Biology subjects

Jones, C.

Publications and source records attributed to Jones, C..

At least 37 records · Page 2Linked to original sources

bioRxiv2026

Streptomyces enrichment in roots during drought is uncoupled from plant benefit and is driven by host suppression of iron uptake and immunity

Drought reshapes plant root microbiota, yet the mechanistic drivers and consequences of this observation remain unclear. We discovered that suppression of host immunity and iron homeostasis is required for Streptomyces enrichment in roots during drought across diverse soils. Genetic and physiological manipulation of these host pathways confirmed their requirement in modulating Streptomyces root enrichment. Drought-induced suppression of iron uptake was conserved across the [~]160 My monocot-eudicot divergence. Some Streptomyces strains enhanced plant growth and rescued iron uptake under drought. These benefits were uncoupled from Streptomyces root enrichment. They were instead shaped by intra-Streptomyces antagonism. We propose a two-step model: drought-driven down regulation of host iron and immune pathways enriches Streptomyces, while intra-genus dynamics fine-tune strain-level assembly and functional outcomes. Our data refine the idea that Streptomyces are enriched in roots during drought in response to a plant cry for help and consequently contribute to alleviation of this abiotic stress.

plant biology↗

bioRxiv2026

PFOA induced metabolic and immune perturbations in a SARS-2 infection model

This study evaluates the impact of PFOA exposure on the metabolome and immune response to SARS-2 using a ferret model. Ferrets were separated into control or PFOA-exposed groups (10/mg/kg/day) and challenged with SARS-2. Longitudinal analyses encompassing clinical assessments, serological profiling, histopathology, and untargeted nuclear magnetic resonance (NMR) metabolomics revealed significant metabolic and immunological perturbations. We found prominent effects of PFOA exposure on metabolism, which resulted in altered metabolic responses to SARS-2 infection. PFOA exposure was also associated with impaired immune function, as evidenced by decreased serum IgG levels, increased viral loads, and prolonged peak infectivity. These findings underscore the consequences of PFOA exposure on host metabolism and immunity during infectious diseases.

pharmacology and toxicology↗

bioRxiv2026

Hog1/p38 and ZAKα drive Shwachman-Diamond syndrome and provide targets to improve cell growth

Shwachman-Diamond syndrome (SDS) is a ribosomopathy characterized by neutropenia, pancreatic insufficiency, skeletal defects, and predisposition to leukemia. Most cases result from biallelic SBDS mutations that impairing 80S ribosome and polysome assembly. In yeast lacking SDO1 (the SBDS ortholog), growth slows dramatically and the p38 ortholog Hog1 signaling is elevated by multiple types of stress. SBDS-deficient HeLa cells exhibited reduced proliferation and slowed cell cycling. The p38 kinase was constitutively activated in SBDS mutants and SDS patient-derived blood cells. Because ZAK detects ribosome dysfunction, its activation links ribosomal defects to stress kinase pathways in SDS. Suppressing p38 or its upstream activator ZAK restored cell growth and reduced stress signaling. These findings reveal an evolutionarily conserved-independent mechanism via p38 drives SDS pathophysiology and identifies stress kinases as potential therapeutic targets for ribosomal dysfunction.

cell biology↗

bioRxiv2026

Characterization of novel cytoplasmic roles for the N-terminal methyltransferase NRMT1

N-terminal methylation of proteins by the trimethylase NRMT1 plays important roles in oncogenesis, development, and aging. As N-terminal methylation has frequently been shown to regulate protein-DNA interactions, and many NRMT1 substrates are transcription factors or regulators of chromatin structure, previous research has focused on how transcriptional regulation by NRMT1 affects cell growth and differentiation. However, we have recently identified a new, cytoplasmic role for NRMT1, inhibiting the eukaryotic elongation factor 1 alpha (eEF1A) methyltransferase METTL13, which indicates NRMT1 could also be acting as a translational regulator. Here we further explore NRMT1 cytoplasmic functions and show that, unlike previously thought, NRMT1 can methylate substrates in the cytoplasm. We also show that while many of these substrates remain bound to NRMT1, it can also interact with a number of non-target ribosomal proteins and proteins associated with the endoplasmic reticulum (ER). To confirm NRMT1 interaction with the ribosome, we performed polysome profiling, which showed a portion of NRMT1 co-migrates with the 40S and 60S subunits but not with actively translating polysomes, indicating NRMT1 may play an early role in translation. To see if NRMT1 was affecting target mRNA selection of ribosomes, we also performed ribosome-sequencing experiments in proliferating and differentiating C2C12 mouse myoblasts. These results show a striking upregulation of translation of soluble proteins with NRMT1 loss and corresponding decrease in translation of transmembrane and signal sequence-containing proteins. We now propose a model where NRMT1 regulates the translation of transmembrane and secreted proteins by facilitating interactions between the ribosome and the ER.

biochemistry↗

bioRxiv2025

Stable Inheritance of Transgene and Yellow Fluorescent Protein Gene Expression in Progeny of Transgenic Cacao (Theobroma cacao) Plants

Genetic engineering tools have the potential to rapidly and precisely improve the genome of slow-to-breed cacao. We previously developed an efficient protocol for transforming cacao using cotyledonary explants derived from secondary somatic embryos via Agrobacterium tumefaciens. In this study, we demonstrate that our transformation protocol is successful in elite cultivars, INIAPG-038 and Matina 1-6, producing fertile seeds with stable visual marker inheritance regardless of whether the transgenic plants were used as the pollen or ovule donor. Three vectors were used in the transformations, each containing genes for enhanced yellow fluorescent protein (eyfp) and neomycin phosphotransferase II (nptII). Three transgenic INIAPG-038 events and one transgenic Matina 1-6 event were used to evaluate seed fertility and the stability of transgene inheritance in cacao seeds and plants. The T1 progeny of these four transgenic events were analyzed for YFP expression and transgene presence. YFP expression segregated at a 1:1 ratio in all events when the transgenic plants were crossed with non-transgenic plants, while a 3:1 segregation was observed when transgenic events were crossed with each other. The transgenic plants exhibited a normal phenotype compared to non-transgenic control plants, producing seeds with a 97% germination rate.

plant biology↗

bioRxiv2025

Shape, Strain, and Stability: Epithelia Under High Strain

Mechanical forces play crucial roles in epithelia tissue morphogenesis and function, yet individual cells often respond differently to the same external force. Strain heterogeneity, the non-uniform deformation of cells under uniform external mechanical stimuli, may underlie tissue-level robustness and guide morphogenetic outcomes. In this study, we applied a defined uniaxial strain to Xenopus laevis epithelial explants and investigated how strain was distributed at the cellular level. Live imaging and quantitative analysis revealed that despite a uniform tissue-level strain, cellular strain was heterogeneous, suggesting variable responses to a uniform mechanical stimulus. To understand the source of this variability, we used an image analysis pipeline to explore multiple aspects of cell morphology. We found that cell intrinsic material properties, represented by Poisson index, had the strongest correlation with strain heterogeneity, suggesting a dominant role in variable mechanical response. We further analyzed how force was distributed at the cellular level using a vinculin force sensor and laser ablation. These experiments demonstrated that forces are primarily transmitted through the medio-apical actomyosin cortex whereas junctional actomyosin facilitates dissipation and remodeling. These findings provide new insights into the physical principles that underlie epithelial resilience and adaptive remodeling, highlighting the importance of distinct functions of junctional and medio-apical actomyosin networks in mechanical adaptation. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=158 SRC="FIGDIR/small/687918v1_ufig1.gif" ALT="Figure 1"> View larger version (40K): org.highwire.dtl.DTLVardef@1d27474org.highwire.dtl.DTLVardef@1db811forg.highwire.dtl.DTLVardef@1fa36dforg.highwire.dtl.DTLVardef@288107_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

bioRxiv2025

siRNA Mediated Genetic Perturbation of Primary Human Leukemia Stem and Progenitor Cells

Acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) are aggressive hematologic malignancies with poor outcomes. Leukemia stem and progenitor cells (LSPCs) are a subset of cells within the bulk tumor thought to be responsible for initiating disease and causing relapse. LSPCs evade chemotherapy partially due to their quiescent state. Therefore, studying this cell subpopulation is critical to identify new disease targets that can better the outcomes of AML/MDS patients. The use of RNAi and genetic approaches is technically challenging in primary leukemia cells and particularly LSPCs. Overcoming this technical hurdle could greatly expand the breath of pre-clinical and mechanistic examination of LSPCs. In this study, we describe a methodology to efficiently introduce siRNA, resulting in effective gene knock down in LSPCs. After isolation of LSPCs from primary patient samples, we showed that electroporation of these cells does not affect cell viability significantly. Further, using siGLO green transfection indicator, we show that RNA is introduced into the nucleus of these cells. siRNA transfection leads to efficient knockdown of target genes and has subsequent biological relevant activity. We have identified a method to effectively knock down genes in leukemia stem and progenitor cells, opening up new avenues to examine LSPC biology in human specimens.

cancer biology↗

bioRxiv2025

Pheromone circuits and transcriptional cascades modulating transcriptional and chromatin states in the Drosophila central brain with social experience

Social experience significantly influences the behavioral and physiological responses of animals, including humans. In many animals, social isolation increases aggression, courtship, locomotion, and feeding while disrupting sleep. This occurs when peripheral neurons detect social signals, such as pheromones, which activate decision-making circuits in the brain. However, the molecular and circuit mechanisms of how chronic social isolation or enrichment alter gene expression and affect neuronal function and behavior remain unclear. In this study, we examined how transcription patterns and chromatin marks in male Drosophila brains change in response to social experience, and the effect of pheromone circuits and transcription factors involved in social circuit function. We focused on pheromone receptors Or47b and Or67d, as well as transcription factors FruM and DsxM. Our findings suggest that social experience affects multiple genes in the central brain. Disrupting Or47b, Or67d, FruM, and DsxM function moderated the transcriptional responses through antagonistic interactions. Specifically, Or47b circuits predominantly mediated transcriptional responses to social isolation through DsxM function, while Or67d and FruM regulated responses to group housing. Notably, mutants of fruM and dsxM exhibited more extensive transcriptional changes in the brain than Or mutants, especially for FruM/DsxM target genes. While social experience did not lead to detectable alterations in the overall chromatin profile in the whole brain, mutants of the four genes resulted in significant changes in the enrichment of H3K4me3 and RNA polymerase II (RNAPolII) compared to wild type. Furthermore, mutants in fruM and dsxM generally eliminated social experience-dependent changes in sleep and locomotion behaviors, whereas Or mutants exhibited more modest disruptions. Overall, our results uncover the pheromone circuits and transcriptional cascades in regulating molecular and behavioral responses to social experience.

neuroscience↗

bioRxiv2025

Surface proteomics reveals arginine metabolism as a vulnerability in high grade serous ovarian cancer

The significant lethality of high-grade serous ovarian cancer (HGSC) is driven by the lack of long-term efficacy of current treatments, underscoring the need for developing additional therapeutics. Cell surface proteins represent attractive therapeutic targets yet remain underexplored in high-grade serous ovarian cancer. Here, we employed cell surface N-glycoproteomics to elucidate the cell surface proteomes of HGSC cells alongside normal epithelial and cancer-associated stromal cells, uncovering new opportunities for therapeutic intervention. Integration of cell surface N-glycoproteomics and functional screening revealed multiple minimally characterized, HGSC-enriched surface proteins that are critical for HGSC proliferation, most notably, SLC7A1. Multi-omic and functional characterization indicated that SLC7A1 is necessary for HGSC migration, protein synthesis and mitochondrial functions likely linked to its role as an arginine transporter. Finally, we demonstrate that elevated surface expression of SLC7A1 in HGSC reflects dysregulated arginine metabolism, pointing to a putative therapeutic vulnerability. Our work identifies SLC7A1 and arginine metabolism as a previously unrecognized molecular vulnerability in HGSC and provides a framework to guide future therapeutic development.

cancer biology↗

bioRxiv2025

Loss of NRMT1 allows expression of multiple differentiation pathways and alters transcription of secreted proteins in C2C12 myoblasts

Muscle stem cells (satellite cells) retain their identity and function through expression of the paired homeobox transcription factor PAX7. PAX7 is able to both stimulate satellite cell proliferation and activate target genes involved in establishing myogenic identity, including myogenic factor 5 (MYF5) and the other myogenic regulatory factors (MRFs). Upregulation of the MRFs promotes commitment to the muscle lineage by initiating withdrawal from the cell cycle, upregulating expression of muscle-specific transcripts, and directing myoblast fusion. We have previously shown that knockout of the N-terminal methyltransferase NRMT1 in C2C12 mouse myoblasts results in significantly decreased Pax7 expression, an inability of the cells to differentiate into myotubes, and abnormal upregulation of osteogenic markers. Here, we use RNA-sequencing to more comprehensively determine how loss of NRMT1 affects the transcriptional profile of proliferating and differentiating C2C12 myoblasts. We see that upon inducing differentiation, NRMT1 knockout cells can downregulate cell cycle, DNA replication, and histone gene expression. Though they also have significantly downregulated Pax7 and Myf5 expression, other muscle-specific transcripts are significantly increased over wild type, indicating the muscle transcriptional program is not completely inhibited. However, signaling pathways involved in the differentiation of other types of mesenchymal and hematopoietic lineages are also increased with NRMT1 loss and expression of chemotactic genes is downregulated. Together, these data indicate that NRMT1 knockout cells can upregulate genes needed for cell cycle withdrawal and muscle specification but fail to suppress markers of other lineages and activate normal chemotactic signaling, which may lead to the observed differentiation phenotypes.

genomics↗

bioRxiv2025

Stiffness sensing fuels matrix-driven metabolic reboot for kidney repair and regeneration

Kidney repair after acute kidney injury (AKI) relies on a finely tuned extracellular matrix (ECM) that provides structural integrity and mechanical cues. As primary ECM architects, fibroblasts and pericytes rapidly mobilize to the injury site post-AKI, yet the ECM-driven repair mechanisms remain incompletely defined. Here, leveraging tissue engineering, genetic and pharmacological models, and multi-omics, we profiled the proteome landscape of decellularized kidney matrix scaffold post-AKI and highlighted microfibrillar-associated protein 2 (Mfap2) as a key core matrisome component primarily sourced from fibroblasts and pericytes. Mfap2 loss disrupted kidney architecture and metabolism, aggravating AKI. Global proteomics revealed that Mfap2 deficiency suppressed tubular 3-hydroxy-3-methylglutaryl-CoA synthase 2 (Hmgcs2) expression via estrogen receptor 2 (Esr2)-mediated transcriptional repression and increased protein succinylation. Phosphoproteomics and spatial transcriptomics further demonstrated a shift in mechanical signaling, with Mfap2 loss hyperactivating mitogen-activated protein kinases and upregulating large tumor suppressor kinase 1 (Lats1) in tubular cells without altering integrin receptor activities. In turn, Lats1 suppressed Esr2 transcription independent of its canonical Yap/Taz effectors, without affecting ubiquitin-mediated Esr2 degradation. Therapeutically, Esr2 agonists restored kidney function in Mfap2-deficient models. These findings position Mfap2 as a key regulator of ECM dynamics and mechanosignaling, linking tissue stiffness to metabolic reprogramming required for kidney repair.

cell biology↗

bioRxiv2025

Volumetric single-molecule tracking inside subcellular structures

The molecular interactions that underpin all cellular functions depend on molecular motion within three-dimensional environments. Large depth-of-field single-molecule localization microscopy (3D-SMLM) methods facilitate these measurements, but their increased optical complexity and bespoke post-processing pipelines can sacrifice important cellular context. Here we combine single-molecule light-field microscopy (SMLFM) with widefield Fourier light-field microscopy for correlative volumetric organelle imaging. The instantaneous acquisition of subcellular volumes improves the sensitivity of molecular organization and diffusion measurements through the rejection of non-specific localizations. We first demonstrate our approach by measuring the molecular organization of a nuclear-localized HaloTag protein relative to cell nuclei. Next, we characterize the molecular diffusion of the soluble protein, calreticulin, in the context of 1-antitrypsin deficiency, which revealed an increase in heterogeneous motion within endoplasmic reticulum inclusions.

biophysics↗

bioRxiv2025

Aromatic Patch in WhiB-Like Transcription Factors Facilitates Primary Sigma Factor Interaction in Mycobacterium tuberculosis

WhiB-like (Wbl) family proteins are a unique family of iron-sulfur ([4Fe-4S]) cluster-bound transcription factors found exclusively in Actinobacteria and actinobacteriophages, including the notoriously persistent pathogen Mycobacterium tuberculosis (Mtb). Despite their critical roles in cell development, stress response and antibiotic resistance, the mechanisms of gene regulation by the Wbl family proteins are not fully understood due to the lack of a canonical DNA-binding motif in most Wbl proteins. Here, we present structural and biochemical evidence demonstrating that all Mtb Wbl proteins bind to the same site in the conserved region 4 of the primary sigma 70 factor facilitated by a previously unrecognized structural motif, the aromatic patch, in the Wbl family. Our phylogenetic findings provide compelling evidence for a complex evolutionary relationship of Wbls between actinobacteria and the associated phages. Together, this work fills a critical gap in our understanding of the function, mechanism and evolutionary origin of Wbls.

biochemistry↗

bioRxiv2025

Social experience alters behaviors by reprogramming the Fruitless pathway and circadian state in Drosophila

From flies to humans, social experience affects various cognitive and behavioral processes. Previous studies have shown that group housing suppresses many behaviors like courtship, aggression, and feeding in Drosophila melanogaster, in addition to resetting the circadian state. Here, we focus on group housing-induced courtship suppression. To determine the mechanisms by which social experience modulates courtship behaviors, we performed bulk tissue RNAseq and single-cell RNAseq from cells expressing FruitlessM (FruM) and DoublesexM (DsxM), two transcription factors that label interconnected neural circuits for socially driven behaviors, from grouped or isolated male brains. These revealed that social isolation alters fru and dsx levels throughout the brain. Knocking down fruM in different fruM-positive neuron subpopulations in the brains has diverse effects on social experience-dependent changes in courtship. Furthermore, group housing increases the expression of stripe (sr) and Hormone receptor-like in 38 (Hr38) genes encoding neural activity-induced transcription factors in most neurons within social circuits. We found that knocking down sr in fruM-positive neurons effectively eliminates the impact of social experience by increasing courtship in group-housed males. Importantly, social experience also alters the expression of FruM/DsxM putative target genes regulating circadian states throughout the brain. Disrupting the function of multiple circadian genes diminishes the effect of group housing on courtship. Our findings suggest that group housing/social enrichment suppresses courtship by reprogramming the circadian arousal state, whereas courtship-elevating effects of social experience rely on unique influences of FruM expression and function in different neurons within social and clock circuits. These results are significant as they point to modulation of circadian arousal state as a possible central strategy for mediating the pleiotropic effects of social experience on organismal responses.

neuroscience↗

bioRxiv2024

Targeted inhibition of Bcl-xL following radiation reduces tumourigenesis in preclinical models of H3K27M-altered diffuse midline glioma

BackgroundDiffuse midline gliomas (DMGs) with histone H3K27M mutations represent a devastating paediatric brain cancer characterized by abysmal prognosis and limited treatment options. The only approved treatment is radiotherapy (RT), but most of the tumours relapse with fatal consequences. In this study, we sought to investigate whether irradiation leads to senescence induction and explore the efficacy of senolytics against DMG. MethodsWe have characterised the senescent phenotype of five genetically heterogeneous H3K27M-altered human DMG cell lines, combining cellular and/or molecular approaches. The sensitivity of senescent cells to Bcl-xL inhibition has been demonstrated in dose/response curves in vitro and in a PDX model of DMG. ResultsHere, we show that ionizing radiation induces senescence and SASP responses in both TP53 mutant and wild-type H3K27M-altered human DMG cell lines. We identify Navitoclax as a potent senolytic agent that selectively targets senescent DMG cells into apoptosis by inhibiting Bcl-xL. Related compounds, such as a proteolysis-targeting chimera (PROTAC)-mediated Bcl-xL degradation and a galacto-conjugated form of Navitoclax also show an effective senolytic activity in senescent cancer cells. Finally, we show that a combination therapy of irradiation and Navitoclax results in reduced tumor burden and increased mouse survival in an orthotopic xenograft DMG model. ConclusionThese results offer a rationale for further clinical development of senolytic therapies as part of multimodal treatment approaches for DMG patients/ Key PointsO_LIIonising irradiation induces senescence in human DMG cells independently of the p53 status. C_LIO_LIBcl-xL inhibition results in apoptosis of human DMG senescent cells in synergy with irradiation. C_LIO_LICombination of irradiation and BcL-xL inhibition reduces tumourigenesis in a PDX model of DMG. C_LI Importance of the StudyH3K27M-altered DMG are devastating paediatric tumours with an abysmal prognosis. The only approved treatment is radiotherapy but this is palliative and tumours almost always relapse with fatal consequences for the patients. In this study, we show that radiotherapy results in senescence induction in five genomically heterogeneous human DMG cell lines. We identify that drugs targeting the anti-apoptotic protein Bcl-xL show a strong senolytic activity in conjunction with radiotherapy both in vitro in DMG cells and in vivo in a PDX model of H3K27M-altered DMG. Treatment with Bcl-xL inhibitor Navitoclax, or related compounds targeting Bcl-xL protein degradation or containing a galactose conjugated form of Navitoclax results in DMG cancer cell apoptosis. As several of these inhibitors are currently being tested in ongoing clinical trials against other diseases, our data support the use of Bcl-xL inhibition mediated senolytics as an adjuvant therapy to radiotherapy to potentially improve outcomes in this challenging disease setting.

cancer biology↗

bioRxiv2024

Differential control of mycobacteria among COVID-19 patients is associated with CD28+ CD8+ T cells

Diseases caused by SARS-CoV-2 and Mycobacterium tuberculosis (M.tb) represent two public health emergencies. In severe disease, both pathogens may share a biological niche in the lower respiratory tract. There is significant potential for SARS-CoV-2 and M.tb infections to be co-present within individuals and enhance or moderate the respective outcomes of either infection. Here, we investigated how whole blood samples, as well as CD4+ and CD8+ T cells, from individuals hospitalised with acute COVID-19 disease respond to mycobacterial challenge. To do this, samples were assessed by ex vivo mycobacterial growth inhibition assays, immune cell phenotyping by mass cytometry, and whole blood cytokine responses to mycobacterial antigens assessed by flow cytometry. These studies identified a subgroup of COVID-19 patients whose blood had an enhanced capacity to inhibit mycobacterial growth. The ability to control mycobacterial growth was associated with the presence of a non M.tb-specific CD28+ CD8+ T cell population, with a particular activation status and migratory phenotype. This work improves our understanding of factors involved in mycobacterial control, and may contribute to the design of novel therapies for TB.

immunology↗

bioRxiv2024

The impact of transplant location on the gut microbiome and resistome in patients undergoing hematopoietic stem cell transplantation at home versus in the hospital

ObjectivesHome-based hematopoietic stem cell transplantation (HCT) is a novel approach that has the potential to improve outcomes, however, the impact of transplant location on the gut microbiome remains uncharacterized. We hypothesized that patients randomized to undergo home HCT would have higher gut taxonomic diversity and lower antimicrobial resistance (AMR) gene abundance compared to those undergoing standard hospital HCT. MethodsWe identified 28 patients enrolled in Phase II randomized trials of home (n=16) v. hospital (n=12) HCT at Duke and performed shotgun metagenomic sequencing of stools to compare taxonomic and AMR gene composition between groups. We performed a secondary analysis of patients from each group transplanted at an outpatient infusion clinic with those who underwent standard inpatient HCT ("outpatient" v. "inpatient"). ResultsNo significant differences in duration of hospitalization were found in those randomized to home v. hospital HCT. Taxonomic and AMR gene - and {beta}-diversity were comparable. In contrast, secondary analyses demonstrated that patients from both home and hospital groups transplanted at an outpatient infusion clinic spent significantly less time in the hospital and demonstrated higher taxonomic -diversity and differential {beta}-diversity compared to standard inpatient HCT, although AMR gene -diversity did not differ, and comparisons were confounded by both differences in transplant type and use of antibiotics. ConclusionsRandomization by transplant location did not impact the gut microbiota to the same extent as the duration of hospitalization, although secondary analyses were heavily confounded. Even when taxonomic differences were observed, AMR genes were similar between groups.

microbiology↗

bioRxiv2024

Whole genome resequencing of a global collection of Napier grass (Cenchrus purpureus) to explore global population structure and QTL governing yield and feed quality traits

Napier grass (Cenchrus purpureus) is a C4 perennial grass species native to Sub-Saharan Africa (SSA), primarily used to feed cattle in SSA. In this study, we sequenced the genomes of 450 Napier grass individuals, sourced from 20 different countries. More than 170 million DNA variants (SNPs and Indels) were detected, of which [~]1% informative SNPs were used to assess genetic diversity in the collection. Our resequencing study provided valuable insights into the genetic diversity across a global Napier grass collection. Furthermore, a genome-wide association study on two independent populations, identified multiple quantitative trait loci (QTL) that were significantly associated with desirable agronomic traits, such as biomass yield, nitrogen and cellulose content. Therefore, our results will serve as a valuable resource in safeguarding and unravelling the patterns of Napier grass genetic diversity, in the face of climate change, and spearhead genomics-based breeding programs to develop high-yielding and drought-tolerant varieties suitable for forage and biofuel production.

plant biology↗