Mapping Resistance to Argentinean Fusarium (Graminearum) Head Blight Isolates in Wheat

Fusarium head blight (FHB) of wheat, caused by Fusarium graminearum (Schwabe), is a destructive disease worldwide, reducing wheat yield and quality. To accelerate the improvement of scab tolerance in wheat, we assessed the International Triticeae Mapping Initiative mapping population (ITMI/MP) for Type I and II resistance against a wide population of Argentinean isolates of F. graminearum. We discovered a total of 27 additive QTLs on ten different (2A, 2D, 3B, 3D, 4B, 4D, 5A, 5B, 5D and 6D) wheat chromosomes for Type I and Type II resistances explaining a maximum of 15.99% variation. Another four and two QTLs for thousand kernel weight in control and for Type II resistance, respectively, involved five different chromosomes (1B, 2D, 6A, 6D and 7D). Furthermore, three, three and five QTLs for kernel weight per spike in control, for Type I resistance and for Type II resistance, correspondingly, involved ten chromosomes (2A, 2D, 3B, 4A, 5A, 5B, 6B, 7A, 7B, 7D). We were also able to detect five and two epistasis pairs of QTLs for Type I and Type II resistance, respectively, in addition to additive QTLs that evidenced that FHB resistance in wheat is controlled by a complex network of additive and epistasis QTLs.

Cross-Resistance of the Codling Moth against Different Isolates of Cydia pomonella Granulovirus Is Caused by Two Different but Genetically Linked Resistance Mechanisms

Cydia pomonella granulovirus (CpGV) is a widely used biological control agent of the codling moth. Recently, however, the codling moth has developed different types of field resistance against CpGV isolates. Whereas type I resistance is Z chromosomal inherited and targeted at the viral gene pe38 of isolate CpGV-M, type II resistance is autosomal inherited and targeted against isolates CpGV-M and CpGV-S. Here, we report that mixtures of CpGV-M and CpGV-S fail to break type II resistance and is expressed at all larval stages. Budded virus (BV) injection experiments circumventing initial midgut infection provided evidence that resistance against CpGV-S is midgut-related, though fluorescence dequenching assay using rhodamine-18 labeled occlusion derived viruses (ODV) could not fully elucidate whether the receptor binding or an intracellular midgut factor is involved. From our peroral and intra-hemocoel infection experiments, we conclude that two different (but genetically linked) resistance mechanisms are responsible for type II resistance in the codling moth: resistance against CpGV-M is systemic whereas a second and/or additional resistance mechanism against CpGV-S is located in the midgut of CpR5M larvae.

Spike Architecture Traits Associated With Type II Resistance to Fusarium Head Blight in Bread Wheat

Fusarium head blight (FHB) remains a devastating disease in bread wheat (Triticum aestivum L.) and other small grains. Genetic resistance to FHB is a complex trait; in addition to active physiological resistance, plant developmental and morphological traits may indirectly affect disease progression and provide a passive mechanism of resistance. In this study, we investigated the relationship between FHB type II resistance and spike architecture traits in a recombinant inbred line (RIL) population of bread wheat. Disease resistance traits were FHB severity at 21 days post inoculation (dpi) and area under the disease progress curve (AUDPC). Spike architecture traits measured were rachis length, spike density, number of spikelets per spike, florets per spike and florets per spikelet. The RIL population showed significant variation for all traits. Heritability values were moderate to high for FHB severity (0.69) and AUDPC (0.63) and high for the spike architecture traits (0.74 - 0.92). FHB severity and AUDPC showed a moderate and significant association with the number of florets per spike (r = 0.38 and r = 0.31, respectively) and with the number of florets per spikelet (r = 0.28 and r = 0.27, respectively), reflecting a greater spread of the fungus in spikes with higher floret number. These results suggest that the number of florets per spike and the number of florets per spikelet should be considered in FHB resistance breeding efforts, because selection of lines with higher number of florets could lead to a correlated selection response towards increased FHB levels under field conditions.

Development of an Evaluation System for Fusarium Resistance in Wheat Grains and Its Application in Assessment of the Corresponding Effects of Fhb1

Fusarium head blight (FHB) caused by Fusarium species is a globally important wheat disease. Host resistance to FHB is composed of multiple mechanisms, including resistance to initial infection (type I), disease spread (type II), toxin accumulation (type III), kernel infection (type IV), and yield loss (type V), of which the last three have been less studied. Traditionally, the Fusarium-damaged kernel rate (FDK; percentage of Fusarium-infected grains) from point- or spray-inoculated experiments was used as the parameter for type IV resistance, which may be problematic because of the influence of type II resistance. Here we propose a new definition for type IV resistance: that is, the resistance against Fusarium infection expressed in wheat grains that have the same chance in contact with the pathogen, under favorable temperature and humidity for infection. Fhb1 confers strong type II resistance, leading to significantly reduced FHB severity and FDK. To investigate the role of Fhb1 in type IV resistance, a pair of near-isogenic lines, R22W (Fhb1 carrier, resistant in terms of type II resistance) and S22V (non-Fhb1, susceptible), along with eight wheat genotypes differing at Fhb1 were inoculated at different grain development stages with Fusarium macrospores both in vivo and in vitro. The in vivo experiments with all florets inoculated demonstrated a significant reduction in thousand kernel weight (TKW) in inoculated grains, regardless of their Fhb1 status and developmental stages. Surprisingly, R22W showed more TKW reduction than S22V, which was supported by the scanning electron microscopy observation that confirmed the more severe degradation of starch granules in R22W grains. The in vitro experiments demonstrated that grains from both R22W and S22V promoted fungal colonization, but no significant difference was found between the two lines. In summary, our results indicated that the proposed type IV evaluation system is effective in determining different grain resistance levels, providing novel tools for FHB resistance breeding. The finding that Fhb1 is not associated with type IV resistance enriches our understanding of this gene.

Genome-wide association mapping revealed syntenic loci QFhb-4AL and QFhb-5DL for Fusarium head blight resistance in common wheat (Triticum aestivum L.)

Background: Fusarium head blight (FHB), primarily caused by Fusarium graminearum, is a major threat to wheat production and food security worldwide. Breeding stably and durably resistant cultivars is the most effective approach for managing and controlling the disease. The success of FHB resistance breeding relies on identification of an effective resistant germplasm. We conducted a genome-wide association study (GWAS) using the high-density wheat 90K single nucleotide polymorphism (SNP) assays to better understand the genetic basis of FHB resistance in natural population and identify associated molecular markers. Results: The resistance to FHB fungal spread along the rachis (Type II resistance) was evaluated on 171 wheat cultivars in the 2016-2017 (abbr. as 2017) and 2017-2018 (abbr. as 2018) growing seasons. Using Illumina Infinum iSelect 90K SNP genotyping data, a genome-wide association study (GWAS) identified 26 loci (88 marker-trait associations), which explained 6.65-14.18% of the phenotypic variances. The associated loci distributed across all chromosomes except 2D, 6A, 6D and 7D, with those on chromosomes 1B, 4A, 5D and 7A being detected in both years. New loci for Type II resistance were found on syntenic genomic regions of chromsome 4AL (QFhb-4AL, 621.85-622.24 Mb) and chromosome 5DL (QFhb-5DL, 546.09-547.27 Mb) which showed high collinearity in gene content and order. SNP markers wsnp_JD_c4438_5568170 and wsnp_CAP11_c209_198467 of 5D, reported previously linked to a soil-borne wheat mosaic virus (SBWMV) resistance gene, were also associated with FHB resistance in this study. Conclusion: The syntenic FHB resistant loci and associated SNP markers identified in this study are valuable for FHB resistance breeding via marker-assisted selection.

Genome-wide association mapping revealed syntenic loci QFhb-4AL and QFhb-5DL for Fusarium head blight resistance in common wheat (Triticum aestivum L.)

Background: Fusarium head blight (FHB), primarily caused by Fusarium graminearum, is a major threat to wheat production and food security worldwide. Breeding stably and durably resistant cultivars is the most effective approach for managing and controlling the disease. The success of FHB resistance breeding relies on identification of an effective resistant germplasm. We performed a genome-wide association study (GWAS) using the high-density wheat 90K single nucleotide polymorphism (SNP) assays to better understand the genetic basis of FHB resistance in natural population and identify associated molecular markers. Results: The resistance to FHB fungal spread along the rachis (Type II resistance) was evaluated on 171 wheat cultivars in the 2016-2017 (abbr. as 2017) and 2017-2018 (abbr. as 2018) growing seasons. Using Illumina Infinum iSelect 90K SNP genotyping data, a genome-wide association study (GWAS) identified 26 loci (88 marker-trait associations), which explained 6.65-14.18% of the phenotypic variances. The associated loci distributed across all chromosomes except 2D, 6A, 6D and 7D, with those on chromosomes 1B, 4A, 5D and 7A being detected in both years. New loci for Type II resistance were found on syntenic genomic regions of chromsome 4AL (QFhb-4AL, 621.85-622.24 Mb) and chromosome 5DL (QFhb-5DL, 546.09-547.27 Mb) which showed high collinearity in gene content and order. SNP markers wsnp_JD_c4438_5568170 and wsnp_CAP11_c209_198467 of 5D, reported previously linked to a soil-borne wheat mosaic virus (SBWMV) resistance gene, were also associated with FHB resistance in this study. Conclusion: The syntenic FHB resistant loci and associated SNP markers identified in this study are valuable for FHB resistance breeding via marker-assisted selection.

Genome-wide association mapping revealed syntenic loci QFhb-4AL and QFhb-5DL for Fusarium head blight resistance in common wheat (Triticum aestivum L.)

Background: Fusarium head blight (FHB), primarily caused by Fusarium graminearum, is a major threat to wheat production and food security worldwide. Breeding stably and durably resistant cultivars is the most effective approach for managing and controlling the disease. The success of FHB resistance breeding relies on identification of effective resistant germplasm. We performed a genome-wide association study (GWAS) using the high-density wheat 90K single nucleotide polymorphism (SNP) assays to better understand the genetic basis of FHB resistance in natural population and identify associated molecular markers. Results: The resistance to FHB fungal spread along the rachis (Type II resistance) was evaluated on 171 wheat cultivars in the 2016-2017 (abbr. as 2017) and 2017-2018 (abbr. as 2018) growing seasons. Using Illumina Infinum iSelect 90K SNP genotyping data, a genome-wide association study (GWAS) identified 26 loci（88 marker-trait associations）, which explained 6.65-14.18% of the phenotypic variances. The associated loci distributed across all chromosomes except 2D, 6A, 6D and 7D, with those on chromosomes 1B, 4A, 5D and 7A being detected in both years. New loci for Type II resistance were found on syntenic genomic regions of chromsome 4AL ( QFhb-4AL , 621.85 Mb - 622.24 Mb) and chromosome 5DL ( QFhb-5DL , 546.09 Mb - 547.27 Mb) which showed highly collinearity in gene content and order. SNP markers wsnp_JD_c4438_5568170 and wsnp_CAP11_c209_198467 of 5D, reported previously linked to a soil-borne wheat mosaic virus (SBWMV) resistance gene, were also associated with FHB resistance in this study. Conclusion: The syntenic FHB resistant loci and associated SNP markers identified in this study are valuable for FHB resistance breeding via marker-assisted selection.

Genome-wide association mapping revealed syntenic loci QFhb-4AL and QFhb-5DL for Fusarium head blight resistance in common wheat (Triticum aestivum L.)

Background:Fusarium head blight (FHB), primarily caused by Fusarium graminearum, is a major threat to wheat production and food security worldwide. Breeding stably and durably resistant cultivars is the most effective approach for managing and controlling the disease. The success of FHB resistance breeding relies on identification of an effective resistant germplasm. We performed a genome-wide association study (GWAS) using the high-density wheat 90K single nucleotide polymorphism (SNP) assays to better understand the genetic basis of FHB resistance in natural population and identify associated molecular markers. Results:The resistance to FHB fungal spread along the rachis (Type II resistance) was evaluated on 171 wheat cultivars in the 2016-2017 and 2017-2018 growing seasons. Using Illumina Infinum iSelect 90K SNP genotyping data, a genome-wide association study (GWAS) identified 26 loci(88 marker-trait associations), which explained 6.65-14.18% of the phenotypic variances. The associated loci distributed across all chromosomes except 2D, 6A, 6D and 7D, with those on chromosomes 1B, 4A, 5D and 7A being detected in both years. New loci for Type II resistance were found on syntenic genomic regions of chromsome 4AL (QFhb-4AL, 621.85 - 622.24 Mb) and chromosome 5DL (QFhb-5DL, 546.09 - 547.27 Mb) which showed highly collinarity in gene content and order. SNP markers wsnp_JD_c4438_5568170 and wsnp_CAP11_c209_198467 of 5D, reported previously linked to a soil-borne wheat mosaic virus (SBWMV) resistance gene, were also associated with FHB resistance in this study. Conclusion:The syntenic FHB resistant loci and associated SNP markers identified in this study are valuable for FHB resistance breeding via marker-assisted selection.