2018
Enhancement of Soybean Through Genetic Engineering
Contributor/Checkoff:
Category:
Sustainable Production
Keywords:
GeneticsGenomics
Lead Principal Investigator:
Harold Trick, Kansas State University
Co-Principal Investigators:
Project Code:
1814
Contributing Organization (Checkoff):
Institution Funded:
Brief Project Summary:

This project will take a genetic engineering approach by utilizing traits outside the scope of conventional breeding to decrease yield loss and improve the value of soybeans. The three objectives of this project are to introduce and evaluate new traits into soybeans for increased SCN resistance, increased fungal resistance, improved resistance to Dectes stem borer. Fungal pathogens and parasitic nematodes are persistent problems that cause large economic losses. The Dectes stem borer is becoming an increasing problem in the state with the potential for significant economic loss. It is timely to find methods to efficiently control these pathogens and pests.

Key Benefactors:
farmers, entomologists, plant pathologists, agronomists

Information And Results
Project Deliverables

Objective 1: Enhance Soybean Cyst Nematode (SCN) resistance in transgenic soybean by modifying gene silencing strategies.

For the past few years we have been evaluating the effectiveness of traits to provide resistance to soybean cyst nematodes (SCN). Many of these traits have been designed to silence specific genes within the nematode and we have demonstrated a reduction in cyst numbers on these transgenic lines. We can further increase the resistance level by 1) using alternative gene sequences of these genes and 2) increasing the levels of small interfering RNA (siRNA) produced by the plant. We have been targeting approximately 200-300 nucleotides of a given nematode gene with our current gene silencing approach. This is approximately 10 to 30% of the entire sequence of most target genes. Although we have demonstrated the effectiveness of this method, targeting alternate sequences of a particular gene may improve the silencing effect. We propose to take two of the genes previously used (one high and one low cyst/egg reduction from the bioassay) and target alternative sequences of the genes for gene silencing. Such a study will provide us with critical data in regards to the selection of future target sequences.

In general, the RNAi mechanism for gene silencing is based on a large (exponential) amplification of siRNA molecules that bind to a specific gene sequence. Many laboratories including our own use this approach to effectively silence the plant’s own genes. For endogenous plant genes, the RNAi mechanism will produce siRNA molecules that recognize the total gene sequence, even if only 10% of the entire gene sequence is targeted, which in turn will cause a very high degree (possibly complete) of gene silencing. Our current methodology produces only siRNAs that correspond to the specific sequence (200 to 300 bp) fragment found in our DNA construction. The quantity of siRNA species does not increase exponentially because the nematode gene target is not found in the plant. We propose to over-express the targeted nematode gene sequence (either in the sense or antisense orientation) together with the RNAi vector construction. This approach should allow the exponential accumulation of siRNA species in the transgenic soybean plants thereby allowing a greater number of siRNA molecules to be ingested by the feeding nematode. This increase in siRNA ingested by the nematode should translate into increased SCN resistance.

To assess the effectiveness of the above strategies greenhouse SCN bioassays on composite plants or transgenic soybean lines, as well as negative controls, will be performed. Lines will be planted into SCN infected soil (~6000 eggs/100 cm3) and grown in the greenhouse for five weeks. Soybean roots will then be washed free of soil and debris, SCN cysts removed from each plant and the number of cysts, eggs and root weight data will be collected for each replicate. Data collected from each bioassay will be examined by analysis of variance with the GLM procedure in SAS.

We have a second transgenic approach to reduce SCN reproduction that is ongoing and an update will be given at the formal proposal presentation in December.

Transgenic lines generated from this research project will be incorporated into elite Kansas lines under the KSC funded project “Breeding and Management of Soybean for Improved Performance”. Where intellectual property rights are involved, the Kansas State University Research Foundation will be advised and they will assist us in the transfer of technology to third parties.

Objective 2: Test the effectiveness of gene silencing constructions for root knot nematode (RKN) resistance using RKN genes homologous to effective SCN genes.

Root-knot nematodes, particularly Meloidogyne incognita, pose an additional risk to soybean production in the United States, accounting for 127,000 tonnes in yield losses annually (Wrather et al., 2006). Although predominantly found in the southern soybean-producing states, M. incognita increasingly is recognized as a threat to soybean production in the Midwest (Allen at al., 2005; Kruger et al., 2008), and periodically is associated with stunted soybean plants in the Kansas River Valley. The nematode causes extensive galling of soybean roots, disrupting root function and resulting in seed yield losses up to and exceeding 50% in infested areas (Allen at al., 2005). Resistant varieties are used to manage M. incognita in the southern U.S., but availability of adapted resistant cultivars is limited for Kansas and the Midwest.

Target genes for RNA silencing will be selected based on research performed by our group evaluating this phenomenon in the soybean/SCN interaction. Genes showing a greater than 40% reduction in cyst or eggs in the soybean system will be our primary targets for the root knot nematode. One of our stable lines demonstrating reduce SCN eggs (containing the prp-17 vector) has also shown a reduction in RKN. Many of the transgenic lines made for SCN control have sequences similar enough to RKN genes so these will also be tested to see if they provide cross protection (i.e. resistance to both SCN and RKN).

Objective 3. Transgenic approaches for increased fungal resistance with emphasis on SDS.

Sudden Death Syndrome (SDS) is caused by Fusarium virguliforme, a soil-borne fungus. Disease symptoms have been attributed to specific toxins produced by the fungus. One study indicated that when the fungal toxin gene FvTox1 was turned off in the pathogen by mutations, no symptoms developed on infected soybeans (Pudake et al., 2013). Our previous work using a gene silencing strategy targeting SCN genes is showing promising results and would serve as a model silencing the FvTox1 gene in F. virguliforme. With Chris Little we have successfully established a seedling assay for testing our transgenics using a hairy root bioassay. We have created silencing vectors for the FvTox1 gene, and plan to challenge the transgenic material with F. virguliforme. A positive result would be indicated by inhibition of fungal growth and absence of the disease.

Additionally, we will investigate a separate approach to produce fungal resistance. Defensins and their relatives are peptides or small proteins that can inhibit antimicrobial growth (De Lucca and Walsh, 1999). These peptides are present in plants, insects, and vertebrates. We have selected three peptides from various sources, optimized expression for soybean, created expression vectors, and transformed soybean cultures. Seeds recovered from transgenics will be used first evaluate growth inhibition on F. virguliforme (SDS) but will screen other pathogens such as Macrophomina phaseolina (charcoal rot). For bioassays we will cooperate with Dr. Chris Little, KSU’s row crop pathologist.

Final Project Results

Update:
To enhance soybean cyst nematode (SCN) resistance in transgenic soybean by modifying gene silencing strategies we have been working on advancing the transgenic lines we have produced. For the first round of crossing, all seeds (about 150 seeds) were planted and are being tested for GOI by PCR, currently gDNA from half of plants were extracted and tested by PCR. There was one plant (Prp17X K11) positive for GOI, which contained intact expression cassette. Additional K11-2363B seedlings were planted for back crossing with this F1 positive plant.

We have performed a second round of crossing with our transgenic soybean with hpRNAi_Y25 and Prp17 to K11-2363B and K12-2333 separately is underway. Approximately 20 plants were used in the crossings and currently pods are forming in these plants. A third round of crossing underway as well as field test plots of a number of events..

As an alternative approach to SCN resistance we are continuing to transform soybean cultures with two genes that together should disrupt SCN mating. We were having initial difficulty in recovering events with one of the genes and suspected that the gene may have a lethal phenotype. To investigate this potential problem we introduced these constructs into Arabidopsis. Two Arabidopsis thaliana events were confirmed to contain the genes and demonstrated that the gene was not lethality to plants. Since then we have confirmed six of our soybean events to contain both constructs and we are currently regenerating these cultures. We are also continuing exploring the possibility to introduce these genes into a bacterium as an alternative delivery method. We are working out the transformation and expression methodologies for this bacterium with our two genes.

Work with the defensin genes was focused on generating plasmids for Agrobacterium transformations. These will be used for hairy root assays and to transform Arabidopsis as a more rapid evaluation of the defensing genes. Constructs were verified by sequencing and we are using those in transformation experiments.

For the eIF knocking down project, more T3 seeds of “400Awash” are available for bioassay test with soybean mosaic virus infection. A bioassay will be set up to test if the transgenic lines have any improved resistance to SMV.

For host-derived RNAi targeting Fusarium virguliforme, the fungus that causes soybean sudden death disease, we have isolated gDNA samples from transgenic callus to confirm presents of the full-length transgenic sequence. To date only one positive by PCR was identified but we are still screening cultures.

The United Soybean Research Retention policy will display final reports with the project once completed but working files will be purged after three years. And financial information after seven years. All pertinent information is in the final report or if you want more information, please contact the project lead at your state soybean organization or principal investigator listed on the project.