A powdery mildew resistance gene was introgressed from Aegilops speltoides into winter wheat and mapped to chromosome 5BL. Closely linked markers will permit marker-assisted selection for the resistance gene. Powdery mildew of wheat (Triticum aestivum L.) is a major fungal disease in many areas of the world, caused by Blumeria graminis f. sp. tritici (Bgt). Host plant resistance is the preferred form of disease prevention because it is both economical and environmentally sound. Identification of new resistance sources and closely linked markers enable breeders to utilize these new sources in marker-assisted selection as well as in gene pyramiding. Aegilops speltoides (2n = 2x = 14, genome SS), has been a valuable disease resistance donor. The powdery mildew resistant wheat germplasm line NC09BGTS16 (NC-S16) was developed by backcrossing an Ae. speltoides accession, TAU829, to the susceptible soft red winter wheat cultivar 'Saluda'. NC-S16 was crossed to the susceptible cultivar 'Coker 68-15' to develop F2:3 families for gene mapping. Greenhouse and field evaluations of these F2:3 families indicated that a single gene, designated Pm53, conferred resistance to powdery mildew. Bulked segregant analysis showed that multiple simple sequence repeat (SSR) and single nucleotide polymorphism (SNP) markers specific to chromosome 5BL segregated with the resistance gene. The gene was flanked by markers Xgwm499, Xwmc759, IWA6024 (0.7 cM proximal) and IWA2454 (1.8 cM distal). Pm36, derived from a different wild wheat relative (T. turgidum var. dicoccoides), had previously been mapped to chromosome 5BL in a durum wheat line. Detached leaf tests revealed that NC-S16 and a genotype carrying Pm36 differed in their responses to each of three Bgt isolates. Pm53 therefore appears to be a new source of powdery mildew resistance.
Fusarium head blight (FHB), primarily caused by Fusarium graminearum, can significantly reduce the grain quality of wheat (Triticum aestivum L.) due to mycotoxin contamination. The objective of this study was to identify quantitative trait loci (QTL) for FHB resistance in the moderately resistant soft red winter wheat cultivar NC‐Neuse. A total of 170 recombinant inbred lines (RILs) from a cross between NC‐Neuse and the susceptible cultivar AGS 2000 were evaluated in inoculated, mist‐irrigated field nurseries. The lines were evaluated for FHB incidence (INC), severity (SEV), Fusarium‐damaged kernels (FDK), and deoxynivalenol (DON) content in seven environments between 2011 and 2014. A 3,419 cM linkage map was developed based on 1839 simple sequence repeat (SSR), diversity array technology (DArT), and single nucleotide polymorphism (SNP) markers. Seven FHB resistance QTL on chromosomes 1A, 1B, 1D, 2A, 4A, 5B, and 6A were mapped. The QTL alleles conferring resistance on 1A, 1B, 2A, 4A, and 6A originated from NC‐Neuse, while the alleles associated with resistance on 1D and 5B originated from AGS 2000. Quantitative trait loci effects ranged from 9 to 12% for INC, from 6 to 11% for SEV, from 8 to 20% for FDK, and from 6 to 18% for DON. The QTL on 5B co‐localized with the Vrn‐B1 locus. Kompetitive Allele‐Specific PCR (KASP) assays were developed for each NC‐Neuse QTL region. A preliminary test using these assays on recent Uniform Southern Winter Wheat Nursery (USWWN) entries indicated Qfhb.nc‐1A, Qfhb.nc‐1B, and Qfhb.nc‐6A as likely the best candidates for use in marker‐assisted selection.
Fusarium head blight (FHB), primarily caused by Fusarium graminearum Schwabe [telemorph: Gibberella zeae Schw. (Petch)], can significantly reduce the grain quality of wheat (Triticum aestivum L.) due to mycotoxin contamination. Two US soft red winter wheat cultivars, Bess and NC‐Neuse, have moderate resistance to FHB. The objective of this study was to validate genomic regions associated with FHB resistance identified in previous studies involving NC‐Neuse and the cultivar Truman, a full‐sib of Bess. A total of 98 doubled haploid lines derived from the cross Bess × NC‐Neuse were evaluated in inoculated, mist‐irrigated field nurseries. The lines were evaluated for FHB incidence, severity, Fusarium‐damaged kernels, and deoxynivalenol content in seven environments between 2011 and 2014. A 3338‐cM linkage map was developed based on 4014 simple sequence repeat and single nucleotide polymorphism markers. Twelve quantitative trait loci (QTL) associated with FHB resistance were identified. NC‐Neuse alleles provided resistance at QTL on five chromosomes and Bess alleles provided resistance at QTL on five other chromosomes. Alignment of linkage maps revealed that five of these QTL were overlapping with previously identified regions. Quantitative trait loci on chromosomes 1A, 4A, and 6A identified in this study overlapped with QTL regions identified in NC‐Neuse, and QTL identified on chromosomes 2B and 3B overlapped with QTL regions identified in Truman. A preliminary test using Kompetitive Allele‐Specific polymerase chain reaction assays on recent Uniform Southern Winter Wheat Scab Nursery entries showed that the assays developed for Qfhb.nc‐2B.1 may be good candidates for use in marker‐assisted selection.
Tomato spotted wilt virus (TSWV) is an important plant pathogen with a wide host range, including the domesticated peanut (Arachis hypogaea L.). After initial outbreaks on peanut during the 1980s, the virus has spread to all peanut-producing states in the U.S. TSWV is transmitted by several species of thrips which are difficult to control with insecticides; therefore, control of TSWV most likely will come from selecting resistant genotypes in breeding programs. Although moderate levels of resistance have been discovered in A. hypogaea, complete virus resistance has not been found. Several Arachis species have desirable genes for plant resistances and tolerate many disease and insect pests better than the cultivated species. The objectives of this study were to (a) evaluate TSWV disease incidence and severity in accessions of Arachis species, and (b) compare levels of TSWV resistance in diploid species to selected A. hypogaea genotypes. In this study, 46 diploid Arachis spp. accessions were evaluated in the greenhouse by artificial inoculation tests for resistance to TSWV. Nine Arachis accessions were observed with no disease symptoms when TSWV isolate 10 was used as opposed to A. hypogaea lines that ranged from moderately to highly susceptible. Additional testing with more virulent isolates identified A. diogoi accession GKP 10602 and A. correntina accession GKP 9530 as highly resistant to the virus. These two accessions are being used as parents in crossing programs to incorporate TSWV resistance genes into A. hypogaea.
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