Biology subjects

Xu, Y.

Publications and source records attributed to Xu, Y..

At least 271 records · Page 15Linked to original sources

bioRxiv2025

The biomolecular profiles of extracellular vesicles from odontogenic stem cell lines depict donor-dependent differences and emphasize their therapeutic and regenerative potential

BackgroundStem cell-derived extracellular vesicles (EVs) hold great promise in regenerative medicine. However, a comprehensive understanding of the regenerative capabilities of EVs from different stem cell sources remains limited. MethodsThis study systematically compares EVs derived from three odontogenic cell types. Analyses includes EV isolation and characterization, cell viability assays, vasculogenesis experiments, proteomic profiling, and miRNA sequencing. ResultsAll three EV types displayed similar surface marker profiles. Dental pulp stem cell-derived EVs showed superior cellular uptake, promoted higher cell proliferation, and enhanced vasculogenesis compared to periodontal ligament stem cell-derived EVs. Gingival fibroblast-derived EVs performed similarly in functional assays. Principal component analysis of miRNA profiles revealed strong biological heterogeneity among EV sources, with donor-specific factors exerting a greater influence on EV characteristics than cellular origin--an aspect underexplored in prior studies. ConclusionsThese findings underscore the complexity of EV functionality and highlight the regenerative potential of dental stem cell-derived EVs.

cell biology↗

bioRxiv2025

FLP-15 functions through the GPCR NPR-3 to regulate local and global search behaviours in Caenorhabditis elegans

Foraging is essential for sustenance and well-being of all organisms. The transition from well-fed to food-deprived conditions in C. elegans triggers a localized exploration of the environment characterized by frequent reorientations. However, over time the cumulative frequency of these reorientations decreases, facilitating the transition to global search behaviour. To investigate the genetic regulation of foraging in C. elegans, we conducted a screen of neuropeptide mutants and identified several candidates involved in modulating this behaviour. Among these, neuropeptide FLP-15 emerged as a key regulator of both local and global search behaviours. Our observations revealed that FLP-15 regulates the frequency and duration of reversals during foraging. Further investigation indicated that FLP-15 is expressed in and functions through the I2 pharyngeal neuron via the G-protein coupled receptor NPR-3. Mutants lacking either flp-15 or npr-3 displayed a significant decrease in reversal frequency during local search behaviours. Interestingly, unlike wild-type animals, the reversal frequency in flp-15 and npr-3 mutants did not decrease over time. This study also describes the expression pattern of NPR-3, in a subset of head neurons, predominantly comprising of dopaminergic neurons. This expression pattern highlights a potential link between neuropeptide signalling and dopaminergic modulation of behaviour. Finally, exogenous dopamine supplementation assays revealed that FLP-15 may regulate foraging by modulating dopamine transmission, highlighting a novel neuropeptide-dopamine interaction involved in the control of foraging behaviours.

neuroscience↗

bioRxiv2025

Identification of immune-mitophagy related gene in PD based on single-cell sequencing and Mendelian randomization

Parkinsons disease (PD) involves dysregulated mitophagy and immuneresponses, though the underlying mechanisms remain unclear. To identify key genes linking these pathways, we integrated single-cell RNA sequencing (GSE157783) with Mendelian randomization(MR) analysis, screening mitophagy-related genes (MRGs) and immune-related genes (IRGs). Differential expression analysis across PD cell subpopulations, combined with MR, revealed four causal genes: SLC11A1and DDX17(protective) and MRAS and PDIA3(risk). These genes were enriched in antigen presentation and calcium signaling pathways and exhibited dynamic expression in astrocytes and microglia during differentiation. Subsequent protein-protein interaction(PPI) network, regulatory (SCENIC), and drug-target analyses further characterized their roles. Validation in MPTP-induced PD mice confirmed behavioral deficits and altered expression of these genes, supporting their functional relevance. Our findings highlight SLC11A1, DDX17, MRAS, and PDIA3 as critical mitophagy-immune hubs in PD, offering mechanistic insights and therapeutic targets. Author SummaryPD is a neurodegenerative disorder linked to mitochondrial dysfunction (mitophagy) and immune dysregulation, yet the interplay between these mechanisms remains poorly understood. Using integrative single-cell sequencing and MR analyses, we identified four key genes-SLC11A1, DDX17, MRAS, and PDIA3-that bridge immune and mitophagy pathways in PD pathogenesis. These genes exhibit causal relationships with PD risk, offering novel insights into diagnostic and therapeutic strategies.

genetics↗

bioRxiv2025

AI-assisted Drug Re-purposing for Human Liver Fibrosis

Liver fibrosis is a severe disease with few treatment options due to the poor quality of the available animal and in vitro models. To address this, we investigated whether a hypothesis generating multi-agent AI system (AI co-scientist) could assist in re-purposing drugs for treatment of liver fibrosis and direct their experimental characterization. A multi-parameter image analysis workflow, which enabled anti-fibrotic efficacy and drug toxicity to be serially assessed in multi-lineage human hepatic organoids grown in microwells (i.e., microHOs), was used to assess the effects of 14 drugs. Remarkably, two of the three AI co-scientist-recommended drugs that targeted epigenomic modifiers exhibited significant anti-fibrotic activity. Analysis of the anti-fibrotic effects of five drugs indicated that two inhibited TGF{beta}-induced intracellular signaling and three drugs altered TGF{beta}-induced mesenchymal cell differentiation. Since all five of the anti-fibrotic drugs reduced TGF{beta}-induced chromatin structural changes, epigenomic changes play an important role in the pathogenesis of liver fibrosis. One AI co-scientist recommended drug is an FDA-approved anti-cancer treatment (Vorinostat) that reduced TGF{beta}-induced chromatin structural changes by 91% and promoted liver parenchymal cell regeneration in microHOs. Hence, the use of AI co-scientist and this microHO platform identified a potential new generation of liver fibrosis treatments that also promote liver regeneration.

bioinformatics↗

bioRxiv2025

Benchmarking Universal Machine Learning Force Fields with Hydrogen-Bonding Cooperativity

Machine learning force fields (MLFFs) offer a promising balance between quantum mechanical (QM) accuracy and molecular mechanics efficiency. While MLFFs have shown strong performance in modeling short-range interactions and reproducing potential energy surfaces, their ability to capture long-range cooperative effects remains underexplored. In this study, we assess the ability of three MLFF models -- ANI, MACE-OFF, and Orb -- to reproduce cooperative interactions arising from environmental induction and dispersion, which are essential for many biomolecular processes. Using a recently proposed framework, we quantify hydrogen bond (H-bond) cooperativity in N-methylacetamide polymers. Our results show that all MLFFs capture cooperativity to some extent, with MACE-OFF yielding the closest agreement with QM data. These findings highlight the importance of evaluating many-body effects in MLFFs and suggest that H-bond cooperativity can serve as a useful benchmark for improving their physical fidelity.

biophysics↗

bioRxiv2025

NF2 loss malignantly transforms human pancreatic acinar cells and enhances cell fitness under environmental stress

Pancreatic ductal adenocarcinoma (PDAC) occurs as a complex, multifaceted event driven by the interplay of tumor permissive genetic mutations, nature of cellular origin and microenvironmental stress. In this study, using primary human pancreatic acinar 3D organoids, we performed CRISPR knockout screen targeting 199 previously underappreciated potential tumor suppressors curated from clinical PDAC samples. Our data revealed significant enrichment of a list of candidates, with NF2 emerging as the top target. Functional validation confirmed that loss of NF2 promotes the transition of PDAC to an invasive state, potentially through extracellular matrix modulation. NF2 inactivation was found to enhance PDAC cell fitness under nutrient starvation. This adaptation not only reinforces the oncogenic state but also confers therapeutical resistance. Additionally, we found that NF2 loss is associated with the fibroblast heterogeneity and cancer-stroma communications in tumor evolution. These findings establish NF2 as a critical tumor suppressor in PDAC and uncover its role in mediating nutrient adaptation and drug resistance. Importantly, this study provides new insights into drug resistance mechanisms and potential therapeutic targets in PDAC.

cancer biology↗

bioRxiv2025

Low level of viral intra-host diversity is associated with severe SFTS disease

Severe fever with thrombocytopenia syndrome virus (SFTSV) is an emerging tick-borne virus that can cause severe clinical symptoms and high fatality. However, the dynamics of SFTSV intra-host diversity during infection and its association with disease severity remain unexplored. Here, we characterized SFTSV iSNVs in longitudinal clinical samples from patients with distinct clinical outcomes. Our analyses revealed that SFTSV intra-host diversity was associated with disease severity and showed distinct patterns in severe and mild cases. Severe cases exhibited paradoxically lower SFTSV intra-host diversity despite higher viral loads, likely driven by reduced selection pressure. Notably, iSNVs linked to viral replication emerged in severe cases, while iSNVs associated with immunity invasion arose in mild cases. Machine learning models showed that intra-host diversity can contribute to classification of SFTS by severity. Our findings, through the lens of within-host viral populations, highlight variations in viral-host interactions during SFTSV infection and provide potential biomarkers for predicting SFTS severity.

pathology↗

bioRxiv2025

SCRIPT: predicting single-cell long-range cis-regulation based on pretrained graph attention networks

Single-cell cis-regulatory relationships (CRRs) are essential for deciphering transcriptional regulation and understanding the pathogenic mechanisms of disease-associated non-coding variants. Existing computational methods struggle to accurately predict single-cell CRRs due to inadequately integrating causal biological principles and large-scale single-cell data. Here, we present SCRIPT (Single-cell Cis-regulatory Relationship Identifier based on Pre-Trained graph attention networks) that infers single-cell CRRs from transcriptomic and chromatin accessibility data. SCRIPT incorporates two key innovations: graph causal attention networks supported by empirical CRR evidence, and representation learning enhanced through pretraining on atlas-scale single-cell chromatin accessibility data. Validation using cell-type-specific chromatin contact data demonstrates that SCRIPT achieves a mean AUC of 0.9, significantly outperforming state-of-the-art methods (AUC: 0.68). Notably, SCRIPT obtains a threefold improvement in predicting long-range CRRs (>100 Kb) compared to existing methods. Applying SCRIPT to Alzheimers disease and schizophrenia, we establish a framework for prioritizing disease-causing variants and elucidating their functional effects in a cell-type-specific manner. By uncovering molecular genetic mechanisms undetected by existing computational methods, SCRIPT provides a roadmap for advancing genetic diagnosis and target discovery.

bioinformatics↗

bioRxiv2025

Interrupting Elmsan1 repression of nuclear Acetyl-CoA production therapeutically reprograms cancer cells

Metabolites are essential substrates for epigenetic modifications. Although nuclear acetyl-CoA constitutes a small fraction of the whole cell pool, it regulates cell fate by locally providing histone acetylation substrate. Here, we combined phenotypic chemical screen and genome-wide CRISPR screen to demonstrate a nucleus-specific acetyl-CoA regulatory mechanism that can be modulated to achieve therapeutic cancer cell reprogramming. While previously thought that nucleus-localized pyruvate dehydrogenase complex (nPDC) is constitutively active, we found that nPDC is constitutively inhibited by the nuclear protein ELMSAN1 through direct interaction. Pharmacologic inhibition of the ELMSAN1-nPDC interaction derepressed nPDC activity, enhancing nuclear acetyl-CoA generation and reprogramming cancer cells to a postmitotic state with diminished cell-of-origin signatures. Reprogramming was synergistically enhanced by histone deacetylase 1/2 inhibition, resulting in inhibited tumor growth, durably suppressed tumor-initiating ability, and improved survival in multiple cancer types in vivo, including therapy-resistant sarcoma patient-derived xenografts and carcinoma cell line xenografts. Our findings highlight the potential of targeting ELMSAN1-nPDC as epigenetic cancer therapy.

cancer biology↗

bioRxiv2025

Hypoxia Exacerbates Kir2.1 Channel Dysfunction in an Andersen-Tawil Syndrome Variant Through a SUMO-Dependent Mechanism

BackgroundAndersen-Tawil Syndrome type 1 (ATS1) is a multisystem channelopathy that predisposes patients to ventricular dysrhythmias and increases the risk of sudden cardiac death. ATS1 arises from loss-of-function mutations in Kir2.1, the inward rectifying potassium channel responsible for most of IK1 in ventricular cardiomyocytes. IK1 is suppressed by SUMOylation, a post- translational modification upregulated in hypoxia, a known proarrhythmic stimulus. We investigated whether current from the ATS1-linked variant Kir2.1-R67Q is inhibited by hypoxia and whether this suppression can be reversed by pharmacological inhibition of the SUMO pathway. MethodsWe used patch-clamp recording to measure IK1 and Kir2.1 currents under acute hypoxia, with and without the SUMO pathway inhibitor TAK-981. To quantify SUMOylation stoichiometry, we applied single molecule photobleaching. A multidisciplinary approach combining electrophysiology, molecular modeling, and optogenetic phosphoinositide was used to measure the impact of Kir2.1- R67Q and SUMOylation on channel interactions with phosphatidylinositol 4,5-bisphosphate (PIP2), a required gating cofactor. ResultsKir2.1 can be modified by up to two SUMO proteins attached to diagonally opposite subunits, with each SUMOylation event reducing current by [~]20%. Heterozygouse channels containing two R67Q subunits were more susceptible to hypoxic suppression than wild type. TAK-981 blocked hypoxic inhibition of IK1 in ventricular cardiomyocytes and abolished Kir2.1 SUMOylation. In cells expressing Kir2.1-R67Q, TAK-981 significantly increased currents and mitigated hypoxic suppression. Computational modeling and optogenetic dephosphorylation revealed that both the R67Q mutation and converge to disrupt Kir2.1- PIP2 interactions, producing synergistic inhibition of channel function. ConclusionsHypoxia-induced SUMOylation and the R67Q mutation synergistically suppress Kir2.1 activity by impairing channel-PIP2 interactions. TAK-981 restores IK1 by preventing SUMOylation under hypoxic conditions and enhancing current through Kir2.1-R67Q channels. These findings support a two-hit model of arrhythmogenesis in ATS1 and identify SUMO pathway inhibition as a potential therapeutic strategy to reduce arrhythmic risk in affected patients.

physiology↗

bioRxiv2025

Inulin reduces Ralstonia invasion by promoting cooperation between Lysinibacillus sphaericus and Pseudoarthrobacter spp.

In field production, beneficial microbial agents are typically applied along with key resources that beneficial microbes prefer to utilize. This practice aims to help the beneficial microbes colonize the field and exert their disease resistance functions. However, the mechanisms by which these key resources influence the colonization and disease resistance effects of beneficial microbes remain unknown. In this study, we found that inulin can enhance the growth capacity of Lysinibacillus sphaericus HR92 and its ability to inhibit Ralstonia solanacearum. Further investigation revealed that inulin can enhance strain HR92s flagellar assembly, bacterial chemotaxis, fatty acid metabolism, and siderophore synthesis capabilities, ultimately improving strain HR92s effectiveness in controlling bacterial wilt. Moreover, adding inulin to the soil can enrich Pseudarthrobacter strains. This genus enhances the expression of genes involved in the synthesis of the antibacterial substance HR92, and competes for nutrients with Ralstonia solanacearum, thereby further inhibiting the occurrence of bacterial wilt disease. Additionally, the combination of inulin and Pseudarthrobacter strains upregulates the valine and leucine pathway genes in strain HR92. These genes play a crucial role in the synthesis of surfactin and the antimicrobial VOC 3-methyl-1-butanol. We have demonstrated that the addition of key resources not only enhances the control efficacy of beneficial bacteria against soil-borne diseases but also enriches the "helpers" of beneficial bacteria in soil. ImportanceRalstonia solanacearum is a plant pathogen that can cause bacterial wilt in several important crops. Given the limitations of beneficial bacterial inoculation, we propose a strategy to enhance the biocontrol efficacy of beneficial microorganisms by utilizing key resources. In this study, we demonstrate that key resources inulin can improve the biological control effects of beneficial bacteria, thereby maintaining plant health. Furthermore, we found that increasing the concentration of inulin altered the diversity of the rhizosphere microbiota and specifically enriched the abundance of Pseudarthrobacter, which compete with pathogens for nutrients on one hand and, on the other hand, synergize with inulin to enhance the biocontrol efficacy of the beneficial bacterium HR92. Together, our study reveals that key resources can enhance the biocontrol efficacy of beneficial bacteria and enrich potential beneficial bacteria in resident microbial communities, further reducing tomato diseases.

microbiology↗

bioRxiv2025

Chromosome-Specific Aneuploidy Engineering via dCas9-Induced Centromeric Chromatin Relaxation

Aneuploidy, the gain or loss of chromosomes, is prevalent in both normal and disease conditions, however, experimental approaches to engineer and study aneuploidy remain limited, leaving its functional significance under-characterized. Here, we present CRISPR-Taiji (CRISPRt), an efficient method for inducing chromosome-specific mis-segregation and aneuploidy generation across all 24 human chromosomes via dead Cas9 (dCas9)-induced centromeric chromatin relaxation. Using CRISPRt with scRNA-seq, we generated the first comprehensive transcriptomic alteration landscape of nearly all autosomal aneuploidies at chromosome-arm resolution. This genotype-phenotype map provides causal evidence linking recurrent aneuploidies in clear cell renal cell carcinoma (ccRCC) to molecular and clinical phenotypes observed in patient tumors. Notably, chromosome 3(p) loss, the ccRCC initiating event, specifically drives strong interferon signaling activation, offering novel insights into ccRCC tumorigenesis and immune modulation. Overall, we establish CRISPRt as a simple, efficient and scalable approach for chromosome-specific aneuploidy engineering and characterization in preclinical models to advance aneuploidy research across diverse biological contexts.

genomics↗

bioRxiv2025

Inference and visualization of multi-scale cell tree for decoding functional diversity with scMustree

AbstractDeciphering cellular heterogeneity and functional diversity is crucial to understanding biological systems and disease mechanisms. Although single-cell RNA sequencing (scRNA-seq) has revolutionized this field, existing methods often fail to characterize the functional associations between cell populations due to the discrete nature of clustering results. We introduce scMustree, a tree- construction algorithm that enables in-depth exploration of functional associations and transitional states among cellular populations. scMustree combines top-down iterative decomposition for high- purity leaf nodes with bottom-up merging based on quantitative functional distances, preserving local continuity and global structural clarity. Benchmarking on real datasets shows that scMustree not only outperforms existing methods in clustering accuracy but also reveals functionally coherent subtypes, anatomically related cell types, and developmentally connected transitions. In case studies, it identifies Alzheimers disease-associated microglial subtypes and captures spatial cell distribution patterns of cell types in developed embryos, demonstrating its utility as a powerful tool for multi-scale exploration of cellular heterogeneity.

bioinformatics↗

bioRxiv2025

stPipe: A flexible and streamlined R/Bioconductor pipeline for preprocessing sequencing-based spatial transcriptomics data

Spatial transcriptomics technology has developed rapidly in recent years, with various sequencing-based platforms such as 10x Visium, Slide-seq and Stereo-seq becoming widely used by researchers. Each platform brings its own set of protocols and customised data analysis pipelines which presents challenges when the goal is to obtain uniformly preprocessed data that is conveniently formatted for downstream analysis. To address the need for simpler, open-source solutions that deal with sequencing-based spatial transcriptomics (sST) data from different platforms, we present stPipe, a comprehensive and modular pipeline for analysing sST data. stPipe handles various analysis steps including (i) data processing from raw paired end FASTQ files to create a spatially resolved gene count matrix; (ii) the collation of relevant quality control metrics during preprocessing to ensure unwanted artefacts can be filtered from further analysis; and (iii) the adoption of standardised data storage containers to allow results to be easily passed on to a wide range of downstream analysis packages tailored to different goals (such as clustering, cell-cell communication analysis and differential expression analysis). stPipe is implemented as an R/Bioconductor package that builds upon functionality in the scPipe software, and offers a flexible preprocessing pipeline that can manage data from all current main-stream sST plaforms. A key use case for stPipe is in methods benchmarking, and we demonstrate how the uniform processing of sST data collected on reference tissue samples from the cadasSTre and SpatialBenchVisium projects is made easier, allowing comparisons between different technology platforms and downstream analysis tools. Our framework thus aims to advance the standardization and optimization of spatial transcriptomics analyses, fostering collaboration and innovation within the research community.

bioinformatics↗

bioRxiv2025

Small non-coding RNAs encapsulating mammalian cells fuel innate immunity

Cell surface RNAs, notably glycoRNAs, have been reported, yet the exact surface RNA compositions in different cell types remain unclear. Here, we introduce a comprehensive suite of methodologies for imaging, profiling, quantifying, and exploring the biological functions of specific surface RNAs. Utilizing these techniques, we have identified diverse non-coding RNAs present on mammalian cell surfaces. We confirm the membrane anchorage and quantify the abundance of several representative RNAs on human primary cells. Notably, we discover a significant prevalence of Y RNAs on the surfaces of human monocytes and B cells. We find that these Y RNAs on human monocyte surfaces enrich extracellular histones, regulating interleukin-6 (IL-6) gene expression and subsequent protein secretion upon histone stimulation via NF-{kappa}B and AP-1 activation. Our study not only presents effective approaches for investigating surface RNAs, but also uncovers a previously unrecognized immune activation pathway mediated by surface Y RNAs on monocytes. In briefA comprehensive profiling of surface RNAs across diverse mammalian blood cell types unveil abundant Y RNAs on the surface of human monocytes. Subsequent investigations uncover functional roles of surface Y RNAs on monocytes as "immune sentinel" to enrich extracellular histones, revealing a previously unknown pathway of innate immune activation. HighlightsNovel methodologies for cell surface RNA mapping, validation and functional interrogation. Sequencing of surface RNAs across various mammalian blood cell types offers detailed maps of surface RNAs. Abundant Y RNAs localize on human monocyte surfaces and capture extracellular histones released by adjacent ruptured cells. Surface Y RNAs enrich extracellular histones to facilitate transcription and secretion of IL-6 through NF-{kappa}B and AP-1 activation.

molecular biology↗

bioRxiv2025

Histone 3 lysine 36 trimethylation by SETD2 shapes an epigenetic landscape in intestinal stem cells to orchestrate lipid metabolism and prevent cell senescence.

The self-renewal capacity of intestinal stem cells (ISCs) declines with aging, leading to a loss of homeostasis and an increased susceptibility to intestinal diseases. Despite the established significance of lipid metabolism and epigenetic regulation in ISC function, the molecular mechanisms that connect these processes to aging-related ISC dysfunction remain elusive. Here, we demonstrate that Histone 3 lysine 36 trimethylation (H3K36me3) caused by SETD2 is critical for ISC stemness. We found that H3K36me3 deficiency results in reduced ISC proliferation and differentiation, disrupts fatty acid oxidation (FAO) metabolism, and induces ISC senescence. Mechanistically, the loss of H3K36me3 triggers the activity of the SWI/SNF chromatin remodeling complex and leads to increased chromatin accessibility and enhancer activation, which alters FAO- and senescence-related gene expression. Importantly, we discover that metabolic intervention can prevent the senescence of ISC due to H3K36me3 deficiency. Our findings reveal a crucial role for H3K36me3 in maintaining the epigenetic landscape that orchestrates FAO metabolism and determines intestinal stem cell functions, emphasizing the role of FAO as a key modulator between H3K36me3 and ISC aging, suggesting that metabolic intervention may help mitigate age-related ISC dysfunction.

cell biology↗

bioRxiv2025

Predictive Ability of Enviromic Modeling in GxE Interactions for Upland Rice Site Recommendations

Enviromics is an omics approach that investigates a phenomenon using all available environmental information. This study explores the use of enviromic covariates in studies of genotype x environment (GxE) interactions in upland rice in Brazil, utilizing a field trial dataset from 143 locations over 27 years, covering diverse environmental conditions. The platforms WorldClim, NASA POWER, and SoilGrids were used to extract data, resulting in 383 environmental covariates. The objective of this study was to evaluate the use of enviromic kernels to integrate GIS and genetic data for predicting upland rice productivity across Brazil and to determine the optimal number of environmental covariates required to ensure model accuracy and stability. The predictive abilities of the enviromic model peaked with around 81 covariates, stabilizing when all 383 were included, suggesting the importance of a comprehensive dataset for accurate predictions. Analysis reveals that environmental dissimilarities are more critical than geographical distance for genotypic variability, reinforcing the need to consider multiple covariates in predictive models. Heritability mapping revealed spatial variations, with regions of high heritability concentrated in southern Brazil, where genetic selection may be more efficient. The clustering of mega-environments was not efficient, highlighting the complexity of GxE interactions, and confirming that pixel-by-pixel enviromic models are a safer approach for recommending breeding actions for upland rice. This study suggests strategies to improve genotype selection for specific conditions, guiding the expansion of rice cultivation into new agricultural areas in Brazil. The findings also contribute to rice-growing regions worldwide, especially in countries cultivating upland rice under diverse conditions. Structured AbstractO_ST_ABSObjectiveC_ST_ABSThis study aimed to evaluate the predictive ability of enviromic models for site-specific recommendations in upland rice, focusing on genotype x environment (GxE) interactions by integrating environmental and phenotypic data. MethodsA total of 734 field trials conducted between 1995 and 2022 across 143 Brazilian locations were analyzed. Environmental data (383 covariates) were retrieved from WorldClim, NASA POWER, and SoilGrids using GIS-based procedures. Statistical analyses included mixed linear models and Random Forest to correct for design effects, estimate heritability, and perform spatial predictions. ResultsEnvironmental dissimilarity better explained genotypic ranking than geographic distance. Predictive ability plateaued after 81 covariates, but adding more covariates reduced variance and increased model stability, supporting the use of comprehensive environmental data. ConclusionsThe study reinforces the need for detailed environmental characterization and the use of comprehensive enviromic models. Pixel-based predictions are more reliable than broad clustering approaches, supporting the use of virtual trials to optimize breeding strategies and resource allocation.

genetics↗

bioRxiv2025

Rapid High-Resolution Analysis of Polysaccharide-Lignin Interactions via Proton-Detected Solid-State NMR with Application to Eucalyptus and Spruce

The plant secondary cell wall, a complex matrix composed of cellulose, hemicellulose, and lignin, is crucial for the mechanical strength and water-proofing properties of plant tissues, and serves as a primary source of biomass for biorenewable energy and biomaterials. Structural analysis of these polymers and their interactions within the secondary cell wall has been heavily relying on 13C-based solid-state NMR techniques. In this study, we explore the application of 1H-detected solid-state NMR techniques for rapid, high-resolution structural characterization of polysaccharides and lignin, demonstrated on the stems of hardwood eucalyptus and softwood spruce. We employed several strategies, including the use of synthesized 2D spectra to resolve central 1H resonances and the combined application of 3D hCCH and hCHH experiments for complete resonance assignment and unambiguous identification of lignin-carbohydrate interactions. Our findings emphasize the central role of acetylated three-fold xylan conformers, rather than two-fold, in stabilizing the carbohydrate-lignin interface, with glucuronic acid sidechains in eucalyptus glucuronoxylan colocalizing with lignin, revised cellulose-lignin interactions involving uncoated microfibril surfaces, and pectin-lignin interactions indicative of early-stage lignification. We also carefully evaluated the interference from tannins in softwood species. These results present a novel approach for rapid structural analysis of lignocellulosic biomaterials without the need for solubilization or extraction.

biophysics↗