Download or read book Effects of the Rhg1 Gene on Resistance to Heterodera Glycines in Soybean Glycine Max written by Yuhong Li and published by . This book was released on 2003 with total page 170 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Characterizing Rhg1 Mediated Soybean Resistance to Soybean Cyst Nematode Using Functional and Computational Approaches written by and published by . This book was released on 2013 with total page 183 pages. Available in PDF, EPUB and Kindle. Book excerpt: Domesticated soybean, Glycine max, is an important world commodity accounting for 68% of world protein meal and 56% of world oilseed production. Soybean cyst nematode (SCN, Heterodera glycines) causes billions of dollars of economic losses annually and is considered the most economically damaging soybean disease. A previously identified locus, termed Rhg1, has a significant impact on SCN resistance, and is currently deployed in most commercially utilized SCN resistant soybean cultivars. The mechanism underlying Rhg1-mediated SCN resistance has remained elusive. This dissertation focuses on functional and computational approaches to define and characterize the genes underlying Rhg1-mediated SCN resistance. We identified three tightly clustered genes at the Rhg1 locus that each contributes to SCN resistance. We further discovered that the DNA encoding these genes is present in multiple copies in SCN-resistant parents, and this causes elevated expression of the genes. Two of the identified genes, Glyma18g02580 and Glyma18g02610, did not carry amino acid polymorphisms between resistant and susceptible Rhg1 haplotypes. The third gene, Glyma18g02590, encoding a predicted &alpha-SNAP protein did contain amino acid polymorphisms relative to the reference soybean genome Williams 82, which is SCN-susceptible. Transgenic expression of any one of these three genes in soybean roots did not discernibly improve resistance, but simultaneous expression of all three genes did enhance SCN resistance. To further explore the evolution and diversity of Rhg1, we used whole genome sequencing, fiber-FISH and related techniques to examine the structural and nucleic acid variation in the genomes of four-dozen soybean accessions. We discovered that the Rhg1 locus is commonly arranged in a single copy in all tested SCN susceptible germplasm, but is present as either a low-copy or high-copy type in SCN-resistant germplasm. These repeat copy classes are also distinguishable by expression level differences, and the presence of related but distinct alleles of the previously identified &alpha-SNAP protein. We also identified differential DNA-methylation at the locus between SCN-resistance and susceptible lines. The identification of the genes that control Rhg1-mediated resistance, and an understanding of their evolution and diversity, should foster efforts to improve the disease resistance that is available to reduce the deleterious impacts of SCN.

Download or read book Investigating RHG1 in the Annual Glycine Species Glycine Max and Glycine Soja written by Derrick J. Grunwald and published by . This book was released on 2021 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Soybean (Glycine max) is a globally important oilseed and protein crop. The world's most damaging pathogen of soybean is soybean cyst nematode (SCN; Heterodera glycines), which routinely causes over $1 billion USD in yield losses in the US each year. Pathogen management relies on the commonly deployed QTL, Resistance to Heterodera glycines 1 (Rhg1). Rhg1 is a multi-gene locus that displays copy number variation: 3 copies in rhg1-a and 4 in rhg1-b. One of the Rhg1 genes encodes an [alpha]-SNAP (alpha Soluble NSF Attachment Protein) that has an unusual set of C-terminal amino acids that disrupt its ability to interact with NSF (N-ethylmaleimide Sensitive Factor), leading to degeneration and collapse of SCN feeding sites. This thesis further characterizes Rhg1 in cultivated and wild soybeans (G. max and G. soja) and molecular interactions of Rhg1-encoded [alpha]-SNAPs. In the work of chapter 2, we discovered that all resistant-type G. max have a chromosome 7 QTL that contains a polymorphic NSF, termed RAN07 (Rhg1-Associated NSF on Chromosome 7). Experiments in vitro demonstrated that RAN07 exhibits a higher affinity than "wild-type" NSF for interaction with resistance-type [alpha]-SNAPs. Subsequent in planta studies demonstrated that RAN07 is required for the viability of soybeans carrying resistance-conferring Rhg1 haplotypes. Additionally, soybean varieties with rhg1-a often carry a QTL on chromosome 11, which we found is associated with an intron retention allele that reduces the overall abundance of "wild-type" [alpha]-SNAP. In the work of chapter 3 we characterized rhg1-a in G. max, focusing on the discovery that rhg1-a haplotypes contain a retrotransposon in the first intron of the Rhg1 [alpha]-SNAP. In chapter 4, we discovered a unique haplotype of Rhg1 termed rhg1-cs in a small subgroup of G. soja, that seems to predate the split of rhg1-a and rhg1-b in G. max. Characterization of rhg1-cs revealed a low copy number and a distinct Rhg1-encoded [alpha]-SNAP. Interestingly, the rhg1-cs G. soja accessions chosen for further study carry resistance to problematic HG type 2.5.7 SCN populations, due to additional uncharacterized resistance mechanisms. Finally, we discovered a novel [alpha]-SNAP encoded on chromosome 11 of one of the rhg1-cs G. soja varieties.

Download or read book Understanding the Mechanism and Epigenetic Regulation of Rhg1 a Major Soybean Cyst Nematode Resistance Locus written by Ryan William Zapotocny and published by . This book was released on 2021 with total page 320 pages. Available in PDF, EPUB and Kindle. Book excerpt: The present thesis research further characterized the mechanisms and epigenetic variation of Rhg1, an important soybean (Glycine max) locus that confers resistance to soybean cyst nematode (SCN; Heterodera glycines). One project discovered a unique N-ethylmaleimide sensitive factor (NSF) variant required for the viability of plants that carry resistance-conferring Rhg1 haplotypes. This variant, termed NSF[RAN07], binds resistant-type [alpha]-SNAP[Rhg1] proteins with improved affinity and reduces the in planta cellular toxicity of resistant-type [alpha]-SNAP[Rhg1]. The NSF[RAN07] variant further highlights the importance of vesicle trafficking during a resistant interaction. While analyzing rhg1-a-containing soybean varieties we discovered a ~4.8kb Copia family retrotransposon within an intron of the gene encoding [alpha]-SNAP[Rhg1LC]. We did not observe anomalous effects on gene expression or protein abundance due to this retrotransposon. I also contributed to a project that identified an [gamma]-SNAP protein as the apparent causal factor in SCN resistance conferred by the cqSCN-006 quantitative trait locus. The largest point of focus in this thesis project was to investigate the role epigenetic status plays in the structurally variable Rhg1 locus. Using a targeted bisulfite sequencing method, I discovered that Rhg1 locus methylation status is associated both with Rhg1 copy number and pedigree. We observed two qualitatively different rhg1-a DNA methylation patterns and observed a correlation between the pattern present and the DNA methylation response to SCN infection (locus CHH hypomethylation or hypermethylation). Intraread DNA methylation was analyzed to determine if methylation changes are concentrated on single dsDNA molecules or spread more evenly across the DNAs from separate cells in the sample. I also report initial progress on three separate projects that lay the groundwork for future exploration of the mechanisms of SCN resistance. In the first, we created and screened transgenic soybeans expressing various combinations of resistant-type [alpha]-SNAP[Rhg1] and either Rhg1-associated NSF[RAN07] or NSF[WT]. Secondly, I performed a Genome-Wide Association Study (GWAS) using recently developed variant analysis tools. Lastly, I outline the construction status and potential utility of targeted epigenetic manipulation constructs. Together, these three projects lay the groundwork for further study into the understanding of SCN resistance and the role epigenetics may play in it.

Download or read book Developing Chemically Mutagenized Soybean Populations for Functional Gene Analyses at the Rhg1 Locus written by Zhou Zhou and published by . This book was released on 2013 with total page 118 pages. Available in PDF, EPUB and Kindle. Book excerpt: Soybean (Glycine max (L.) Merr.) cyst nematode (SCN) (Heterodera glycines Ichinohe), an obligate sedentary endoparasite, is the most economically destructive pathogen in soybean production and causes over $1 billion in annual losses in the United States. Planting resistant cultivars is the primary management method to control SCN for the long-term purpose, but the nature of genetic resistance is little known. The Rhg1 (Resistance to H. glycines ) locus on chromosome 18 is found as a major quantitative trait locus (QTL) that contributes resistance to SCN. The chemical mutagen ethylmethane sulfonate (EMS) can be utilized to induce genetic mutations in soybean populations, which screened by an efficient reverse genetic strategy known as Targeting Induced Local Lesions IN Genomes (TILLING) for functional gene analyses. The objective of this study was to analyze the function of SNAP gene ( Glyma18g02590 ) at rhg1 allele from `Forrest' (`Peking'-derived SCN resistant cultivar) using TILLING. Soybean cultivar `Forrest' seeds were mutagenized with EMS and grown to generate M1 plants. M1 plants were self-pollinated to produce approximately 3000 M2 plants. Genomic DNAs were extracted from young leaves of individual M2 plants and quantified to normalize concentration of DNAs. The DNA samples were then pooled eight-fold in 96-well plates for mutations screening by TILLING. Moreover, 12 phenotypic traits including chlorophyll deficiency, leaf shape, branch architecture, seed color, seed weight, fatty acid phenotype were identified in the mutagenized population, analyzed and archived in this study.

Download or read book The Effect of the Soybean Gene Rhg1 on Reproduction of Heterodera Glycines in the Field and Greenhouse and Associated Effects on Agronomic Traits written by Eric Alan Brucker and published by . This book was released on 2004 with total page 116 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Investigation of Resistance to Heterodea Glycines scn in Soybean Plant Introductions pi 467312 and 507354 written by Peiqin Lu and published by . This book was released on 2007 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Soybean cyst nematode (SCN) Heterodera glycines Ichinohe is the most serious pest of soybean [Glycine max (L.) Merr.] in the world. The effectiveness of breeding soybean SCN resistant cultivars is reduced by the variation of SCN population and narrow genetic basis of resistant soybean cultivars. Hence, it is important to investigate new soybean SCN resistant sources for new genes that confer resistance to SCN field populations such as HG type 1.2.7 to provide durable resistance. Soybean plant introductions PI 467312 and PI 507354, are unique, with resistance to SCN multiple HG types respectively. However, the genetic basis of SCN resistance in these PIs is not known. The objectives of this study are to investigate the inheritance of resistance to SCN HG types 0, 1.2.7, and 1.3.6.7 in PI 467312 and the SCN resistance to SCN HG types 2.5.7 and 1.2.7 in PI 507354, to identify and map quantitative trait loci (QTL) associated with resistance to SCN HG types 0, 1.2.7, 1.3.6.7 in PI 467312 and resistance to SCN HG types 2.5.7, and 1.2.7 in PI 507354. The study showed that resistance to HG types 1.2.7, and 1.3.6.7 in Pop 467 were conditioned by one dominant and two recessive genes (Rhg rhg rhg) and resistance to HG type 0 was controlled by three recessive genes (rhg rhg rhg). Resistance to both HG types 2.5.7 and 1.2.7 in Pop 507 fit a one dominant and 3 recessive gene model (Rhg rhg rhg rhg). Two to three QTLs were associated with resistance to each HG type (race) in both populaitons.

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 Atypical Variants of the Soybean SNARE soluble NSF Attachment Protein Receptors recycling Machinery Underlie Rhg1 mediated Resistance to Soybean Cyst Nematode written by Adam Milton Bayless and published by . This book was released on 2017 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Glycine max (soybean) is the world's most widely grown legume. The most damaging soybean pathogen in terms of yield loss is the soybean cyst nematode (Heterodera glycines, SCN), which causes annual U.S. yield losses valuing over $1 billion USD. Glycine species encode multiple defenses against SCN, but of these, the Rhg1 (Resistance to Heterodera glycines 1) locus is the strongest known resistance locus, and is used in all commercial SCN-resistant soybeans. The Rhg1 resistance phenotype triggers death of the nematode-induced feeding site, thereby shutting off nutrition from the now sedentary nematode. Previous studies misidentified Rhg1 as a leucine-rich repeat receptor kinase, however, later genetic mapping studies excluded this kinase and defined Rhg1 to a narrow genetic interval of 11 putative candidate genes. The focus of this dissertation has been to identify the gene(s) conferring Rhg1 resistance and determine how they molecularly function during SCN-resistance. We identified the genes conferring Rhg1 function and discovered that Rhg1 is an unusual disease resistance locus. Rhg1 is an ~30 kb block of four different genes that is tandemly repeated up to 10 times. Gene silencing and resistance complementation indicated that three different Rhg1 genes, including an usual [alpha]-SNAP allele (alpha-Soluble-NSF Attachment Protein), contribute to SCN-resistance. Two distinct Rhg1 phenotypic classes have long been known by soybean growers. In a follow up, we determined that Rhg1 repeat copy number (Rhg1 high copy: 4 or more blocks, Rhg1 low copy: 3 or fewer blocks) defines these phenotypic Rhg1 classes, and moreover, that Rhg1 high copy vs. low copy haplotypes encode distinct polymorphic [alpha]-SNAP proteins. Subsequently, we characterized both Rhg1 high and low copy [alpha]-SNAP proteins. We found that, unlike the WT Rhg1 [alpha]-SNAP protein encoded by SCN susceptible soybeans, either resistance-type [alpha]-SNAP is impaired in normal interactions with the N-ethylmaleimide Sensitive Factor (NSF). High expression of either Rhg1 resistance-type [alpha]-SNAP impeded WT NSF functions and hindered vesicular trafficking. Finally, within syncytia of the high copy Rhg1 variety Fayette, we detected that the ratio of resistance-type [alpha]-SNAPs increases relative to WT [alpha]-SNAPs, suggesting that a semi-dominant negative mechanism dependent on [alpha]-SNAP ratios may underlie Rhg1 resistance. Later investigations with low copy Rhg1 soybeans showed that overall WT [alpha]-SNAP abundance was strikingly low compared to SCN-susceptible or high copy Rhg1 soybeans. We then re-explored NSF loci in low copy Rhg1 varieties and discovered a novel NSF allele with unique N-domain polymorphisms, which we termed RAN07 (Rhg1 associated NSF on chromosome 07). We found that NSFRAN07 was present within and needed for the viability of all soybean germplasm that carries high or low copy resistance-conferring Rhg1. Biochemical assays showed that NSFRAN07 polymorphisms improve upon WT-NSF for compatibility with Rhg1 resistance type [alpha]-SNAPs. In planta studies revealed that NSFRAN07 more effectively complements the cytotoxic properties of Rhg1 resistance-type [alpha]-SNAPs. We further demonstrated that a separate WT [alpha]-SNAP locus on chromosome 11, which maps near a putative minor resistance QTL, does not produce a stable protein. These findings suggest that replacement and/or rewiring of both [alpha]-SNAP and NSF - the core components of the SNARE recycling machinery - underlie Rhg1-mediated SCN resistance. Lastly, we discovered that low copy Rhg1 haplotypes harbor an intact 4.77 kb Copia retrotransposon within intron 1 of the resistance type [alpha]-SNAP. No significant impacts of this Copia element on low copy [alpha]-SNAP production were observed. This Rhg1Low Copy associated Copia (RAC) was not detected in SCN-susceptible or Rhg1 high copy soybeans, but was present in all three Rhg1 repeats in all examined low copy Rhg1 soybean accessions.

Download or read book Investigating Soybean Cyst Nematode Resistance written by Katelyn Butler and published by . This book was released on 2018 with total page 187 pages. Available in PDF, EPUB and Kindle. Book excerpt: Soybean cyst nematode (SCN; Heterodera glycines) is consistently ranked as the most economically damaging pathogen of soybean, a globally important oilseed and protein crop. To manage this persistent pathogen, growers rely primarily on crop rotation and genetic resistance. For decades, Rhg1 has been the primary resistance locus deployed in most commercial soybean varieties. Resistance at Rhg1 is conferred by three types of gene products not previously known to mediate plant defense. Gene copy number variation and expression/localization differences contribute to this resistance. In the present work we demonstrate that Rhg1 can also confer resistance in potato and Arabidopsis against the cyst nematodes Globodera pallida, Globodera rostochiensis and Heterodera schactii. This supports the hypothesis that Rhg1 evolved to interfere with conserved cyst nematode infection processes. This finding suggests biotechnology-based management strategies for cyst nematodes in other crops. SCN evolution necessitates new resistance sources in soybean. The remainder of this thesis describes the identification and characterization of novel resistance genes from two independent SCN resistance QTL originating from Glycine soja accession PI 468196, cqSCN-006 and cqSCN-007. I discovered that altered regulation of a ɣ-SNAP protein encoded at cqSCN-006 confers resistance. An [alpha]-SNAP protein contributes to Rhg1-mediated resistance, underscoring the importance of SNAP proteins and their associated activity in cyst nematode pathogenesis. cqSCN-006 resistant plants exhibit differential accumulation of the ɣ-SNAP protein and expression of alternative splice forms at infection sites. Little is known about the function of ɣ-SNAPs in any system, and even less in plants. I have identified a role of ɣ-SNAPs in SCN response. I also report progress towards identifying the gene encoding resistance at G. soja QTL cqSCN-007. While no gene(s) has been confirmed to confer resistance, a RAD21-like gene is the strongest candidate. The upstream region of the resistant allele contains a large deletion and exhibits differences in gene expression. Studies of cyst nematode resistance continually expand plant defense paradigms. The work in this thesis reveals additional intricacies of this pathosystem, laying the groundwork for further exploration of soybean-SCN interaction and improved plant protection strategies.

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 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 Identification and Evaluation of Quantitative Trait Loci Associated with Resistance to HG Type 2 and Seed Quality Traits from Two Bi Parental Mapping Populations Segregating for Soybean Cyst Nematode Resistance written by Adam Brown and published by . This book was released on 2021 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Soybean cyst nematode (SCN), Heterodera glycines Ichinohe, is the most economically devastating pathogen of soybean (Glycine max [L.] Merr.) Overuse of the resistance source PI88788 has led to development of new HG types of SCN in the fields. Major genes, Rhg1 and Rhg4, provide resistance to most HG types. The objectives of this thesis were: 1) identify minor QTL contributing to SCN resistance in two recombinant inbred line populations derived from a cross between the susceptible cultivar, Neptune, and resistant LD07-3419 (PI43764-derived), and between resistant cultivar OAC 13-87C-SCN (PI88788-derived) and LD07-3419 (PI43764); 2) assess the relationship between SCN resistance and yield and seed quality. One of the four identified QTL, which is located on chromosome 6 is potentially novel; however, this result needs to be confirmed. SCN resistance was negatively correlated with protein but not with oil concentration or yield. These findings may facilitate breeding for SCN resistance.

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 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 Near Infrared Spectroscopy Used to Determine Genetic Resistance to Heterodera Glycines Ichinohe IN Glycine Max L Merr written by Christopher Michael Fender and published by . This book was released on 2001 with total page 176 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 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