High fat intake sustains sorbitol intolerance after antibiotic-mediated Clostridia depletion from the gut microbiota.

Carbohydrate intolerance, commonly linked to the consumption of lactose, fructose, or sorbitol, affects up to 30% of the population in high-income countries. Although sorbitol intolerance is attributed to malabsorption, the underlying mechanism remains unresolved. Here, we show that a history of antibiotic exposure combined with high fat intake triggered long-lasting sorbitol intolerance in mice by reducing Clostridia abundance, which impaired microbial sorbitol catabolism. The restoration of sorbitol catabolism by inoculation with probiotic Escherichia coli protected mice against sorbitol intolerance but did not restore Clostridia abundance. Inoculation with the butyrate producer Anaerostipes caccae restored a normal Clostridia abundance, which protected mice against sorbitol-induced diarrhea even when the probiotic was cleared. Butyrate restored Clostridia abundance by stimulating epithelial peroxisome proliferator-activated receptor-gamma (PPAR-γ) signaling to restore epithelial hypoxia in the colon. Collectively, these mechanistic insights identify microbial sorbitol catabolism as a potential target for approaches for the diagnosis, treatment, and prevention of sorbitol intolerance.

Serum Amyloid A Proteins Induce Pathogenic Th17 Cells and Promote Inflammatory Disease.

Lymphoid cells that produce interleukin (IL)-17 cytokines protect barrier tissues from pathogenic microbes but are also prominent effectors of inflammation and autoimmune disease. T helper 17 (Th17) cells, defined by RORγt-dependent production of IL-17A and IL-17F, exert homeostatic functions in the gut upon microbiota-directed differentiation from naive CD4+ T cells. In the non-pathogenic setting, their cytokine production is regulated by serum amyloid A proteins (SAA1 and SAA2) secreted by adjacent intestinal epithelial cells. However, Th17 cell behaviors vary markedly according to their environment. Here, we show that SAAs additionally direct a pathogenic pro-inflammatory Th17 cell differentiation program, acting directly on T cells in collaboration with STAT3-activating cytokines. Using loss- and gain-of-function mouse models, we show that SAA1, SAA2, and SAA3 have distinct systemic and local functions in promoting Th17-mediated inflammatory diseases. These studies suggest that T cell signaling pathways modulated by the SAAs may be attractive targets for anti-inflammatory therapies.

Feeding-dependent VIP neuron-ILC3 circuit regulates the intestinal barrier.

The intestinal mucosa serves both as a conduit for the uptake of food-derived nutrients and microbiome-derived metabolites, and as a barrier that prevents tissue invasion by microorganisms and tempers inflammatory responses to the myriad contents of the lumen. How the intestine coordinates physiological and immune responses to food consumption to optimize nutrient uptake while maintaining barrier functions remains unclear. Here we show in mice how a gut neuronal signal triggered by food intake is integrated with intestinal antimicrobial and metabolic responses that are controlled by type-3 innate lymphoid cells (ILC3)1-3. Food consumption rapidly activates a population of enteric neurons that express vasoactive intestinal peptide (VIP)4. Projections of VIP-producing neurons (VIPergic neurons) in the lamina propria are in close proximity to clusters of ILC3 that selectively express VIP receptor type 2 (VIPR2; also known as VPAC2). Production of interleukin (IL)-22 by ILC3, which is upregulated by the presence of commensal microorganisms such as segmented filamentous bacteria5-7, is inhibited upon engagement of VIPR2. As a consequence, levels of antimicrobial peptide derived from epithelial cells are reduced but the expression of lipid-binding proteins and transporters is increased8. During food consumption, the activation of VIPergic neurons thus enhances the growth of segmented filamentous bacteria associated with the epithelium, and increases lipid absorption. Our results reveal a feeding- and circadian-regulated dynamic neuroimmune circuit in the intestine that promotes a trade-off between innate immune protection mediated by IL-22 and the efficiency of nutrient absorption. Modulation of this pathway may therefore be effective for enhancing resistance to enteropathogens2,3,9 and for the treatment of metabolic diseases.

Wild grass-derived alleles represent a genetic architecture for the resilience of modern common wheat to stresses.

This review explores the integration of wild grass-derived alleles into modern bread wheat breeding to tackle the challenges of climate change and increasing food demand. With a focus on synthetic hexaploid wheat, this review highlights the potential of genetic variability in wheat wild relatives, particularly Aegilops tauschii, for improving resilience to multifactorial stresses like drought, heat, and salinity. The evolutionary journey of wheat (Triticum spp.) from diploid to hexaploid species is examined, revealing significant genetic contributions from wild grasses. We also emphasize the importance of understanding incomplete lineage sorting in the genomic evolution of wheat. Grasping this information is crucial as it can guide breeders in selecting the appropriate alleles from the gene pool of wild relatives to incorporate into modern wheat varieties. This approach improves the precision of phylogenetic relationships and increases the overall effectiveness of breeding strategies. This review also addresses the challenges in utilizing the wheat wild genetic resources, such as the linkage drag and cross-compatibility issues. Finally, we culminate the review with future perspectives, advocating for a combined approach of high-throughput phenotyping tools and advanced genomic techniques to comprehensively understand the genetic and regulatory architectures of wheat under stress conditions, paving the way for more precise and efficient breeding strategies.

Kismet/CHD7/CHD8 affects gut microbiota, mechanics, and the gut-brain axis in Drosophila melanogaster.

The gut microbiome affects brain and neuronal development and may contribute to the pathophysiology of neurodevelopmental disorders. However, it is unclear how risk genes associated with such disorders affect gut physiology in a manner that could impact microbial colonization and how the mechanical properties of the gut tissue might play a role in gut-brain bidirectional communication. To address this, we used Drosophila melanogaster with a null mutation in the gene kismet, an ortholog of chromodomain helicase DNA-binding protein (CHD) family members CHD7 and CHD8. In humans, these are risk genes for neurodevelopmental disorders with co-occurring gastrointestinal symptoms. We found that kismet mutant flies have a significant increase in gastrointestinal transit time, indicating the functional homology of kismet with CHD7/CHD8 in vertebrates. Rheological characterization of dissected gut tissue revealed significant changes in the mechanics of kismet mutant gut elasticity, strain stiffening behavior, and tensile strength. Using 16S rRNA metagenomic sequencing, we also found that kismet mutants have reduced diversity and abundance of gut microbiota at every taxonomic level. To investigate the connection between the gut microbiome and behavior, we depleted gut microbiota in kismet mutant and control flies and quantified the flies' courtship behavior. Depletion of gut microbiota rescued courtship defects of kismet mutant flies, indicating a connection between gut microbiota and behavior. In striking contrast, depletion of the gut microbiome in the control strain reduced courtship activity, demonstrating that antibiotic treatment can have differential impacts on behavior and may depend on the status of microbial dysbiosis in the gut prior to depletion. We propose that Kismet influences multiple gastrointestinal phenotypes that contribute to the gut-microbiome-brain axis to influence behavior. We also suggest that gut tissue mechanics should be considered as an element in the gut-brain communication loop, both influenced by and potentially influencing the gut microbiome and neurodevelopment.

A novel natural variation in the promoter of GmCHX1 regulates conditional gene expression to improve salt tolerance in soybean.

Identification and characterization of soybean germplasm and gene(s)/allele(s) for salt tolerance is an effective way to develop improved varieties for saline soils. Previous studies identified GmCHX1 (Glyma03g32900) as a major salt tolerance gene in soybean, and two main functional variations were found in the promoter region (148/150 bp insertion) and the third exon with a retrotransposon insertion (3.78 kb). In the current study, we identified four salt-tolerant soybean lines, including PI 483460B (Glycine soja), carrying the previously identified salt-sensitive variations at GmCHX1, suggesting new gene(s) or new functional allele(s) of GmCHX1 in these soybean lines. Subsequently, we conducted quantitative trait locus (QTL) mapping in a recombinant-inbred line population (Williams 82 (salt-sensitive) × PI 483460B) to identify the new salt tolerance loci/alleles. A new locus, qSalt_Gm18, was mapped on chromosome 18 associated with leaf scorch score. Another major QTL, qSalt_Gm03, was identified to be associated with chlorophyll content ratio and leaf scorch score in the same chromosomal region of GmCHX1 on chromosome 3. Novel variations in a STRE (stress response element) cis-element in the promoter region of GmCHX1 were found to regulate the salt-inducible expression of the gene in these four newly identified salt-tolerant lines including PI 483460B. This new allele of GmCHX1 with salt-inducible expression pattern provides an energy cost efficient (conditional gene expression) strategy to protect soybean yield in saline soils without yield penalty under non-stress conditions. Our results suggest that there might be no other major salt tolerance locus similar to GmCHX1 in soybean germplasm, and further improvement of salt tolerance in soybean may rely on gene-editing techniques instead of looking for natural variations.

Clinical characteristics of infantile hemangiomas with aggressive, persistent, and destructive ulceration.

BACKGROUND/OBJECTIVES: Ulceration is a common complication of infantile hemangioma (IH). Severe, persistent ulceration occurs in a minority of patients. This study aims to characterize the clinical features of IH with aggressive ulceration (AU). METHODS: Multicenter retrospective study of clinical features of IH with AU. RESULTS: Thirty-five patients with AU were identified and included in the study. The majority of AU occurred in segmental IH (23/35, 65%). Segmental IH with AU were large (≥10 cm2 ; 16/23, 69%, p < .001) with a thin (<3 mm) superficial component (16/23, 69%, p < .001). Localized IH with AU had a thick (>3 mm) superficial component (11/12, 92%, p < .001). All diaper area IH with AU (9/35) were segmental with thin superficial component (100%, p = .02). IH with AU in the head/neck (10/35) were more commonly localized (67%) and mixed (62.5%), while segmental, thick superficial morphology was more common on trunk (9/35) and upper extremities (7/35). CONCLUSIONS: IH resulting in AU differ in clinical features by anatomic site. Those in the diaper area are nearly always segmental with thin superficial component, whereas other sites tend to be localized, mixed, with thick superficial component. These distinct phenotypes may prove useful in the clinical setting for physicians to identify patterns of IH ulceration with increased risk of aggressive, persistent ulceration.

Oxidative Mechanisms and Cardiovascular Abnormalities of Cirrhosis and Portal Hypertension.

In patients with portal hypertension, there are many complications including cardiovascular abnormalities, hepatorenal syndrome, ascites, variceal bleeding, and hepatic encephalopathy. The underlying mechanisms are not yet completely clarified. It is well known that portal hypertension causes mesenteric congestion which produces reactive oxygen species (ROS). ROS has been associated with intestinal mucosal injury, increased intestinal permeability, enhanced gut bacterial overgrowth, and translocation; all these changes result in increased endotoxin and inflammation. Portal hypertension also results in the development of collateral circulation and reduces liver mass resulting in an overall increase in endotoxin/bacteria bypassing detoxication and immune clearance in the liver. Endotoxemia can in turn aggravate oxidative stress and inflammation, leading to a cycle of gut barrier dysfunction → endotoxemia → organ injury. The phenotype of cardiovascular abnormalities includes hyperdynamic circulation and cirrhotic cardiomyopathy. Oxidative stress is often accompanied by inflammation; thus, blocking oxidative stress can minimize the systemic inflammatory response and alleviate the severity of cardiovascular diseases. The present review aims to elucidate the role of oxidative stress in cirrhosis-associated cardiovascular abnormalities and discusses possible therapeutic effects of antioxidants on cardiovascular complications of cirrhosis including hyperdynamic circulation, cirrhotic cardiomyopathy, and hepatorenal syndrome.

The Late Embryogenesis Abundant Proteins in Soybean: Identification, Expression Analysis, and the Roles of GmLEA4_19 in Drought Stress.

Late embryogenesis abundant (LEA) proteins play important roles in regulating plant growth and responses to various abiotic stresses. In this research, a genome-wide survey was conducted to recognize the LEA genes in Glycine max. A total of 74 GmLEA was identified and classified into nine subfamilies based on their conserved domains and the phylogenetic analysis. Subcellular localization, the duplication of genes, gene structure, the conserved motif, and the prediction of cis-regulatory elements and tissue expression pattern were then conducted to characterize GmLEAs. The expression profile analysis indicated that the expression of several GmLEAs was a response to drought and salt stress. The co-expression-based gene network analysis suggested that soybean LEA proteins may exert regulatory effects through the metabolic pathways. We further explored GnLEA4_19 function in Arabidopsis and the results suggests that overexpressed GmLEA4_19 in Arabidopsis increased plant height under mild or serious drought stress. Moreover, the overexpressed GmLEA4_19 soybean also showed a drought tolerance phenotype. These results indicated that GmLEA4_19 plays an important role in the tolerance to drought and will contribute to the development of the soybean transgenic with enhanced drought tolerance and better yield. Taken together, this study provided insight for better understanding the biological roles of LEA genes in soybean.

Machine learning models outperform deep learning models, provide interpretation and facilitate feature selection for soybean trait prediction.

Recent growth in crop genomic and trait data have opened opportunities for the application of novel approaches to accelerate crop improvement. Machine learning and deep learning are at the forefront of prediction-based data analysis. However, few approaches for genotype to phenotype prediction compare machine learning with deep learning and further interpret the models that support the predictions. This study uses genome wide molecular markers and traits across 1110 soybean individuals to develop accurate prediction models. For 13/14 sets of predictions, XGBoost or random forest outperformed deep learning models in prediction performance. Top ranked SNPs by F-score were identified from XGBoost, and with further investigation found overlap with significantly associated loci identified from GWAS and previous literature. Feature importance rankings were used to reduce marker input by up to 90%, and subsequent models maintained or improved their prediction performance. These findings support interpretable machine learning as an approach for genomic based prediction of traits in soybean and other crops.

Haplotype mapping uncovers unexplored variation in wild and domesticated soybean at the major protein locus cqProt-003.

KEY MESSAGE: The major soy protein QTL, cqProt-003, was analysed for haplotype diversity and global distribution, and results indicate 304 bp deletion and variable tandem repeats in protein coding regions are likely causal candidates. Here, we present association and linkage analysis of 985 wild, landrace and cultivar soybean accessions in a pan genomic dataset to characterize the major high-protein/low-oil associated locus cqProt-003 located on chromosome 20. A significant trait-associated region within a 173 kb linkage block was identified, and variants in the region were characterized, identifying 34 high confidence SNPs, 4 insertions, 1 deletion and a larger 304 bp structural variant in the high-protein haplotype. Trinucleotide tandem repeats of variable length present in the second exon of gene Glyma.20G085100 are strongly correlated with the high-protein phenotype and likely represent causal variation. Structural variation has previously been found in the same gene, for which we report the global distribution of the 304 bp deletion and have identified additional nested variation present in high-protein individuals. Mapping variation at the cqProt-003 locus across demographic groups suggests that the high-protein haplotype is common in wild accessions (94.7%), rare in landraces (10.6%) and near absent in cultivated breeding pools (4.1%), suggesting its decrease in frequency primarily correlates with domestication and continued during subsequent improvement. However, the variation that has persisted in under-utilized wild and landrace populations holds high breeding potential for breeders willing to forego seed oil to maximize protein content. The results of this study include the identification of distinct haplotype structures within the high-protein population, and a broad characterization of the genomic context and linkage patterns of cqProt-003 across global populations, supporting future functional characterization and modification.

Breeding for disease resistance in soybean: a global perspective.

KEY MESSAGE: This review provides a comprehensive atlas of QTLs, genes, and alleles conferring resistance to 28 important diseases in all major soybean production regions in the world. Breeding disease-resistant soybean [Glycine max (L.) Merr.] varieties is a common goal for soybean breeding programs to ensure the sustainability and growth of soybean production worldwide. However, due to global climate change, soybean breeders are facing strong challenges to defeat diseases. Marker-assisted selection and genomic selection have been demonstrated to be successful methods in quickly integrating vertical resistance or horizontal resistance into improved soybean varieties, where vertical resistance refers to R genes and major effect QTLs, and horizontal resistance is a combination of major and minor effect genes or QTLs. This review summarized more than 800 resistant loci/alleles and their tightly linked markers for 28 soybean diseases worldwide, caused by nematodes, oomycetes, fungi, bacteria, and viruses. The major breakthroughs in the discovery of disease resistance gene atlas of soybean were also emphasized which include: (1) identification and characterization of vertical resistance genes reside rhg1 and Rhg4 for soybean cyst nematode, and exploration of the underlying regulation mechanisms through copy number variation and (2) map-based cloning and characterization of Rps11 conferring resistance to 80% isolates of Phytophthora sojae across the USA. In this review, we also highlight the validated QTLs in overlapping genomic regions from at least two studies and applied a consistent naming nomenclature for these QTLs. Our review provides a comprehensive summary of important resistant genes/QTLs and can be used as a toolbox for soybean improvement. Finally, the summarized genetic knowledge sheds light on future directions of accelerated soybean breeding and translational genomics studies.

Differentially reset transcriptomes and genome bias response orchestrate wheat response to phosphate deficiency.

Phosphorus (P) is an essential macronutrient for all organisms. Phosphate (Pi) deficiency reduces grain yield and quality in wheat. Understanding how wheat responds to Pi deficiency at the global transcriptional level remains limited. We revisited the available RNA-seq transcriptome from Pi-starved wheat roots and shoots subjected to Pi starvation. Genome-wide transcriptome resetting was observed under Pi starvation, with a total of 917 and 2338 genes being differentially expressed in roots and shoots, respectively. Chromosomal distribution analysis of the gene triplets and differentially expressed genes (DEGs) revealed that the D genome displayed genome induction bias and, specifically, the chromosome 2D might be a key contributor to Pi-limiting triggered gene expression response. Alterations in multiple metabolic pathways pertaining to secondary metabolites, transcription factors and Pi uptake-related genes were evidenced. This study provides genomic insight and the dynamic landscape of the transcriptional changes contributing to the hexaploid wheat during Pi starvation. The outcomes of this study and the follow-up experiments have the potential to assist the development of Pi-efficient wheat cultivars.

Classification Methods and Identification of Reniform Nematode Resistance in Known Soybean Cyst Nematode-Resistant Soybean Genotypes.

Plant parasitic nematodes are a major yield-limiting factor of soybean in the United States and Canada. It has been indicated that soybean cyst nematode (SCN; Heterodera glycines Ichinohe) and reniform nematode (RN; Rotylenchulus reniformis Linford and Oliveira) resistance could be genetically related. For many years, fragmentary data have shown this relationship. This report evaluates RN reproduction on 418 plant introductions (PIs) selected from the U.S. Department of Agriculture Soybean Germplasm Collection with reported SCN resistance. The germplasm was divided into two tests of 214 PIs reported as resistant and 204 PIs reported as moderately resistant to SCN. The defining and reporting of RN resistance changed several times in the last 30 years, causing inconsistencies in RN resistance classification among multiple experiments. Comparison of four RN resistance classification methods was performed: (i) ≤10% as compared with the susceptible check, (ii) using normalized reproduction index (RI) values, and using (iii) transformed data log10(x), and (iv) transformed data log10(x + 1) in an optimal univariate k-means clustering analysis. The method of transformed data log10(x) was selected as the most accurate for classification of RN resistance. Among 418 PIs with reported SCN resistance, the log10(x) method grouped 59 PIs (15%) as resistant and 130 PIs (31%) as moderately resistant to RN. Genotyping of a subset of the most resistant PIs to both nematode species revealed their strong correlation with rhg1-a allele. This research identified genotypes with resistance to two nematode species and potential new sources of RN resistance that could be valuable to breeders in developing resistant cultivars.

Large-scale analysis reveals spatiotemporal circadian patterns of cilia transcriptomes in the primate brain.

Cilia are dynamic subcellular systems, with core structural and functional components operating in a highly coordinated manner. Since many environmental stimuli sensed by cilia are circadian in nature, it is reasonable to speculate that genes encoding cilia structural and functional components follow rhythmic circadian patterns of expression. Using computational methods and the largest spatiotemporal gene expression atlas of primates, we identified and analyzed the circadian rhythmic expression of cilia genes across 22 primate brain areas. We found that around 73% of cilia transcripts exhibited circadian rhythmicity across at least one of 22 brain regions. In 12 brain regions, cilia transcriptomes were significantly enriched with circadian oscillating transcripts, as compared to the rest of the transcriptome. The phase of the cilia circadian transcripts deviated from the phase of the majority of the background circadian transcripts, and transcripts coding for cilia basal body components accounted for the majority of cilia circadian transcripts. In addition, adjacent or functionally connected brain nuclei had large overlapping complements of circadian cilia genes. Most remarkably, cilia circadian transcripts shared across the basal ganglia nuclei and the prefrontal cortex peaked in these structures in sequential fashion that is similar to the sequential order of activation of the basal ganglia-cortical circuitry in connection with movement coordination, albeit on completely different timescales. These findings support a role for the circadian spatiotemporal orchestration of cilia gene expression in the normal physiology of the basal ganglia-cortical circuit and motor control. Studying orchestrated cilia rhythmicity in the basal ganglia-cortical circuits and other brain circuits may help develop better functional models, and shed light on the causal effects cilia functions have on these circuits and on the regulation of movement and other behaviors.

Soybean (Glycine max) Haplotype Map (GmHapMap): a universal resource for soybean translational and functional genomics.

Here, we describe a worldwide haplotype map for soybean (GmHapMap) constructed using whole-genome sequence data for 1007 Glycine max accessions and yielding 14.9 million variants as well as 4.3 M tag single-nucleotide polymorphisms (SNPs). When sampling random subsets of these accessions, the number of variants and tag SNPs plateaued beyond approximately 800 and 600 accessions, respectively. This suggests extensive coverage of diversity within the cultivated soybean. GmHapMap variants were imputed onto 21 618 previously genotyped accessions with up to 96% success for common alleles. A local association analysis was performed with the imputed data using markers located in a 1-Mb region known to contribute to seed oil content and enabled us to identify a candidate causal SNP residing in the NPC1 gene. We determined gene-centric haplotypes (407 867 GCHs) for the 55 589 genes and showed that such haplotypes can help to identify alleles that differ in the resulting phenotype. Finally, we predicted 18 031 putative loss-of-function (LOF) mutations in 10 662 genes and illustrated how such a resource can be used to explore gene function. The GmHapMap provides a unique worldwide resource for applied soybean genomics and breeding.

Interferon γ neutralization reduces blood pressure, uterine artery resistance index, and placental oxidative stress in placental ischemic rats.

Preeclampsia (PE) is characterized by maternal hypertension, intrauterine growth restriction, and increased cytolytic natural killer cells (cNKs), which secrete interferon γ (IFNγ). However, the precise role of IFNγ in contributing to PE pathophysiology remains unclear. Using the reduced uterine perfusion pressure (RUPP) rat model of placental ischemia, we tested the hypothesis that neutralization of IFNγ in RUPPs will decrease placental reactive oxygen species (ROS) and improve vascular function resulting in decreased MAP and improved fetal growth. On gestation day (GD) 14, the RUPP procedure was performed and on GDs 15 and 18, a subset of normal pregnant rats (NP) and RUPP rats were injected with 10 µg/kg of an anti-rat IFNγ monoclonal antibody. On GD 18, uterine artery resistance index (UARI) was measured via Doppler ultrasound and on GD 19, mean arterial pressure (MAP) was measured, animals were euthanized, and blood and tissues were collected for analysis. Increased MAP was observed in RUPP rats compared with NP and was reduced in RUPP + anti-IFNγ. Placental ROS was also increased in RUPP rats compared with NP rats and was normalized in RUPP + anti-IFNγ. Fetal and placental weights were reduced in RUPP rats, but were not improved following anti-IFNγ treatment. However, UARI was elevated in RUPP compared with NP rats and was reduced in RUPP + anti-IFNγ. In conclusion, we observed that IFNγ neutralization reduced MAP, UARI, and placental ROS in RUPP recipients. These data suggest that IFNγ is a potential mechanism by which cNKs contribute to PE pathophysiology and may represent a therapeutic target to improve maternal outcomes in PE.

Identification and characterization of novel QTL conferring internal detoxification of aluminium in soybean.

Aluminium (Al) toxicity inhibits soybean root growth, leading to insufficient water and nutrient uptake. Two soybean lines ('Magellan' and PI 567731) were identified differing in Al tolerance, as determined by primary root length ratio, total root length ratio, and root tip number ratio under Al stress. Serious root necrosis was observed in PI 567731, but not in Magellan under Al stress. An F8 recombinant inbred line population derived from a cross between Magellan and PI 567731 was used to map the quantitative trait loci (QTL) for Al tolerance. Three QTL on chromosomes 3, 13, and 20, with tolerant alleles from Magellan, were identified. qAl_Gm13 and qAl_Gm20 explained large phenotypic variations (13-27%) and helped maintain root elongation and initiation under Al stress. In addition, qAl_Gm13 and qAl_Gm20 were confirmed in near-isogenic backgrounds and were identified to epistatically regulate Al tolerance via internal detoxification instead of Al3+ exclusion. Phylogenetic and pedigree analysis identified the tolerant alleles of both loci derived from the US ancestral line, A.K.[FC30761], originally from China. Our results provide novel genetic resources for breeding Al-tolerant soybean and suggest that internal detoxification contributes to soybean tolerance to excessive soil Al.

Genetic characterization of qSCN10 from an exotic soybean accession PI 567516C reveals a novel source conferring broad-spectrum resistance to soybean cyst nematode.

KEY MESSAGE: The qSCN10 locus with broad-spectrum SCN resistance was fine-mapped to a 379-kb region on chromosome 10 in soybean accession PI 567516C. Candidate genes and potential application benefits of this locus were discussed. Soybean cyst nematode (SCN, Heterodera glycines Ichinohe) is one of the most devastating pests of soybean, causing significant yield losses worldwide every year. Genetic resistance has been the major strategy to control this pest. However, the overuse of the same genetic resistance derived primarily from PI 88788 has led to the genetic shifts in nematode populations and resulted in the reduced effectiveness in soybean resistance to SCN. Therefore, novel genetic resistance resources, especially those with broad-spectrum resistance, are needed to develop new resistant cultivars to cope with the genetic shifts in nematode populations. In this study, a quantitative trait locus (QTL) qSCN10 previously identified from a soybean landrace PI 567516C was confirmed to confer resistance to multiple SCN HG Types. This QTL was further fine-mapped to a 379-kb region. There are 51 genes in this region. Four of them are defense-related and were regulated by SCN infection, suggesting their potential role in mediating resistance to SCN. The phylogenetic and haplotype analyses of qSCN10 as well as other information indicate that this locus is different from other reported resistance QTL or genes. There was no yield drag or other unfavorable traits associated with this QTL when near-isogenic lines with and without qSCN10 were tested in a SCN-free field. Therefore, our study not only provides further insight into the genetic basis of soybean resistance to SCN, but also identifies a novel genetic resistance resource for breeding soybean for durable, broad-spectrum resistance to this pest.