Powdery mildew is a major fungal disease in wheat growing areas worldwide. A novel source of resistance to wheat powdery mildew present in the germplasm line NC97BGTD7 was genetically characterized as a monogenic trait in greenhouse and field trials using F(2) derived lines from a NC97BGTD7 X Saluda cross. Microsatellite markers were used to map and tag this resistance gene, now designated Pm34. Three co-dominant microsatellite markers linked to Pm34 were identified and their most likely order was established as: Xbarc177-5D, 5.4cM, Pm34, 2.6cM, Xbarc144-5D, 14cM, Xgwm272-5D. These microsatellite markers were previously mapped to the long arm of the 5D chromosome and their positions were confirmed using Chinese Spring nullitetrasomic Nulli5D-tetra5A and ditelosomic Dt5DL lines. Pm2, the only other known Pm gene on chromosome 5D, has been mapped to the short arm and its specificity is different from that of Pm34.

A single gene controlling powdery mildew resistance was identified in the North Carolina germplasm line NC96BGTD3 (NCD3) using genetic analysis of F(2) derived lines from a NCD3 X Saluda cross. Microsatellite markers linked to this Pm gene were identified and their most likely order was Xcfd7, 10.3 cM, Xgdm43, 8.6 cM, Xcfd26, 11.9 cM, Pm gene. These markers and the Pm gene were assigned to chromosome 5DL by means of Chinese Spring Nullitetrasomic (Nulli5D-tetra5A) and ditelosomic (Dt5DL) lines. A detached leaf test showed a distinctive disease reaction to six pathogen isolates among the NCD3 Pm gene, Pm2 (5DS) and Pm34 (5DL). An allelism test showed independence between Pm34 and the NCD3 Pm gene. Together, the tests provided strong evidence for the presence of a novel Pm gene in NCD3, and this gene was designated Pm35.

Soybean [Glycine max (L.) Merr.] oil typically contains 2-4% stearic acid. Seed oil with 20% stearic acid would be useful for solid fat applications, both for its cooking properties and health benefits. Breeding lines with high stearic acid have been developed, but many suffer from agronomic problems. This study identifies a new source of high stearic acid, determines its relationship with another high stearic locus and presents molecular markers for it is use in breeding. TCJWB03-806-7-19, a 'Holladay' mutant with high stearic acid, was crossed to two FAM94-41-derived lines that contained a point mutation in a seed-specific isoform of a Δ9-stearoyl-acyl carrier protein-desaturase (SACPD-C). Fatty acid analysis was performed over two growing seasons with F(2)-derived lines and transgressive segregation for stearic acid content was observed. Sequencing of SACPD isoforms in TCJWB03-806-7-19 revealed the deletion of an 'A' nucleotide in exon 3 of SACPD-B, which results in a protein whose final 28 amino acids are predicted to differ from Williams 82 SACPD-B. Sorting intolerant from tolerant (SIFT) analysis revealed that this frameshift mutation may affect SACPD-B protein function. Allele-specific genotyping for the SACPD-C point mutation and SACPD-B nucleotide deletion was performed in both populations. Additive effects and R(2) for stearic acid were +3.3 and 0.55 for SACPD-C and +1.9 and 0.19 for SACPD-B. Average stearic acid in lines homozygous for both mutations was 14.6%. This SACPD-B mutation represents a novel high stearic allele.

Key message fap1 mutation is caused by a G174A change in GmKASIIIA that disrupts a donor splice site recognition and creates a GATCTG motif that enhanced its expression. Abstract Soybean oil with reduced palmitic acid content is desirable to reduce the health risks associated with consumption of this fatty acid. The objectives of this study were: to identify the genomic location of the reduced palmitate fap1 mutation, determine its molecular basis, estimate the amount of phenotypic variation in fatty acid composition explained by this locus, determine if there are epistatic interactions between the fap1 and fap nc loci and, determine if the fap1 mutation has pleiotropic effects on seed yield, oil and protein content in three soybean populations. This study detected two major QTL for 16:0 content located in chromosome 5 (GmFATB1a, fap nc ) and chromosome 9 near BARCSOYSSR_09_1707 that explained, with their interaction, 66-94 % of the variation in 16:0 content in the three populations. Sequencing results of a putative candidate gene, GmKASIIIA, revealed a single unique polymorphism in the germplasm line C1726, which was predicted to disrupt the donor splice site recognition between exon one and intron one and produce a truncated KASIIIA protein. This G to A change also created the GATCTG motif that enhanced gene expression of the mutated GmKASIIIA gene. Lines homozygous for the GmKASIIIA mutation (fap1) had a significant reduction in 16:0, 18:0, and oil content; and an increase in unsaturated fatty acids content. There were significant epistatic interactions between GmKASIIIA (fap1) and fap nc for 16:0 and oil contents, and seed yield in two populations. In conclusion, the fap1 phenotype is caused by a single unique SNP in the GmKASIIIA gene.

The genetic effects of long‐term random mating and natural selection aided by genetic male sterility were evaluated in two soybean [Glycine max (L.) Merr.] populations designated RSII and RSIII. These populations were evaluated in the field at three locations, each with two replications. Genotypic and phenotypic correlations were estimated to determine the effects of 26 generations of random mating. Data was collected on flowering date (R2), maturity date (R8), plant height, lodging, yield, seed weight, protein concentration, and oil concentration. The genotypic correlation between yield and protein was not significant and small (<|0.2|) in both populations, however negative in RSII. The genotypic correlation between yield and oil was not significant but positive in both populations. In contrast, for both populations the genotypic correlations between protein and oil were significantly negative and large (>|0.5|). As these populations were randomly mated for many generations, linkage phase disequilibrium is likely close to zero; therefore, it was concluded that pleiotropic effects, probably caused by interrelated physiological processes, maintain the negative association between oil and protein. The genetic correlations between yield and protein or oil in these populations, however, do suggest that with the right breeding scheme, the negative associations can be reduced and allow for improvement in more than one trait simultaneously.

Powdery mildew of wheat (Triticum aestivum L.) is a major fungal disease caused by Blumeria graminis DC f. sp. tritici A microsatellite linkage map was developed for the T. monococcum‐derived powdery mildew resistant gene present in the North Carolina germplasm line NCBGT96A6 (NCA6). Genetic analysis of F2‐derived lines from the cross NCA6 × ‘Saluda’ indicated a single gene controlled powdery mildew resistance. Four microsatellite markers linked to the NCA6 Pm gene mapped to chromosome 7AL. The most likely order was Xcfa2123‐0.9 cM–Xbarc121‐1.7 cM resistance gene/Xcfa2019‐3.0 cM‐Xgwm332 A detached‐leaf test indicated the disease reaction response of the NCA6 Pm gene was different from the five known alleles at the Pm1 locus on 7AL. Deletion interval mapping showed a large physical to genetic distance ratio for these microsatellite marker loci. This may be due to suppressed recombination between the introgressed T. monococcum segment and the homologous region of the T. aestivum cultivar Saluda. Our results suggested that the NCA6 Pm gene is likely a novel source of resistance to powdery mildew but additional allelism studies are needed to establish the relationship between this locus and the other known Pm loci on 7AL.

The genetic effects of long‐term random mating and natural selection aided by genetic male sterility were evaluated in two soybean [Glycine max (L.) Merr.] populations: RSII and RSIII. Population means, variances, and heritabilities were estimated to determine the effects of 26 generations of random mating. The 10% highest yielding lines from each population were selected. Data was collected on flowering date, maturity date, plant height, lodging score, seed yield, seed weight, protein concentration (PC), and oil concentration (OC). RSII had a mean seed yield, PC, and OC of 2163 kg ha−1, 416 g kg−1, and 193 g kg−1, respectively. Entry‐mean heritability for seed yield, PC, and OC was estimated at 36, 68, and 57%, respectively. Theoretical response to selection was 183 kg ha−1 and, after selection, the realized gain was 161 kg ha−1. RSIII had a mean seed yield, PC, and OC of 2300 kg ha−1, 416 g kg−1, and 190 g kg−1, respectively. The entry‐mean heritability estimates for seed yield, PC, and OC were 57, 87, and 91%, respectively. Theoretical response to selection was 300 kg ha−1 and, after selection, realized gain was an increase of 139 kg ha−1. Despite not reaching their theoretical yield potential, the best lines from both populations compared well to check cultivars. The significant genetic variances and heritabilities observed demonstrate that the breakage of linkage blocks by long‐term random mating and natural selection were effective in producing competitive lines.

Two new sources of elevated seed stearic acid were identified and the feasibility of an elevated stearic acid, high oleic acid germplasm was studied. Soybean [Glycine max (L.) Merr.] oil typically contains 2-4% stearic acid. Oil with at least 20% stearic acid is desirable because of its improved baking properties and health profile. This study identifies two new sources of high stearic acid and evaluates the interaction of high stearic and oleic acid alleles. TCHM08-1087 and TCHM08-755, high stearic acid 'Holladay' mutants, were crossed to FAM94-41-3, a line containing a point mutation in a seed-specific isoform of a Δ9-stearoyl-acyl carrier protein-desaturase (SACPD-C). F2-derived lines were evaluated for fatty acid content in four field environments. Sequencing of SACPDs in TCHM08-1087 and TCHM08-755 revealed distinct deletions of at least one megabase encompassing SACPD-C in both lines. After genotyping, the additive effect for stearic acid was estimated at +1.8% for the SACPD-C point mutation and +4.1% for the SACPD-C deletions. Average stearic acid in lines homozygous for the deletions was 12.2%. A FAM94-41-3-derived line and TCHM08-1087-11, a selection from TCHM08-1087, were crossed to S09-2902-145, a line containing missense mutations in two fatty acid desaturases (FAD2-1A and FAD2-1B). F1 plants were grown in a greenhouse and individual F2 seed were genotyped and phenotyped. No interaction was observed between either FAD2-1A or FAD2-1B and any of the SACPD-C mutant alleles. Seed homozygous mutant for SACPD-C/FAD2-1A/FAD2-1B contained 12.7% stearic acid and 65.5% oleic acid while seed homozygous for the SACPD-C deletion and mutant for FAD2-1A and FAD2-1B averaged 10.4% stearic acid and 75.9% oleic acid.