Identification of QTLs for Resistance to Fusarium Head Blight Using a Doubled Haploid Population Derived from Southeastern United States Soft Red Winter Wheat Varieties AGS 2060 and AGS 2035.

Fusarium head blight (FHB), caused primarily by the fungus Fusarium graminearum, is one of the most damaging diseases of wheat, causing significant loss of yield and quality worldwide. Warm and wet conditions during flowering, a lack of resistant wheat varieties, and high inoculum pressure from corn stubble contribute to frequent FHB epidemics in the southern United States. The soft red winter wheat variety AGS 2060 is moderately susceptible (as opposed to susceptible) to FHB and regularly found in pedigrees of resistant breeding lines. AGS 2060 does not carry any known resistance genes or quantitative trait loci (QTL). A QTL mapping study was conducted to determine the location and genetic effect of its resistance using a doubled haploid mapping population produced from a cross between wheat varieties AGS 2060 and AGS 2035 (FHB susceptible). The population was genotyped using the Illumina iSelect single nucleotide polymorphism (SNP) array for wheat and phenotyped in Baton Rouge and Winnsboro, Louisiana and Newport, Arkansas in 2018 and 2019. The effect of genotype was significant for Fusarium damaged kernels (FDK) and deoxynivalenol (DON) content across all locations and years, indicating genetic variation in the population. The study detected 13 QTLs (one each on chromosome 1A, 1B, 1D, 2A, 2B, 6A, 6B, 7A, and 7B, and two each on 5A and 5B) responsible for the reduction of FDK and/or DON. Of these, nine QTLs for FHB resistance were identified in Winnsboro, Louisiana, in 2019. QTLs on chromosomes 2A and 7A could be valuable sources of resistance to both DON and FDK over several environments and were likely the best candidates for use in marker-assisted selection. Consistently expressed QTLs on chromosomes 5A, 6B, and 7A were potentially newly identified sources of resistance to FHB in soft red winter wheat.

Correction: Genome-wide microarray analysis leads to identification of genes in response to herbicide, metribuzin in wheat leaves.

[This corrects the article DOI: 10.1371/journal.pone.0189639.].

Genome-wide microarray analysis leads to identification of genes in response to herbicide, metribuzin in wheat leaves.

Herbicides are an important component of weed management in wheat, particularly in the southeastern US where weeds actively compete with wheat throughout the winter for nutrients and reduce tillering and ultimately the yield of the crop. Some wheat varieties are sensitive to metribuzin, a low-cost non-selective herbicide, leading to leaf chlorosis, stand loss, and decreased yield. Knowledge of the genetics of herbicide tolerance in wheat is very limited and most new varieties have not been screened for metribuzin tolerance. The identification of genes associated with metribuzin tolerance will lead to the development of molecular markers for use in screening breeding lines for metribuzin tolerance. AGS 2035 and AGS 2060 were identified as resistant and sensitive to metribuzin in several previous field screening experiments as well as controlled condition screening of nine varieties in the present study. Genome-wide transcriptome profiling of the genes in AGS 2035 and AGS 2060 through microarray analysis identified 169 and 127 genes to be significantly (2-fold, P>0.01) up- and down-regulated, respectively in response to metribuzin. Functional annotation revealed that genes involved in cell wall biosynthesis, photosynthesis and sucrose metabolism were highly responsive to metribuzin application. (Semi)quantitative RT-PCR of seven selected differentially expressed genes (DEGs) indicated that a gene coding for alkaline alpha-galactosidase 2 (AAG2) was specifically expressed in resistant varieties only after one and two weeks of metribuzin application. Integration of the DEGs into our ongoing mapping effort and identification of the genes within the QTL region showing significant association with resistance in future will aid in development of functional markers for metribuzin resistance.