Glufosinate resistance in Palmer amaranth (Amaranthus palmeri S. Watson) was recently detected in three accessions from Arkansas, USA. Amaranthus palmeri is the first and only broadleaf weed species resistant to this herbicide, and the resistance mechanism is still unclear. A previous study characterized the glufosinate resistance level in the accessions from Arkansas. A highly glufosinate-resistant accession was further used to investigate the mechanism conferring glufosinate resistance in A. palmeri. Experiments were designed to sequence the herbicide target enzyme cytosolic and chloroplastic glutamine synthetase isoforms (GS1 and GS2, respectively) and quantify copy number and expression. Absorption, translocation, and metabolism of glufosinate using the 14C-labeled herbicide were also evaluated in the resistant and susceptible accessions. The glufosinate-resistant accession had an increase in copy number and expression of GS2 compared with susceptible plants. All accessions showed only one GS1 copy and no differences in expression. No mutations were identified in GS1 or GS2. Absorption (54% to 60%) and metabolism (13% to 21%) were not different between the glufosinate-resistant and glufosinate-susceptible accessions. Most residues of glufosinate (94% to 98%) were present in the treated leaf. Glufosinate translocation to tissues above the treated leaf and in the roots was not different among accessions. However, glufosinate translocation to tissues below the treated leaf (not including roots) was greater in the resistant A. palmeri (2%) compared with the susceptible (less than 1%) accessions. The findings of this paper strongly indicate that gene amplification and increased expression of the chloroplastic glutamine synthetase enzyme are the mechanisms conferring glufosinate resistance in the A. palmeri accession investigated. Thus far, no additional resistance mechanism was observed, but further investigations are ongoing.
Fine mapping and functional validation of the Ligon lintless-2 (Li2) fiber mutant elucidates the genetics and development of one of the longest single-celled fi
Soybean is a globally significant legume crop, providing essential protein and oil for human and livestock nutrition. Improving oil and protein content simultaneously without compromising yield has been challenging due to the quantitative nature of these traits and their interrelationships. This study aims to deepen our understanding of the molecular basis soybean of seed weight, protein, and oil content to facilitate marker-assisted breeding to enhance these traits. In this research, a Genome-Wide Association Study (GWAS) was conducted utilizing 285 diverse soybean accessions from maturity group V, employing genotyping through the SoySNP50K platform. These accessions were tested in three environmental conditions of the southeast US for three traits: 100-seed weight, protein, and oil content. The study identified 18, 23, and 26 SNPs significantly associated with 100-seed weight, seed oil, and protein content. Colocalized protein and oil content regions were discovered on chromosomes 15, 16, and 20. Chromosomes 15 and 20 are well documented to have pleiotropic but opposite effects on oil and protein content, but both regions contain genes that affect individual traits, such as FAD2-1 and nodulin MtN21. A 1.92 Mb region on chromosome 11 exhibits a target region to improve oil and seed weight without affecting protein content. This study highlights key genomic regions and candidate genes influencing seed weight, protein, and oil content, with some regions affecting multiple traits. Hence, these findings provide a valuable foundation for marker-assisted selection to optimize seed weight and simultaneously enhance oil and protein content in soybean breeding programs.
Traits such as seed weight, shelling percent, percent sound mature kernels, and seed dormancy determines the quality of peanut seed. Few QTL (quantitative trait loci) studies using biparental mapping populations have identified QTL for seed dormancy and seed grade traits. Here, we report a genome-wide association study (GWAS) to detect marker–trait associations for seed germination, dormancy, and seed grading traits in peanut. A total of 120 accessions from the U.S. peanut mini-core collection were evaluated for seed quality traits and genotyped using Axiom SNP (single nucleotide polymorphism) array for peanut. We observed significant variation in seed quality traits in different accessions and different botanical varieties. Through GWAS, we were able to identify multiple regions associated with sound mature kernels, seed weight, shelling percent, seed germination, and dormancy. Some of the genomic regions that were SNP associated with these traits aligned with previously known QTLs. For instance, QTL for seed dormancy has been reported on chromosome A05, and we also found SNP on the same chromosome associated with seed dormancy, explaining around 20% of phenotypic variation. In addition, we found novel genomic regions associated with seed grading, seed germination, and dormancy traits. SNP markers associated with seed quality and dormancy identified here can accelerate the selection process. Further, exploring the function of candidate genes identified in the vicinity of the associated marker will assist in understanding the complex genetic network that governs seed quality.
Poa annua L. (annual bluegrass) is a common weed in turfgrass and has been reported resistant to 12 different herbicide sites of action, with various combinations of multiple‐herbicide resistance having been identified. To quantify the extent of herbicide‐resistant P. annua, the ResistPoa Project (resistpoa.org) surveyed 1349 P. annua populations for resistance to nine sites of action and one plant growth retardant. Herein, we report results from sequencing of known target site mutations found in 5‐enolpyruvylshikimate‐3 phosphate synthase (EPSPS), acetolactate synthase (ALS), photosystem II protein D (psbA), and 𝛼‐tubulin genes. Populations were sequenced using either capillary or amplicon sequencing (AmpSeq), depending on the complexity of the gene, and were analyzed for target‐site resistance. After additional resistance screening, a total of 389 suspected resistant populations were sequenced—131 for ALS, 83 for EPSPS, 93 for psbA, and 82 for 𝛼‐tubulin. From the resistant populations, 64 displayed resistance to multiple sites of action. After sequencing, it was determined that target‐site resistance was the common form of resistance for all sites of action outside of psbA with 65.6% of ALS populations, 73.5% of EPSPS, 39.8% of psbA, and 91.5% of 𝛼‐tubulin having presented a target‐site mutation.