Edited by: Jose Luis Gonzalez Hernandez, South Dakota State University, United States
Reviewed by: Shaobin Zhong, North Dakota State University, United States; Zhi Zheng, Plant Industry (CSIRO), Australia
This article was submitted to Plant Breeding, a section of the journal Frontiers in Plant Science
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Fusarium head blight (FHB) is a devastating fungal disease of small-grain cereals that results in severe yield and quality losses. FHB resistance is controlled by resistance components including incidence, field severity, visual rating index, Fusarium damaged kernels (FDKs), and the accumulation of the mycotoxin deoxynivalenol (DON). Resistance conferred by each of these components is partial and must be combined to achieve resistance sufficient to protect wheat from yield losses. In this study, two biparental mapping populations were analyzed in Canadian FHB nurseries and quantitative trait loci (QTL) mapped for the traits listed above. Nine genomic loci, on 2AS, 2BS, 3BS, 4AS, 4AL, 4BS, 5AS, 5AL, and 5BL, were enriched for the majority of the QTL controlling FHB resistance. The previously validated FHB resistance QTL on 3BS and 5AS affected resistance to severity, FDK, and DON in these populations. The remaining seven genomic loci colocalize with flowering time and/or plant height QTL. The QTL on 4B was a major contributor to all field resistance traits and plant height in the field. QTL on 4AL showed contrasting effects for FHB resistance between Eastern and Western Canada, indicating a local adapted resistance to FHB. In addition, we also found that the 2AS QTL contributed a major effect for DON, and the 2BS for FDK, while the 5AL conferred mainly effect for both FDK/DON. Results presented here provide insight into the genetic architecture underlying these resistant components and insight into how FHB resistance in wheat is controlled by a complex network of interactions between genes controlling flowering time, plant height, local adaption, and FHB resistance components.
Fusarium head blight (FHB), or scab, mainly caused by the fungus
Chemical fungicides and agronomic practices have proven to be only partially effective at controlling FHB (
Two main mechanisms can explain the FHB resistance in wheat: physiological resistance (active) and disease escape (passive) (
Progress in breeding FHB-resistant cultivars has been hindered by the lack of effective resistance sources and the quantitative nature of FHB resistance. FHB resistance is a polygenic trait controlled by multiple genes that can have either major or minor effects and is significantly affected by the interaction of genotype and environment (
Genetic studies have identified as many as 556 QTL for FHB resistance on all 21 chromosomes in wheat (
In the present study, we aimed to characterize and identify the genetic architecture of different FHB-resistant components including incidence, severity, FDK, and DON from a multi-parental population created by crossing FL62R1 with the two elite Canadian wheat cultivars Stettler and Muchmore. FL62R1 is a wheat line with good FHB resistance derived from the four-way cross QG22.24 / Alsen // SS Blomidon / Alsen that targeted to combine both type I and type II resistance from QG22.24 and Alsen, respectively (
Two spring wheat (
The two DH populations were evaluated for FHB resistance in disease nurseries at Ottawa, Ontario, and Carman, Manitoba in 2015 and 2016 with three biological replications and a random complete block design (RCBD) in single meter rows. At the Ottawa nursery, grain spawn inoculation was used, as described by
A spray approach was used to inoculate plants at the Carman disease nursery. When ∼50% of plants reached anthesis, a mixture of four local
At 18–21 days post-inoculation, FHB incidence (INC) was scored as an estimate of the percentage of infected heads within the plot, and severity (SEV) was measured as an estimate of infected spikelets in an infected head. Visual rating index (VRI) was estimated from INC and SEV using the formula: VRI = (INC × SEV)/100. Plants were harvested with minimum air force to prevent the loss of low weight infected kernels and a visual assessment of kernel damage in the collected seed was used to estimate kernel damage, expressed as percentage of FDK. The concentration of DON in grain was evaluated by commercial enzyme linked immunosorbent assay (ELISA) kits, Neogen Veratox® (Lansing, MI, United States) for DON 5/5 ELISA kits (
Genomic DNA was extracted from the two DH populations using the BioSprint 96 Extraction Platform and DNA Plant Kit (Qiagen, Hilden, Germany). DNA was resuspended in purified water and quantified with a Quant-iTTM PicoGreen® dsDNA Assay Kit (Thermo Fisher Scientific Inc., Bartlesville, OK, United States). All DNA samples were diluted to 50 ng/μl for SNP array genotyping. The two DH populations were genotyped with the Illumina iSelect 90K SNP array (
Genetic maps were developed with Mapdisto (
Statistical analysis of the available phenotypic data was performed in R 3.30 (
Considering all lines from the two populations analyzed, INC ranged from 0 to 100% at both Carman and Ottawa with a mean value of approximately 70–80% (
Phenotypic variation and heritability (
Location | Trait | Pop | Year | Range | Mean | Location | Trait | Pop | Year | Range | Mean | ||
Ottawa | DA (days) | MM | 15_16 | 39–61 | 50.05 | 0.791 | Carman | DA | MM | 15_16 | 38–55 | 45.11 | 0.876 |
15 | 45–61 | 50.9 | 0.845 | 15 | 41–48 | 45.0 | 0.862 | ||||||
16 | 39–61 | 49.2 | 0.747 | 16 | 38–55 | 45.2 | 0.902 | ||||||
ST | 15_16 | 39–72 | 51.31 | 0.803 | ST | 15_16 | 38–57 | 44.65 | 0.740 | ||||
15 | 45–66 | 52.1 | 0.899 | 15 | 38–50 | 44.0 | 0.774 | ||||||
16 | 39–72 | 50.5 | 0.846 | 16 | 41–57 | 45.3 | 0.895 | ||||||
DON (ppm) | MM | 15_16 | 0.2–45.7 | 7.35 | 0.641 | DON | MM | 15_16 | 3.4–38 | 13.70 | NA | ||
15 | 0.3–45.7 | 8.3 | 0.764 | 15 | 5.5–29 | 14.48 | NA | ||||||
16 | 0.2–41.5 | 6.2 | 0.672 | 16 | 3.4–38 | 12.92 | NA | ||||||
ST | 15_16 | 0.1–43.5 | 7.39 | 0.596 | ST | 15_16 | 2.6–42 | 16.41 | NA | ||||
15 | 0.25–43.5 | 9.5 | 0.845 | 15 | 2.7–42 | 16.77 | NA | ||||||
16 | 0.1–33.3 | 5.3 | 0.583 | 16 | 2.6–39 | 16.043 | NA | ||||||
FDK (%) | MM | 15_16 | 0–49 | 10.18 | 0.589 | FDK | MM | 15_16 | 1.3–39.3 | 12.70 | NA | ||
15 | 0–50 | 8.1 | 0.645 | 15 | 3.3–39.3 | 16.31 | NA | ||||||
16 | 0–47 | 12.3 | 0.728 | 16 | 1.34–3 | 9.098 | NA | ||||||
ST | 15_16 | 0–47 | 8.54 | 0.590 | ST | 15_16 | 2.18–35.9 | 15.22 | NA | ||||
15 | 0–34 | 5.5 | 0.747 | 15 | 3.7–35.9 | 20.33 | NA | ||||||
16 | 0–47 | 11.6 | 0.648 | 16 | 2.18–31.9 | 10.105 | NA | ||||||
HT (cm) | MM | 15_16 | 47–110 | 81.18 | 0.800 | HT | MM | 15_16 | NA | NA | NA | ||
15 | 60–110 | 88.8 | 0.844 | 15 | NA | NA | NA | ||||||
16 | 47–108 | 73.6 | 0.739 | 16 | 50–116.7 | 92.7 | 0.858 | ||||||
ST | 15_16 | 56.5–113.5 | 81.02 | 0.879 | ST | 15_16 | NA | NA | NA | ||||
15 | 66–120 | 93.9 | 0.886 | 15 | NA | NA | NA | ||||||
16 | 47–107 | 78.1 | 0.814 | 16 | 60–121.7 | 95.4 | 0.889 | ||||||
INC (%) | MM | 15_16 | 10–100 | 87.47 | 0.555 | INC | MM | 15_16 | 20–100 | 71.65 | 0.648 | ||
15 | 20–100 | 88.8 | 0.662 | 15 | 20–100 | 72.0 | 0.697 | ||||||
16 | 10–100 | 85.5 | 0.480 | 16 | 20–95 | 71.3 | 0.885 | ||||||
ST | 15_16 | 10–100 | 85.91 | 0.672 | ST | 15_16 | 10.1–100 | 74.83 | 0.760 | ||||
15 | 15–100 | 85.2 | 0.719 | 15 | 10–95 | 75.3 | 0.600 | ||||||
16 | 10–100 | 86.6 | 0.738 | 16 | 30–100 | 74.4 | 0.874 | ||||||
SEV (%) | MM | 15_16 | 5–100 | 44.76 | 0.620 | SEV | MM | 15_16 | 5–85 | 27.37 | 0.700 | ||
15 | 5–100 | 44.2 | 0.769 | 15 | 5–85 | 29.5 | 0.708 | ||||||
16 | 5–95 | 45.4 | 0.698 | 16 | 5–80 | 25.2 | 0.844 | ||||||
ST | 15_16 | 5–100 | 40.19 | 0.821 | ST | 15_16 | 5–95 | 34.17 | 0.849 | ||||
15 | 5–100 | 37.3 | 0.851 | 15 | 5–95 | 40.9 | 0.695 | ||||||
16 | 5–100 | 43.1 | 0.875 | 16 | 5–70 | 27.4 | 0.875 |
Distribution of phenotypic traits from field trials in different years and locations. Fusarium damaged kernels (FDKs), incidence (INC), and severity (SEV) at
Positive correlation was observed among all FHB resistance components, while DA and HT showed mostly negative correlation with FHB traits (
Phenotypic correlation between Fusarium head blight-resistance components and associated traits at two field locations for two populations. The areas of the circles show the absolute value of the corresponding correlation coefficients (
The correlation between greenhouse type II resistance in the Stettler population (
Quantitative trait loci analysis identified a large number of loci that contributed the different resistance components (
Nine major QTL identified for FHB-resistant components across four environments in the Muchmore and Stettler populations.
QTLChra | 2AS | 2BS | 3BS | 4AS | 4AL* | 4BS | 5AS | 5AL | 5BL | ||||||||||||||||||
Pos (cM)b | 38.7–73.9 | 1.3–44.6 | 5.2–14.4 | 20–65 | 23–37; 163–216 | 5–52 | 97.7–213 | 75–92 | 60–113 | ||||||||||||||||||
PhysPos (Mb)c | 37–55 | 42–364 | 8.8–16 | 6.9–39 | 641–742 | 8.4–223 | 416–657 | 33–86 | 448–583 | ||||||||||||||||||
LODd | Ade | PVf | LOD | Ad | PV | LOD | Ad | PV | LOD | Ad | PV | LOD | Ad | PV | LOD | Ad | PV | LOD | Ad | PV | LOD | Ad | PV | LOD | Ad | PV | |
MO15 | 7.0 | 1.8 | 10 | 2.8 | 1.2 | 4.9 | 2.9 | 2.9 | 27 | 6.7 | 1.7 | 11 | |||||||||||||||
MO16 | 9.4 | 2.4 | 20 | 7.4 | 2 | 16 | |||||||||||||||||||||
MW15 | 9.2 | 1.9 | 13 | 6.5 | 1.6 | 8.7 | 7.2 | −1.7 | 9.7 | 8.7 | 2 | 13 | 5 | 1.4 | 6.9 | ||||||||||||
MW16 | 5.8 | 1.5 | 9 | 4.2 | 1.3 | 6.9 | 3.4 | −1.2 | 5.9 | 4.4 | 1.2 | 6.3 | 3.4 | 1.1 | 5.2 | ||||||||||||
SO15 | 4.1 | 2 | 6.7 | 3.5 | 1.7 | 4.5 | 13 | 3.9 | 24 | 6.5 | 2.5 | 9.8 | |||||||||||||||
SO16 | 12 | 1.9 | 28 | 2.7 | −0.9 | 5.2 | |||||||||||||||||||||
SW15 | 3.8 | 1.7 | 5.9 | 8.8 | 2.7 | 15 | 5.1 | −2 | 7.9 | 6.7 | 2.3 | 11 | |||||||||||||||
SW16 | 4.6 | 2 | 7.2 | 11 | 3.2 | 19 | 7.7 | 2.6 | 12 | 3.5 | 1.7 | 5.3 | 2.6 | 1.4 | 3.7 | ||||||||||||
MO15 | 3.3 | 1.4 | 6.7 | 4.1 | 1.6 | 8.5 | 13 | 3.3 | 35 | 4.4 | 4 | 8.9 | |||||||||||||||
MO16 | 14 | 3.4 | 14 | 6.9 | 3.2 | 13 | |||||||||||||||||||||
MW15 | 6.9 | 2 | 11 | 11 | 2.7 | 18 | 4.1 | −1.6 | 6.1 | ||||||||||||||||||
MW16 | 2.7 | 0.8 | 3.9 | 6.9 | 2.1 | 11 | 9.3 | 1.6 | 15 | 3.5 | 1 | 5.4 | 4.4 | 1.1 | 6.8 | ||||||||||||
SO15 | 4.9 | 4.9 | 8.5 | 5.8 | 2 | 10 | 4 | 1.3 | 7.1 | 4.8 | −1.5 | 8.4 | |||||||||||||||
SO16 | 12 | 3.8 | 27 | ||||||||||||||||||||||||
SW15 | 6.8 | 2.3 | 13 | 2.9 | 1.5 | 5.4 | |||||||||||||||||||||
SW16 | 8.8 | 1.9 | 15 | 5.5 | 1.5 | 9.4 | |||||||||||||||||||||
MO15 | 2.7 | 3.5 | 6.7 | 5.5 | 5.3 | 14 | |||||||||||||||||||||
MO16 | 3.5 | 4.8 | 9.4 | ||||||||||||||||||||||||
MW15 | 3.2 | 2.9 | 5.4 | 3.3 | −2.9 | 5.4 | 8.4 | 5.1 | 16 | ||||||||||||||||||
MW16 | 4.9 | 4 | 8.5 | ||||||||||||||||||||||||
SO15 | 5.4 | −5.1 | 9.2 | 7.9 | 6.5 | 15 | 7.6 | −6.3 | 13 | ||||||||||||||||||
SO16 | 7.3 | −7.1 | 17 | ||||||||||||||||||||||||
SW15 | 3.7 | 2.9 | 5.1 | 19 | 5.9 | 19 | |||||||||||||||||||||
SW16 | 2.8 | 2.3 | 3.5 | 13 | 6.9 | 8.7 | 4.2 | 2.8 | 5.4 | ||||||||||||||||||
MO15 | 5.6 | 6.9 | 10 | 7 | 7.7 | 14 | 3.6 | 5.8 | 7.8 | 3.3 | 5.1 | 6.4 | |||||||||||||||
MO16 | 5 | 5.9 | 11 | 2.5 | 4.5 | 6.9 | |||||||||||||||||||||
MW15 | 3.2 | 2.5 | 5.2 | 6.6 | −3.7 | 11 | 3.2 | 2.5 | 4.9 | ||||||||||||||||||
MW16 | 2.5 | 2 | 4.1 | 3.4 | 2.4 | 5.6 | 4.3 | 4.3 | 7.1 | ||||||||||||||||||
SO15 | 8.7 | 8.2 | 13 | 3.4 | 6.6 | 5.1 | 4.3 | 4.3 | 3.5 | 12 | −10 | 20 | |||||||||||||||
SO16 | 10 | −10 | 23 | ||||||||||||||||||||||||
SW15 | 4 | 3.6 | 6.3 | 2.9 | 3.1 | 4.6 | 4.2 | 4.5 | 7.1 | ||||||||||||||||||
SW16 | 4.3 | 3.8 | 7.6 | 2.5 | −2.8 | 4.1 | 3.6 | 4 | 5.8 | ||||||||||||||||||
MO15 | 5.6 | 6.4 | 11 | 6.6 | 7 | 14 | 5.8 | 6.5 | 12 | 3.5 | 4.9 | 6.9 | |||||||||||||||
MO16 | 3.5 | 4.3 | 7.7 | 8.3 | 3.7 | 7 | 4.2 | 5.1 | 11 | ||||||||||||||||||
MW15 | 6.4 | 3.7 | 10 | 8.2 | −4.2 | 14 | 4.6 | 3.1 | 7.3 | 2.8 | 2.4 | 4.5 | |||||||||||||||
MW16 | 3.9 | 2.6 | 6.7 | 3.8 | 2.6 | 6.5 | |||||||||||||||||||||
SO15 | 4.3 | −5.5 | 6.5 | 8.8 | 7.9 | 14 | 3.8 | 5.9 | 5.6 | 12 | −9.8 | 20 | |||||||||||||||
SO16 | 2.6 | −4.2 | 5.2 | 8.1 | 7.8 | 17 | 10 | −9 | 23 | ||||||||||||||||||
SW15 | 2.6 | 2.9 | 4.2 | 4.2 | 4.2 | 6.7 | 8.4 | 5.5 | 15 | ||||||||||||||||||
SW16 | 4 | 3.9 | 7.1 | 3.5 | −3.5 | 5.8 | 8.3 | 5.7 | 15 | ||||||||||||||||||
MO15 | 6.6 | 0.7 | 9 | 2.7 | −0.4 | 3.3 | 20 | −1.3 | 35 | ||||||||||||||||||
MO16 | 2.5 | 0.7 | 6.2 | 5.4 | −1.1 | 14 | |||||||||||||||||||||
MW15 | 36 | −1.3 | 50 | 6.3 | 0.5 | 6.5 | |||||||||||||||||||||
MW16 | 4.9 | −0.6 | 4.4 | 38 | −1.9 | 49 | 3.7 | 0.5 | 3.2 | ||||||||||||||||||
SO15 | 3.4 | 0.6 | 4.9 | 4.1 | 0.7 | 6.4 | 6.7 | −0.9 | 11 | 6 | 0.9 | 9.8 | 6.6 | 1 | 11 | ||||||||||||
SO16 | 7.6 | 0.2 | 17 | ||||||||||||||||||||||||
SW15 | 19 | −0.8 | 22 | 3.4 | −0.3 | 4.2 | 7 | 0.4 | 9.2 | ||||||||||||||||||
SW16 | 32 | −0.9 | 11 | 12 | 1.3 | 20 | |||||||||||||||||||||
MO15 | 30 | −7.6 | 58 | 2.7 | −1.6 | 2.9 | |||||||||||||||||||||
MO16 | 5.6 | −2.6 | 9.1 | 16 | −5.4 | 38 | 5.3 | −2.5 | 8.6 | ||||||||||||||||||
MW16 | 2.9 | −1.8 | 3.1 | 32 | −7.1 | 50 | 5.2 | −2.4 | 5.6 | ||||||||||||||||||
SO16 | 27 | −7.2 | 50 | 2.8 | −2 | 4.4 | 6.7 | 2.8 | 8.8 | ||||||||||||||||||
SW16 | 37 | −7.5 | 57 | 6.4 | −2.6 | 7 |
QTLs of Fusarium head blight resistance, flower time, and plant height anchored on the Chinese Spring reference 1.0 (CS Ref 1.0). The marker located at the peak of the QTL identified by blast on CS Ref 1.0 was used to localize QTL.
4BS: The 4BS genomic locus, from 7.04 to 42.02 Mb on the CS Ref 1.0 assembly, is the region with the highest number of QTL identified in this study. It was detected across almost all environments for the FHB resistance traits and plant height (
3BS: QTL identified on 3BS were localized to an interval between 6.68 and 11.58 Mb on the CS Ref 1.0 assembly. QTL for SEV, FDK, and DON were stably detected in both populations at Carman in 2015 with relatively large effects, with PV of 7–19%. During the 2016 trial, QTL also were found for these components except for SEV in the Stettler population. No QTL was found for INC in this genomic locus. QTL for VRI were identified in the Stettler population in 2015 and the Muchmore population in 2016. At Ottawa, the only QTL in this region was identified for DON in the 2015 Stettler population. No DA or HT QTL were found in the 3BS region.
4AL and 4AS: The QTL from 4AL (physical position from 641.4 to 692.4 Mb on the CS assembly) were mainly detected in the 2015 trials. For the Muchmore population, stable QTL were found at both Carman and Ottawa for SEV, FDK, DON, and VRI, while QTL for INC were only detected at Carman in this region. For the Stettler population, QTL were also found for SEV, FDK, DON, and VRI on 4AL at Ottawa, while this region only had a QTL for DON at Carman. In 2016 the 4AL region had a smaller impact on FHB resistance, with only a minor effect for DON QTL found in the Muchmore population at Carman. One of the largest and most significant QTL in the entire dataset was found for DA in the 4AL region. It was detected in each population, year, and location, except for Stettler at Ottawa in 2016, and had a large impact with PV ranging from 10.9 to 49.8%. The common parental line, FL62R1, contributed to longer DA and taller plants, though at Ottawa, the locus contributed to FHB resistance but increased FHB susceptibility at Carman.
In the region on 4AS (∼12.2–38.7 Mb), QTL were only detected in the Stettler population. SEV was the most stable QTL detected at Ottawa and Carman. The alleles contributed by Stettler conferred better disease resistance at the 4AS QTL.
5AL and 5AS: The 5AL genomic locus covered the region from 528.6 to 584.7 Mb on the CS Ref 1.0 assembly. QTL from this region were observed for all of the traits, though each was not consistent across environments. The largest effect 5AL QTL were for DON at Ottawa; the Muchmore population in 2016 with a PV of 16%, followed by a 9.8% PV from the Stettler population in 2015. Minor QTL for DA and HT were found on the 5AL region in both populations.
FHB resistance QTL were found on 5AS in the Muchmore population only. In 2015, 5AS QTL were found in Ottawa and Carman (contributing up to 11% PV). In 2016, a 5AS QTL for DON was detected in Carman, in addition to an FDK QTL at Ottawa. VRI and SEV 5AS QTL were found at both sites in 2016.
5BL: QTL from this region were located from 551.0 to 582.5 Mb in the CS 1.0 reference genome. The 5BL QTL were only identified in the Stettler population, where they were responsible for a large phenotypic effect on FHB resistance at Ottawa in 2015 and 2016, with PV as high as 13.3% for INC and 22.7% for SEV. In all cases, alleles from Stettler contributed to disease resistance at the 5BL locus. A major QTL with large effect for DA was detected in the 5BL interval in the Stettler population, with Stettler responsible for delayed anthesis.
2AS and 2BS: The 2AS QTL were localized from 36.6 to 58.4 Mb on the CS Ref 1.0 assembly. This region conferred resistance for almost all of the resistance components in both the Stettler and Muchmore populations in both years of testing at the Carman site. No QTL was detected on 2AS at Ottawa.
The 2BS QTL region controlled the majority of FHB resistance traits in the Muchmore population at Ottawa in 2015 and 2016.
FHB resistance in wheat is a complex trait and controlled by several resistance components including INC, SEV, DON accumulation, FDK, and spreading (greenhouse). A better understanding of the genetic architecture underlying these different components may enable the development of wheat cultivars with better resistance to FHB. In the present study, a systematic analysis of different components was undertaken with two large bi-parental mapping populations, revealing how different FHB resistance components, plant height and flowering time, interact.
There was a moderate to high heritability displayed across the FHB resistance components tested, which is in agreement with previous findings, indicating that genetic variation plays a main role in the phenotypic variation of these FHB traits (
FHB type II resistance (resistance to fungal spread in the spike) is determined by point inoculation in the greenhouse, while SEV is routinely used as an estimate for field FHB spread/type II resistance (
A higher negative correlation was observed between plant height and FHB resistance components at Ottawa than at Carman. This is likely the result of the different FHB inoculation approaches utilized at each location: grain spawn at Ottawa and spray treatment at Carmen. The spawn approach relies on wind or water splashes to spread FHB spores from the ground surface to spikes and establish infection (
A large number of loci that control different FHB resistance were identified, with genomic loci on 2AS, 2BS, 3BS, 4AS, 4AL, 4BS, 5AS, 5AL, and 5BL enriched with QTL for one or more traits. The genomic locus 4BS from FL62R1 conferred the most stable FHB resistance, with INC, SEV, FDK, and DON QTL identified at all tested environments, in both the Stettler and Muchmore populations. A major QTL for plant height was also identified in this region of 4BS that can be attributed to the presence of the semi-dwarf allele of
The largest effect and most extensively characterized FHB resistance QTL is
In addition to genetic background, the method of inoculation, the aggressiveness of the
The 5AS QTL was only found in the Muchmore population and showed variable effects on different resistance components. As observed for 3BS (
The remaining genomic loci controlling FHB resistance (2AS, 2BS, 4AS, 4AL, 5AL, and 5BL) identified in this study were all found to colocalize with flowering time or flowering time and plant height. The large number of FHB resistance loci associated with flowering time indicates that a complex flowering regulatory network was involved in controlling disease resistance in the populations tested. The establishment of FHB infection needs a favorable environment for disease establishment and the appropriate susceptible stage of plant development, namely, the early flowering stage at the time of fungal introduction (
The chromosome arms 4AL and 5BL contain two major genomic loci that showed the largest effect for DA and minor effects for HT. The 4AL QTL were found to control SEV, FDK, and DON, with the largest effect on SEV. QTL from 4A have previously been reported in durum wheat (
The 5BL QTL region has a major effect for DA and a minor effect for height in the Stettler population, with the QTL from Stettler delaying time to anthesis. The major vernalization gene
We identified FHB resistance QTL for FHB syntenic region on 2AS and 2BS colocalized with the major flower control genes
Finally, intensive research have been conducted for types I and II of FHB resistance in wheat. Despite the importance of FDK for grain quality and DON for food safety, little research was performed on FDK and DON. Recently,
The genetic architecture of high-level FHB resistance for different resistance components from FL62R1 were identified. It is concluded that FL62R1 confers Sumai 3 levels of resistance through the interaction of
For future research into the genetic control of FHB resistance, there is a need to clearly characterize the important resistant loci, from the magnitude of their effects to the effect on different resistant components, especially in elite cultivar genetic backgrounds. This is especially true for the major resistance gene
From a breeding perspective, due to the complexity of the network controlling flowering time, its association with FHB resistance, and local adaption properties, it is important to completely identify the haplotypes of the major flowering time gene(s) in existing breeding programs. By fine-tuning the complex network from local adapted haplotypes (or alleles), and combining
The datasets generated for this study can be found in FigShare,
PF conceived this study and acquired fund for this study. PF, WZ, KB, and RC designed the experiment. FJ and FE developed DH populations. HR contributed to seed increasing of DH populations. KB, PG, BP, and WZ performed the experiments. AB-B, GF, and ZR contributed to field trials and disease evaluation. WZ and KB analyzed the data and interpreted the results. WZ, KB, and PF wrote the manuscript. All authors contributed to the article and approved the submitted version.
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
The authors thank Ron DePauw for Stettler and Muchmore germplasm, Janet Condie for technical assistance with the 90K SNP genotyping, and Daoquan Xiang for critically reviewing the manuscript.
The Supplementary Material for this article can be found online at: