Winter wheat requires a period of low temperatures to accelerate flowering (vernalization). This requirement could make winter wheat more vulnerable to elevated global temperature via insufficient vernalization. All known vernalization genes are cloned according to qualitative variation in vernalization requirement between spring and winter wheat, but the genes controlling quantitative variation for more or less vernalization requirement among winter wheat cultivars remain unknown. We report here that the gene for the vernalization requirement duration in winter wheat was cloned using a BC1F2:3 population that segregated in a 3:1 ratio of early-flowering plants and late-flowering plants after vernalization for 3 weeks. The positional cloning of the gene for vernalization requirement duration demonstrated that this trait is controlled by TaVRN-A1 at the protein level. The Ala180 in vrn-A1a, encoded by the dominant allele for 3–week vernalization, was mutated to Val180 in vrn-A1b, encoded by the recessive allele for 6–week vernalization. Further studies with in vitro protein pull-down assays and immunoprecipitation analyses indicated that the mutated Val180 in vrn-A1b protein decreased the ability to bind with TaHOX1 (the first homeobox protein in Triticum aestivum). The direct binding of TaVRN-A1 and TaHOX1 proteins was confirmed in the nucleus of living plant cells by bimolecular fluorescence complementation (BiFC) analyses. The TaHOX1 gene was found to be upregulated by low temperatures, and to have a significant genetic effect on heading date, suggesting that TaHOX1 functions in the flowering pathway in winter wheat.

Yellow rust, also known as stripe rust, is caused by Puccinia striiformis Westend. f. sp. tritici Eriks (PST) and is one of the most common and persistent wheat (Triticum aestivum L.) diseases worldwide. A mapping population of recombinant inbred lines from the cross of ‘Jagger’ (moderately resistant) × ‘2174’ (moderately susceptible) was tested at three sites in Washington where predominant races PST‐114 and PST‐116 naturally occurred, at Rossville, KS, where PST‐100 was inoculated, and in Beijing, China, where a predominant Chinese stripe rust race CYR32 was inoculated on adult plants. A major quantitative trait locus for adult‐plant stripe rust resistance was located on the short arm of chromosome 2A (QYr.osu‐2A), where Jagger was found to carry markers for resistance gene Yr17 from Aegilops ventricosa Tausch (syn. Triticum ventricosum). Therefore, Yr17 is likely the resistance gene on chromosome 2A in Jagger. Markers for Yr17 were found to occur frequently in cultivars from the southern Great Plains but only occasionally in cultivars from other U.S. wheat regions. A novel resistance gene was mapped on the long arm of chromosome 5A (QYr.osu‐5A), for which the Jagger allele showed consistent resistance to multiple races of the stripe rust pathogen. A significant genetic effect of the resistance gene Lr34/Yr18 from 2174 was detected only when the population was tested with CYR32 in China.

Powdery mildew caused by Blumeria graminis f. sp. tritici is an important wheat disease in China and other parts of the world. Wild emmer (Triticum turgidum var. dicoccoides) is the immediate progenitor of cultivated tetraploid and hexaploid wheats and thus an important resource for wheat improvement. Wild emmer accession IW2 collected from Mount Hermon, Israel, is highly resistant to powdery mildew at the seedling and adult plant stages. Genetic analysis using an F(2) segregating population and F(2:3) families, derived from a cross between susceptible durum cultivar Langdon and wild emmer accession IW2, indicated that a single dominant gene was responsible for the resistance of IW2. Bulked segregant and molecular marker analyses detected that six polymorphic SSR, one ISBP, and three EST-STS markers on chromosome 3BL bin 0.63-1.00 were linked to the resistance gene. Allelic variations of resistance-linked EST-STS marker BE489472 revealed that the allele was present only in wild emmer but absent in common wheat. Segregation distortion was observed for the powdery mildew resistance allele and its linked SSR markers with preferential transmission of Langdon alleles over IW2 alleles. The resistance gene was introgressed into common wheat by backcrossing and marker-assisted selection. Since no designated powdery mildew resistance gene has been found on chromosome 3BL, the resistance gene derived from wild emmer accession IW2 appears to be new one and was consequently designated Pm41.

Leaf rust, caused by Puccinia triticina Eriks, is one of the most common and persistent wheat diseases in the US Great Plains. We report that the Lr34 gene was mapped in the center of a QTL for leaf rust reaction and explained 18-35% of the total phenotypic variation in disease severity of adult plants in a Jagger x 2174 population of recombinant inbred lines (RILs) field-tested for 3 years. The sequence of the complete Lr34 gene was determined for the susceptible Jagger allele and for the resistant 2174 allele. The two alleles had exactly the same sequence as the resistant allele reported previously in Chinese Spring at three polymorphic sites in intron 4, exon 11, and exon 12. A G/T polymorphism was found in exon 22, where a premature stop codon was found in the susceptible Jagger allele (Lr34E22s), confirming a previous report, due to a point mutation compared with the resistant 2174 allele (Lr34E22r). We have experimentally demonstrated a tight association between the point mutation at exon 22 of Lr34 and leaf rust susceptibility in a segregating biparental population. A PCR marker was developed to distinguish between the Lr34E22r and Lr34E22s alleles. A survey of 33 local hard winter wheat cultivars indicated that 7 cultivars carry the Lr34E22s allele and 26 cultivars carry the Lr34E22r allele. This study significantly improves our genetic understanding of allelic variation in the Lr34 gene and provides a functional molecular tool to improve leaf rust resistance in a major US wheat gene pool.