No abstract

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.

Aegilops markgrafii (Greuter) Hammer is an important source of genes for resistance to abiotic stresses and diseases in wheat (Triticum aestivum L.). A series of six wheat ‘Alcedo’-Ae. markgrafii chromosome disomic addition lines, designated as AI(B), AII(C), AIII(D), AV(E), AIV(F), and AVIII(G) carrying the Ae. markgrafii chromosomes B, C, D, E, F, and G, respectively, were tested with SSR markers to establish homoeologous relationships to wheat and identify markers useful in chromosome engineering. The addition lines were evaluated for resistance to rust and powdery mildew diseases. The parents Alcedo and Ae. markgrafii accession ‘S740-69’ were tested with 1500 SSR primer pairs and 935 polymorphic markers were identified. After selecting for robust markers and confirming the polymorphisms on the addition lines, 132 markers were considered useful for engineering and establishing homoeologous relationships. Based on the marker analysis, we concluded that the chromosomes B, C, D, E, F, and G belong to wheat homoeologous groups 2, 5, 6, 7, 3, and 4, respectively. Also, we observed chromosomal rearrangements in several addition lines. When tested with 20 isolates of powdery mildew pathogen (Blumeria graminis f. sp. tritici) from five geographic regions of the United States, four addition lines [AIII(D), AV(E), AIV(F), and AVIII(G)] showed resistance to some isolates, with addition line AV(E) being resistant to 19 of 20 isolates. The addition lines were tested with two races (TDBJ and TNBJ) of the leaf rust pathogen (Puccinia triticina), and only addition line AI(B) exhibited resistance at a level comparable to the Ae. markgrafii parent. Addition lines AII(C) and AIII(D) had been previously identified as resistant to the Ug99 race group of the stem rust pathogen (Puccinia graminis f. sp. tritici). The addition lines were also tested for resistance to six United States races (PSTv-4, PSTv-14, PSTv-37, PSTv-40, PSTv-51, and PSTv-198) of the stripe rust pathogen (Puccinia striiformis f. sp. tritici); we found no resistance either in Alcedo or any of the addition lines. The homoeologous relationships of the chromosomes in the addition lines, molecular markers located on each chromosome, and disease resistance associated with each chromosome will allow for chromosome engineering of the resistance genes.