plants and their parents. Several F1 and F2 families from each cross, 98 F3 families from cross PI 89772 x Lee 68, 74 F3 families from cross PI 88788 x PI 89772, and 80 F3 families from cross Lee 68 x PI 209332 were tested with an inbred line of H.glycines developedon 88788. Approximately 8,000 individual plants growing in pots containing 200 cm3 of sterilized soil were inoculated with 4,010 eggs and J2/pot. Thity days after inoculation the number of females that developed on each plant was determined. Cluster analysis revealed sets of families with a low mean number of femalesand low variance, intermediate means and high variance, and high means witha low variance, indicating F3 plants came from, respectively, homozygous resistant, heterozygous or segreganting, and homozygous susceptible F2 plants. Thus, resistance classes were considered as quantitative parameters having different levels of resistance as opposed to only two classes, either or susceptible. Chi-square analysis of segregation of phenotypic data indicated two genes confer resistance torace of H.glycines. One gene acts as a major gene (Rhgx) and the other a minor gene (Rhgy) in conferring resistance of the parents PI 89772 (Rhgx1?Rhgx1?Rhgy1?Rhgy1?) PI 88788 (Rhgx2?Rhgx2?Rhgy2?Rhgy2/), and PI 209332 (Rhgx3?Rhgx3?Rhgy3?Rhgy3) to H.glycine race 3. The same genes may occur in PI 209332 as in PI 89772, but support for this hypothesis must be obtained by studying the cross PI 209332 x PI 89772. The same major (Rhgx) and minor (Rhgy) genes occur in PI 89772 (Rhgx1?Rhgx1?Rhgy1?Rhgy1?) and PI 88788 (Rhgx2?Rhgx2?Rhgy2?Rhgy2?). The phenotypic ratios obtained in this research indicate that epsitasis occurs between loci Rhgyx and geney.

Download or read book An Analysis of Signaling Processes Leading to a Defense Response in Soybean written by and published by . This book was released on 2017 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Plant-parasitic nematodes are the cause of devastating yield loss in vital agricultural crops around the world. Heterodera glycines , also referred to as soybean cyst nematode, is the main pathogen of Glycine max (soybean) causing more loss than all other pathogens of G. max combined. The resultant economic impact due to H. glycines in United States soybean production alone is estimated to account for an annual one-billion-dollar loss. Natural resistant genotypes have been found in trials to combat this pathogen. Of the resistant varieties identified, G. max [Peking/PI 548402] and G. max [PI 88788] are the major sources of resistance. Identification of genes expressed in the cells of which the nematode parasitizes, the syncytia, exclusively undergoing the resistant/incompatible reaction from the two major sources of resistance mentioned previously have identified a number of candidate genes presumed to function in defense to H. glycines parasitism. Prior to this work, success has been obtained by selection of a number of these candidate genes in functional analysis to show involvement in defense. This work is aimed at functionally identifying signaling components involved in the defense reaction. Reverse genetic studies of NON-RACE SPECIFIC DISEASE RESISTANCE 1 Glycine max homolog, Gm-NDR1-1, has confirmed a functional role in the defense to H. glycines to G. max. Gene expression studies revealed both effector-triggered immunity (ETI) and pattern-triggered immunity (PTI) components to be regulated by Gm-NDR1-1. Furthermore, induction in the heterologous expression of Gm-NDR1-1 in Gossypium hirsutum (cotton) suppressed Meloidogyne incognita parasitism. Harpin treatment has been evaluated due to the knowledge of NDR1s capability of being harpin-induced (HIN1). Expression studies of the harpin treatment did in fact induce Gm-NDR1-1. The analysis further provides ev

Download or read book Characterization of the Spatial Distribution of Heterodera Glycines Ichinohe 1955 Nematoda Soybean Cyst Nematode in Two Michigan Fields written by Maria Felicitas Avendaño and published by . This book was released on 2003 with total page 482 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book An Analysis of Signaling Processes Leading to a Defense Response in Soybean written by Brant Trey McNeece and published by . This book was released on 2017 with total page 225 pages. Available in PDF, EPUB and Kindle. Book excerpt: Plant-parasitic nematodes are the cause of devastating yield loss in vital agricultural crops around the world. Heterodera glycines, also referred to as soybean cyst nematode, is the main pathogen of Glycine max (soybean) causing more loss than all other pathogens of G. max combined. The resultant economic impact due to H. glycines in United States soybean production alone is estimated to account for an annual one-billion-dollar loss. Natural resistant genotypes have been found in trials to combat this pathogen. Of the resistant varieties identified, G. max[Peking/PI 548402] and G. max[PI 88788] are the major sources of resistance. Identification of genes expressed in the cells of which the nematode parasitizes, the syncytia, exclusively undergoing the resistant/incompatible reaction from the two major sources of resistance mentioned previously have identified a number of candidate genes presumed to function in defense to H. glycines parasitism. Prior to this work, success has been obtained by selection of a number of these candidate genes in functional analysis to show involvement in defense. This work is aimed at functionally identifying signaling components involved in the defense reaction. Reverse genetic studies of NON-RACE SPECIFIC DISEASE RESISTANCE 1 Glycine max homolog, Gm-NDR1-1, has confirmed a functional role in the defense to H. glycines to G. max. Gene expression studies revealed both effectortriggered immunity (ETI) and pattern-triggered immunity (PTI) components to be regulated by Gm-NDR1-1. Furthermore, induction in the heterologous expression of GmNDR1-1 in Gossypium hirsutum (cotton) suppressed Meloidogyne incognita parasitism. Harpin treatment has been evaluated due to the knowledge of NDR1’s capability of being harpin-induced (HIN1). Expression studies of the harpin treatment did in fact induce GmNDR1-1. The analysis further provides evidence of NDR1 role in defense by displaying the harpin-induced response of NDR1 in resistance to infection of Rotylenchulus reniformis. Receptors are known to function through signaling components in plant defense. Therefore, the conserved downstream signaling component of multiple diverse stimuli, mitogen-activated protein kinases (MAPKs) were functionally characterized in G. max for their role in resistance to H. glycines via the reverse genetic parasitism assays and evaluated to observe the effect on defense gene expression.