Evaluation of Septoria Nodorum Blotch (SNB) Resistance in Glumes of Wheat (Triticum aestivum L.) and the Genetic Relationship With Foliar Disease Response

Septoria nodorum blotch (SNB) is a necrotrophic disease of wheat prominent in some parts of the world, including Western Australia (WA) causing significant losses in grain yield. The genetic mechanisms for resistance are complex involving multiple quantitative trait loci. In order to decipher comparable or independent regulation, this study identified the genetic control for glume compared to foliar resistance across four environments in WA against 37 different isolates. High proportion of the phenotypic variation across environments was contributed by genotype (84.0% for glume response and 82.7% for foliar response) with genotype-by-environment interactions accounting for a proportion of the variation for both glume and foliar response (14.7 and 16.2%, respectively). Despite high phenotypic correlation across environments, most of the eight and 14 QTL detected for glume and foliar resistance using genome wide association analysis (GWAS), respectively, were identified as environment-specific. QTL for glume and foliar resistance neither co-located nor were in LD in any particular environment indicating autonomous genetic mechanisms control SNB response in adult plants, regulated by independent biological mechanisms and influenced by significant genotype-by- environment interactions. Known Snn and Tsn loci and QTL were compared with 22 environment-specific QTL. None of the eight QTL for glume or the 14 for foliar response were co-located or in linkage disequilibrium with Snn and only one foliar QTL was in LD with Tsn loci on the physical map. Therefore, glume and foliar response to SNB in wheat is regulated by multiple environment-specific loci which function independently, with limited influence of known NE-Snn interactions for disease progression in Western Australian environments. Breeding for stable resistance would consequently rely on recurrent phenotypic selection to capture and retain favorable alleles for both glume and foliar resistance relevant to a particular environment.

Genes Associated with Foliar Resistance to Septoria Nodorum Blotch of Hexaploid Wheat (Triticum aestivum L.)

The genetic control of host response to the fungal necrotrophic disease Septoria nodorum blotch (SNB) in bread wheat is complex, involving many minor genes. Quantitative trait loci (QTL) controlling SNB response were previously identified on chromosomes 1BS and 5BL. The aim of this study, therefore, was to align and compare the genetic map representing QTL interval on 1BS and 5BS with the reference sequence of wheat and identify resistance genes (R-genes) associated with SNB response. Alignment of QTL intervals identified significant genome rearrangements on 1BS between parents of the DH population EGA Blanco, Millewa and the reference sequence of Chinese Spring with subtle rearrangements on 5BL. Nevertheless, annotation of genomic intervals in the reference sequence were able to identify and map 13 and 12 R-genes on 1BS and 5BL, respectively. R-genes discriminated co-located QTL on 1BS into two distinct but linked loci. NRC1a and TFIID mapped in one QTL on 1BS whereas RGA and Snn1 mapped in the linked locus and all were associated with SNB resistance but in one environment only. Similarly, Tsn1 and WK35 were mapped in one QTL on 5BL with NETWORKED 1A and RGA genes mapped in the linked QTL interval. This study provided new insights on possible biochemical, cellular and molecular mechanisms responding to SNB infection in different environments and also addressed limitations of using the reference sequence to identify the full complement of functional R-genes in modern varieties.

Genetic resistance to yellow rust infection of the wheat ear is controlled by genes controlling foliar resistance and flowering time

Yellow rust (YR), or stripe rust, is a fungal infection of wheat (Triticum aestivum L.) caused by the pathogen Puccinia striiformis f. sp. tritici (Pst). While much research has focused on YR infection of wheat leaves, we are not aware of reports investigating the genetic control of YR resistance in other wheat structures, such as the ears. Here we use an eight-founder population to undertake genetic analysis of glume YR infection in wheat ears. Five quantitative trait loci (QTL) were identified, each explaining between 3.4% and 6.8% of the phenotypic variation. Of these, three (QYrg.niab-2D.1, QYrg.niab-4D.1 and QYrg.niab-5A.1) co-located with QTL for leaf YR resistance previously identified in the same population. Additional leaf YR resistance QTL previously identified in the population were not detected as controlling glume resistance, with the remaining two glume YR QTL linked to genetic loci controlling flowering time. The first, QYrg.niab-2D. 1, mapped to the major flowering time locus Photoperiod-D1 (Ppd-D1), with the early-flowering allele from the founder Soissons conferring reduced glume YR resistance. The second, QYrg.niab-4A.1, was identified in one trial only, and was located close to a flowering time QTL. This indicates earlier flowering results in increased glume YR susceptibility, likely due to exposure of tissues during environmental conditions more favourable for Pst infection. Collectively, our results provide first insights into the genetic control of YR resistance in glumes, ontrolled by subsets of QTL for leaf YR resistance and flowering time. This work provides specific genetic targets for the control of YR resistance in both the leaves and the glumes, and may be especially relevant in Pst-prone agricultural environments where earlier flowering is favoured.

Evaluation of Septoria nodorum blotch (SNB) resistance in glumes of wheat (Triticum aestivum L.) in multiple field environments and the genetic relationship with foliar disease response

Septoria nodorum blotch (SNB) is a necrotrophic disease of wheat prominent in some parts of the world, including Western Australia (WA) causing significant losses in grain yield. The genetic mechanisms for resistance are complex involving multiple quantitative trait loci. In order to decipher comparable or independent regulation, this study identified the genetic control for glume compared to foliar resistance across four environments in WA against 37 different isolates. High proportion of the phenotypic variation across environments was contributed by genotype (84.0% for glume response and 82.7% for foliar response) with genotype-by-environment interactions accounting for a proportion of the variation for both glume and foliar response (14.7% and 16.2%, respectively). Despite high phenotypic correlation across environments, most of the eight and 14 QTL detected for glume and foliar resistance, respectively, were identified as environment-specific. QTL for glume and foliar resistance neither co-located nor were in LD in any particular environment indicating autonomous genetic mechanisms control SNB response in adult plants, regulated by independent biological mechanisms and influenced by significant genotype-by-isolate-by environment interactions. Known Snn and Tsn loci and QTL were compared with 22 environment-specific QTL. None of the eight QTL for glume or the 14 for foliar response were co-located or in linkage disequilibrium with Snn and only one foliar QTL was in LD with Tsn loci on the physical map. Therefore, known NE-Snn interactions are of limited relevance to glume and foliar SNB response in WA environments and other biological mechanisms are likely to prevail for host resistance and susceptibility.

Foliar resistance to Rhizoctonia solani in Arabidopsis is compromised by simultaneous loss of ethylene, jasmonate and PEN2 mediated defense pathways

Rhizoctonia solani causes damaging yield losses on most major food crops. R. solani isolates belonging to anastomosis group 8 (AG8) are soil-borne, root-infecting pathogens with a broad host range. AG8 isolates can cause disease on wheat, canola and legumes, however Arabidopsis thaliana is heretofore thought to possess non-host resistance as A. thaliana ecotypes, including the reference strain Col-0, are resistant to AG8 infection. Using a mitochondria-targeted redox sensor (mt-roGFP2) and cell death staining, we demonstrate that both AG8 and a host isolate (AG2-1) of R. solani are able to infect A. thaliana roots. Above ground tissue of A. thaliana was found to be resistant to AG8 but not AG2. Genetic analysis revealed that ethylene, jasmonate and PENETRATION2-mediated defense pathways work together to provide resistance to AG8 in the leaves which subsequently enable tolerance of root infections. Overall, we demonstrate a significant difference in defense capabilities of above and below ground tissue in providing resistance to R. solani AG8 in Arabidopsis.

LATE BLIGHT RESISTANCE OF WILD POTATO SPECIES UNDER FIELD CONDITIONS IN THE NORTHWEST OF RUSSIA

Background. Despite the great efforts made by breeders, late blight remains a paramount cause of significant potato harvest losses. Introgression of various resistance genes from wild Solanum L. species is the main method to increase the resistance in potato cultivars. Field resistance is considered to be more durable than those induced by the action of single R genes. To this end, resistance sources should be selected from а wide range of species under severe natural infection.Material and methods. As the material for evaluation, 1141 accessions of 99 wild potato species belonging to 15 taxonomic series according to the system of J. Hawkes were used. Each accession was assessed for 3–5 years. A 1–9 point scale was employed to score the damage of plants every week starting from the first symptoms of the disease, where 9 meant the absence of any symptoms, and 1 the entirely damaged plant. The plants scoring 6 to 9 points were considered resistant.Results and conclusions. As a result of the long-term field observations, wild potato species, represented in the current evaluation by numerous accessions, were characterized for foliar resistance to late blight; individual introductions resistant to late blight were also identified. Some of those studied in the 1980s showed high resistance in the end of the 1990s through the 2000s. The highest percentage of resistant accessions/species was identified among the species with areas of distribution in Mexico. A group of Central American species and large part of species with areas of distribution in South America expressed high level of interspecific polymorphism in foliar resistance to late blight.

Temporal Dynamics of Fusarium virguliforme Colonization of Soybean Roots

Soybean sudden death syndrome (SDS) caused by Fusarium virguliforme is one of the most yield limiting soybean diseases in the United States. SDS disease symptoms include root rot and foliar symptoms induced by fungal toxins. Soybean cultivar resistance is one of the most effective SDS disease management options, but no cultivar displays complete resistance. Soybean SDS foliar symptoms are the primary phenotype used to screen and breed for SDS resistance. Root rot or root colonization measures are seldom utilized, partly due to the lack of convenient and accurate methods for quantification of F. virguliforme. In this study, greenhouse and field experiments were conducted to determine the temporal dynamics of F. virguliforme colonization of soybean roots using quantitative real-time PCR (qPCR). The infection coefficient (IC), or ratio of F. virguliforme DNA to soybean DNA, was determined in soybean cultivars with different SDS foliar resistance ratings. In greenhouse experiments, F. virguliforme was detected in all cultivars 7 days after planting (DAP), with a peak in IC at 14 DAP. All soybean cultivars developed SDS foliar symptoms, but F. virguliforme soybean root colonization levels did not significantly correlate with SDS foliar symptom severity. In field experiments, SDS foliar symptoms developed among soybean cultivars in alignment with provided foliar resistance ratings; however, the F. virguliforme IC were not significantly different between SDS foliar symptomatic and asymptomatic cultivars. F. virguliforme was detected in all cultivars at the first sample collection point 25 DAP (V3 vegetative growth stage), and the IC increased throughout the season, peaking at the last sample collection point 153 DAP (postharvest). Collectively, appearance and disease severity ratings of SDS foliar symptoms were not associated with F. virguliforme quantity in roots, suggesting a need to include F. virguliforme root colonization in breeding efforts to screen soybean germplasm for F. virguliforme root infection resistance. The findings also demonstrates root colonization of the pathogen on nonsymptomatic soybean cultivars leading to persistence of the pathogen in the field, and possible hidden yield loss.