Biology subjects

Zheng, Y.

Publications and source records attributed to Zheng, Y..

At least 73 records · Page 4Linked to original sources

bioRxiv2026

BCG vaccination mitigates tau pathology and restores cognitive function in PS19 mice.

Retrospective studies in patients with non-muscle invasive bladder cancer (NMIBC) have reported a significant reduction in Alzheimers disease (AD) incidence (12-78%) among Bacillus Calmette-Guerin (BCG) recipients versus controls. To investigate the underlying mechanisms, we evaluated BCG in the PS19 mouse model of tauopathy. We found that BCG administration reduced hippocampal phospho-tau and microgliosis while preserving neuronal markers. In vivo volumetric T2-MRI demonstrated attenuation of brain atrophy accompanied by increased glutamate-weighted CEST-MRI signals. Functionally, BCG-treated mice showed improved performance in the novel object recognition test (NORT), as well as improved body-weight maintenance and survival. Transcriptomic profiling of the hippocampus revealed near complete normalization of the PS19 disease-associated gene expression signature towards that of healthy controls. Flow cytometric profiling of brain myeloid populations demonstrated a reduction in activated resident microglia, but total microglia cells remain elevated. Moreover, an increase of the co-stimulatory marker CD80 on the recruited peripheral myeloid cells ensues following BCG treatment. Consistent with this shift in myeloid state, primary brain myeloid cells from BCG-treated mice also exhibited enhanced phagocytosis of FITC-labeled tau fibrils and increased lactate production. Together, these findings indicate that BCG induces systemic and CNS myeloid cell reprogramming that limits neuroinflammation, enhances tau clearance, and rescues cognitive and neurodegenerative phenotypes in a tauopathy model. BCG is a safe, readily available therapy that merits consideration as a preventive agent against dementia. One sentence summaryBCG therapy prevents tauopathy in PS19 mouse model.

neuroscience↗

bioRxiv2026

Temporal-deviation-driven community detection uncovers early-warning signals for critical transitions in complex diseases

Early detection of critical transitions in complex diseases is crucial for timely clinical intervention. However, as patients often provide only a single snapshot, identifying sample-specific early-warning signals (EWS) from a dynamical evolution perspective remains challenging, coupled with high-dimensional noise amplification. Here, we present TD-COM, a framework for detecting personalized EWS of critical transitions via single-sample community detection. By constructing a temporal perturbation map STDN, TD-COM captures latent dynamical perturbations inferred from static individual profiles. Synergizing these temporaldeviation signals with static topological features, TD-COM implements a multilevel node filtering strategy during community detection, effectively suppressing single-sample noise. Validated on hour-scale, multi-year, and multi-decade transcriptomic data, TD-COM robustly detects critical states preceding clinical deterioration and uncovers their underlying molecular mechanisms. Comparative experiments demonstrate that TD-COM outperforms existing methods in accuracy and topological robustness. Thus, TD-COM provides a generalizable framework for personalized early warning of complex diseases, particularly when longitudinal sampling is infeasible.

bioinformatics↗

bioRxiv2026

A diagnostic plasma omics-biomarker for Alzheimer's disease informed by microglial single-cell transcriptomics: A pilot study

BackgroundThe current biomarker framework for the diagnosis and staging of Alzheimers disease (AD) relies mainly on neuropathological features; thus, its performance for diagnosis is limited prior to the initiation of neurodegeneration. Here, we leveraged transcriptomic data to develop a new framework for omic-informed blood-based diagnostic biomarkers for AD from early-stage. MethodsMicroglial gene expression from single-nucleus (sn)RNA-seq data was analyzed via 6 statistical methods to identify candidate panels of genes predictive of AD. A total of 78 gene panels, 30-2000 genes in size, were selected and evaluated for their ability to distinguish AD patients from controls. Three top-ranked panels of 300, 50 and 30 genes were transferred to blood (monocyte) transcriptomic data obtained from living subjects via a graph-based mapping approach based on optimal transport statistics. ResultsThe 300-panel method resulted in an AUC of 0.7 and moderate accuracy (75%) in classifying AD; however, the accuracy in predicting cognitively normal patients was lower (53%). While the 300 genes provided high accuracy, inspection of the distribution of p values for the gene set revealed that the panel could be greatly reduced in size to capture the most significant differences between AD patients and cognitively normal individuals. The accuracy and specificity of the 50 and 30 panels demonstrated similar AUC values but improved the balance between the prediction of AD patients and normal controls. Specifically, the 50-gene panel resulted in an AUC of 0.7, with 65% AD accuracy and 71% normal accuracy. ConclusionsIntegrating multiomics datasets into the AD biomarker discovery pipeline offers a powerful modality to increase precision and comprehensiveness in AD research and clinical applications.

genomics↗

bioRxiv2026

Lamins and lineage-relevant transcription factors coordinate gene expression in lineage development

HighlightsO_LILamin-A and lamin-B1 are essential for midgestational embryogenesis. C_LIO_LILamin-A/B1 are required for proper yolk sac endoderm (YSE) gene regulation. C_LIO_LILamin-A/B1 maintain LADs organization and chromatin interactions in YSE. C_LIO_LILamin-A/B1 and YSE transcription factors support proper YSE gene expression. C_LI Lamins are intermediate filament proteins functioning as ubiquitous structural components of the nuclear lamina that interact with and organize the Lamina-Associated chromatin Domains (LADs). LADs remodel during development and lamins maintain LADs and gene expression profile specific to a given cell type. How ubiquitous lamins achieve cell-type-specific functions during development remains unknown. We show lamin-A and -B1 are required for mouse midgestational embryogenesis and maintain LADs, 3D chromatin interactions, and gene expression in the yolk sac endoderm (YSE). Both lamin-regulated genes and remodeled LADs in YSE cells contain binding motifs of YSE-relevant transcription factors. By analyzing changes in chromatin interactions upon lamin-A and -B1 knockout, we reveal that chromatin neighborhoods maintained by these lamins can influence gene expression orchestrated by YSE-relevant transcription factors. Our findings explain how the ubiquitously expressed lamins can collaborate with lineage-relevant transcription factors to maintain LADs and gene expression programs in specific cell types.

developmental biology↗

bioRxiv2026

Imageomics defines granular morphological changes of human skin with age and reveals a rejuvenating effect of xenografting

Rejuvenating aging human skin is a major therapeutic goal, but objective, quantitative measures of intrinsic aging are limited. We performed a cross-sectional histological study of UV-protected buttock and abdominal skin in adults spanning multiple decades of life to identify features that reliably track age. Epidermal thickness measured between rete ridges was unchanged, but rete ridge size declined linearly with age: ridges became shorter and thinner in both sites, though rete ridge number decreased only in the abdomen. Consistent with these structural changes, proliferative cells (Ki67+) per ridge and expression of integrin {beta}4 (ITGB4), a putative stem-cell marker, were reduced in aged skin. We combined these biomarkers into a predictive model that estimated skin age more accurately than any single marker. To test whether the model detects longitudinal change, we analyzed aged abdominal skin before and after xenografting onto young or aged mice, a procedure previously reported to rejuvenate human skin in young but not aged recipient mice. Both individual biomarkers and the imaging model indicated rejuvenation regardless of host age; however, notably, engraftment efficiency was lower in aged hosts, with surviving grafts showing younger histological phenotypes. These results provide quantitative criteria for assessing intrinsic skin aging and suggest that the process of engraftment itself is sufficient to induce rejuvenation-like changes.

pathology↗

bioRxiv2026

LNGCN: A Distance-Aware Dynamics Network for Protein-Protein Interaction Prediction

High-throughput PPI screening requires not only interaction discrimination but also stable, calibrated scores for candidate prioritization and efficient experimental allocation. Conventional graph neural networks may over-smooth deep residue representations, reducing score separation among high-confidence candidates. We therefore developed LNGCN, a distance-aware continuous-time graph framework for experimental PPI prioritization. LNGCN integrates residue-level structural graphs with liquid neural dynamics, uses radial distance to drive continuous graph evolution, and applies hierarchical calibration to convert raw outputs into prioritization scores. It performed robustly on balanced human, 1:10 imbalanced, and cross-species yeast bench-marks. On the imbalanced dataset, the top 5% of candidates achieved 85.1% precision. LNGCN also preserved residue-level representation diversity better than conventional GCN variants. In FGF23-FGFR1c--Klotho, SHP2 signaling, Tdk1 oligomer-dependent binding, and a TPR study, it enriched known partners near the ranking top, and experimentally supported novel interactions. Overall, LNGCN enables sustained enrichment of experimentally relevant PPI candidates.

bioinformatics↗

bioRxiv2026

CREB/CRTC2-Induced GPR65 Orchestrates Th17 Metabolic Fitness and Pathogenic Effector Function

GPR65 has been shown to be a critical regulator of Th17 cell pathogenicity. Loss of GPR65 in mice results in a decrease in Th17 cells and reduced susceptibility to a mouse model of multiple sclerosis. The CREB/CRTC2 pathway has emerged as an important regulator of immune function. We have previously shown that the CREB/CRTC2 pathway modulates autoimmune disease by promoting differentiation of Th17 cells. In this study we performed RNA-seq to identify Th17 genes regulated by the CREB/CRTC2 pathway. Our RNA-seq analysis led us to uncover the first mechanism of regulation of the orphan receptor GPR65 by the CREB/CRTC2 pathway. We show that GPR65 is a target of the CREB/CRTC2 pathway through expression studies and chromatin immunoprecipitation. In addition, we show that targeting GPR65 with small molecules alters the expression of IL-17A. Understanding the regulation of GPR65 will be crucial in developing small molecules to treat patients with Th17 cell-mediated disorders.

immunology↗

bioRxiv2026

Tumor Heterogeneity Induces Pro- and Anti-metastatic Myeloid Cell Phenotypes in Breast Cancer Lung Metastasis

Metastasis is a major cause of cancer-related mortality, yet targeting metastatic cells directly has been largely unsuccessful due to their plasticity and heterogeneity. Myeloid cells play diverse pro- and anti-metastatic functions and are an attractive alternative target for treating metastasis, but how tumor heterogeneity influences myeloid cell phenotypes during metastasis remains poorly understood. Here, we profiled myeloid cells from primary tumors and matched metastatic lungs of 12 heterogeneous and differentially metastatic patient-derived xenograft models of breast cancer. Comparative analysis of cell type abundances revealed distinct myeloid remodeling specific to primary tumors or metastatic lungs. Beyond compositional differences, we identified gene expression programs that were associated with metastatic burden, such as number or size of metastatic nodules, indicating distinct microenvironmental requirements for metastatic seeding and outgrowth. Examining these metastasis-associated programs using time-course datasets, we discovered an evolution from anti- to pro-metastatic monocyte phenotypes during metastatic progression. We further showed that this phenotypic shift was driven by an increase in two distinct myeloid-derived suppressor cell signatures, and a transcriptionally regulated impairment of monocyte differentiation leading to the depletion of non-classical monocytes. Our results comprehensively dissect the heterogeneity of myeloid cell phenotypes across primary tumor and metastatic sites, opening novel avenues for myeloid-targeting therapies specific to metastasis.

cancer biology↗

bioRxiv2026

An interferon independent innate immune response to double stranded RNA in embryonic stem cells

In vertebrate early embryos and embryonic stem cells, the interferon (IFN)-centered double-stranded RNA (dsRNA) sensing and signaling pathway is markedly suppressed, implying the existence of an alternative repertoire of dsRNA sensors in these stages. We recently reported that dsRNA treatment triggers translation inhibition using Prkra as a sensor in zebrafish and mouse early embryos. Independently, here we show that dsRNA stimulates the expression of a subset of interferon-stimulated genes (ISGs) in the absence of IFN production, establishing a defensive state in mouse embryonic stem cells (mESCs). Upon dsRNA stimulation, the multifunctional DExD/H-box RNA helicase Dhx9 is recruited into dsRNA-induced condensates, where it promotes the recruitment and functional suppression of the Mdm2/Cul4A ubiquitin ligase machinery by excluding their substrate adaptor Ddb1, thereby stabilizing p53 and Stat1. Dhx9, p53 and Stat1 then cooperate to stimulate an ISG response. This signaling is important for the defense against ZIKV infection in mESCs as well as other dsRNA stresses. Such a cascade is conserved in human ESCs, while in zebrafish embryos, p53 but not Stat1 is required for the transcriptional response. Our findings define an immediate, cell-autonomous innate immune pathway operating in ESCs and vertebrate embryos.

immunology↗

bioRxiv2026

Aberrant retinal structure and vasculature in mouse models of dominant retinopathies caused by CRX homeodomain mutations

CRX is a transcription factor essential for photoreceptor differentiation and functional development. Two missense mutations in CRX homeodomain, CRXE80A and CRXK88N, are linked to early-onset dominant retinopathies. Molecular studies have revealed distinct profiles of perturbed gene expression in differentiating photoreceptors of knock-in mouse models, resulting from altered DNA binding activities of mutant CRX proteins. This study characterizes concurrent retinal and vascular alterations in knock-in mouse models. Fated cones are present in heterozygous and homozygous CrxE80A and CrxK88N mutants at birth, but subsequent cone differentiation is rapidly compromised. Expression of rod marker rhodopsin (RHO) is absent in CrxK88N/Nretinae but present in other mutants through adulthood. Notably, as compared to wildtype controls, RHO expression is prematurely activated in neonatal CrxE80A mutants. Among tested mutants, only CrxE80A/+retinae elaborate rod outer segments but still lose visual function by young adulthood. The presence of irregular retinal rosettes is a striking pathological phenotype in all mutants. Retinal rosettes displace the localization of inner neurons without affecting their cell numbers during retinal development. Retinal vessels develop close contact with rosette structures. In summary, disrupted photoreceptor differentiation leads to the loss of visual function and formation of retinal rosettes. The presence of retinal rosettes secondarily impairs the localization of inner neurons and vasculature. A deeper understanding of these cellular underpinnings will inform pathogenesis of CRX homeodomain mutations.

neuroscience↗

bioRxiv2026

OmicClaw: executable and reproducible natural-language multi-omics analysis over the unified OmicVerse ecosystem.

Advances in bulk, single-cell and spatial omics have transformed biological discovery, yet analysis remains fragmented across packages with incompatible interfaces, heterogeneous dependencies and limited workflow reproducibility. Here, we present OmicClaw, an executable natural-language framework for multi-omics analysis built on the unified OmicVerse ecosystem and the J.A.R.V.I.S. runtime. OmicVerse organizes upstream processing, preprocessing, single-cell, spatial, bulk-transcriptomic and foundation-model workflows into a shared AnnData-centered interface spanning more than 100 methods. J.A.R.V.I.S. converts this ecosystem into a bounded analytical action space through a registry-grounded, state-aware and recoverable execution layer that validates prerequisites, preserves provenance and supports iterative repair, while enabling conversational, notebook and visual interfaces to operate over the same live analytical state. Rather than relying on unconstrained code generation, OmicClaw translates user requests into traceable workflows over live omics objects. Across a benchmark of 15 tasks spanning scRNA-seq, spatial transcriptomics, RNA velocity, scATAC-seq, CITE-seq and multiome analysis, ov.Agent improved rubric-based performance over bare one-shot large language model baselines, particularly for long-horizon multi-step workflows. OmicClaw further supports external agent access through an MCP-compatible server and a beginner-friendly web platform for interactive analysis, code execution and million-scale visualization. Together, OmicClaw provides a practical foundation for reproducible human-AI collaboration in modern multi-omics research

bioinformatics↗

bioRxiv2026

Reconstructing biologically coherent cellular profiles from imaging-based spatial transcriptomics

In imaging-based spatial transcriptomics, transcript-to-cell assignment shapes downstream biological interpretation including cell typing, ligand-receptor inference, and niche characterization. However, two-dimensional segmentation of volumetric tissue often yields mixed cellular profiles, while cells without detected nuclei are missed entirely, distorting the aforementioned downstream analyses. We present TRACER, which refines cellular representations in imaging-based transcriptomics by leveraging gene-gene coherence and spatial co-localization of transcripts observed directly in the data, without requiring external annotations or reference atlases. TRACER resolves mixed cellular profiles and reconstructs partial cells whose nuclei are not detected, enabling more complete representation of cells within the tissue section. We also introduce coherence-based metrics that quantify transcriptional purity and conflict, enabling platform-agnostic benchmarking of segmentation quality. Across diverse platforms, tissues, and segmentation methodologies, TRACER consistently and reproducibly improves the coherence of cellular profiles and the quality of downstream analyses.

systems biology↗

bioRxiv2026

Synora: vector-based boundary detection for spatial omics

Tumor-stroma boundaries are critical microenvironmental niches where malignant and non-malignant cells exchange signals that shape invasion, immune modulation and therapeutic response. Spatial omics platforms now resolve these interfaces at single-cell scale, but computational boundary detection remains challenging because heterogeneous neighborhoods can arise either from true compartment interfaces or from unstructured immune infiltration. Here we present Synora, a modality-agnostic computational framework that identifies tumor boundaries using only cell coordinates and binary tumor/non-tumor annotations, making it readily applicable across a broad range of spatial omics modalities. Synora introduces orientedness, a novel metric that quantifies directional neighborhood asymmetry and distinguishes true boundary cells, where neighbors are spatially segregated by type, from infiltrated regions where cell types intermingle randomly. By integrating orientedness with traditional diversity measures into a unified BoundaryScore, Synora achieves robust boundary identification across synthetic datasets with ground-truth boundaries, maintaining performance under realistic perturbations including 50% missing cells and 25% infiltration. Application to 15 Visium HD spatial transcriptomic datasets across multiple cancer types reveals consistent boundary-enriched gene signatures and cell-type spatial gradients. Validation on a CODEX multiplexed protein dataset demonstrates that Synoras precise boundary identification enables discovery of clinically relevant cellular neighborhoods and disease-associated spatial patterns missed by frequency-based approaches. Synora enables boundary-aware spatial analyses by making tissue interfaces quantifiable from minimal inputs, helping to standardize interface detection and comparison across spatial omics platforms and biological contexts.

bioinformatics↗

bioRxiv2026

Microhomology-Mediated Tandem Duplication Drives Tandem Repeat Formation Across Life

Tandem repeats (TR) are common genomic elements that are highly variable and with major functional consequences. Yet, the evolutionary trajectory for their formation remains poorly understood. One proposed mechanism is microhomology-mediated tandem duplication (MTD), in which single-copy DNA segments flanked by microhomology undergo tandem duplication (TD) and can further expand into TRs. Although MTD was first identified in the fission yeast Schizosaccharomyces pombe, its universal occurrence and postulated role in TR evolution have not been established. Using whole-genome deep sequencing and new analytical tools, we show that MTDs occur de novo universally across bacteria, archaea, fungi, and viruses. Further analysis of 2,245 reference genomes and millions of isolate genomes from 103 prokaryotic and eukaryotic microbial species, combined with human population TD data, somatic-germline mutations, and disease-associated variants, reveals that MTDs are consistently the dominant TD-forming mechanism across domains of life. Evidence suggests that MTDs have initiated the formation of the majority of existing TRs in genomes. Importantly, MTDs also prevail in human pathogenic TR mutations, including those linked to cancers. Mechanistically, deletion of the conserved mutator gene Rad27 specifically increased de novo MTD frequency in the budding yeast Saccharomyces cerevisiae, implicating Rad27-mediated Okazaki fragment maturation in MTD formation. These findings establish MTD as a universal and functionally significant mechanism for TR genesis. Graphic abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=121 SRC="FIGDIR/small/708716v1_ufig1.gif" ALT="Figure 1"> View larger version (37K): org.highwire.dtl.DTLVardef@db9ff1org.highwire.dtl.DTLVardef@e1a14corg.highwire.dtl.DTLVardef@124be79org.highwire.dtl.DTLVardef@15531ea_HPS_FORMAT_FIGEXP M_FIG C_FIG Significance StatementMicrohomology-mediated tandem duplications (MTDs) represent a universal mechanism driving tandem repeat formation across all domains of life--from viruses to humans. These duplications initiate genome evolution by expanding into functional tandem repeats and are the predominant form of pathogenic tandem duplications in human cancers and heritable disorders. Critically, disruption of the conserved Okazaki fragment processing pathway promotes MTD formation, establishing a fundamental link between DNA replication fidelity and genomic plasticity.

microbiology↗

bioRxiv2026

Spatial correspondences of Audiovisual Stimuli on Double Flash Illusion Perception and its Cognitive Modeling

Perceptual processing integrates information from multiple sensory modalities to form a coherent representation of the environment. A classic example of such is the Sound-Induced Flash Illusion (SIFI), where the perceived number of visual flashes is altered by conflicting auditory stimuli. While the SIFI is a well-established phenomenon of multisensory integration, the influence of physical spatial characteristics--specifically stimulus eccentricity and spatial congruence--on integration levels remains debated.To address this gap, this study used the SIFI paradigm to investigate the effect of visual stimulus spatial location and the spatial congruence between auditory and visual stimuli on audiovisual integration. In Experiments 1 and 2, we found that when spatial attention was controlled via cueing, unimodal visual performance remained consistent across locations. However, the susceptibility to SIFI increased progressively from the central to the peripheral visual field, exhibiting a spatial pattern of Gaussian distribution. Bayesian modeling further supported this by showing that this spatial modulation was driven by an increase in the integration weight assigned audiovisual representations in the periphery, rather than changes in sensory uncertainty alone. Conversely, Experiment 3 demonstrated that the spatial congruence of audiovisual stimuli did not affect the SIFI or alter the integration processing. These findings refine our current understanding of the spatial modulation upon audiovisual integration. By incorporating the visual systems spatial properties into a Bayesian framework, we provide a computational explanation for the eccentricity-dependent nature of multisensory integration.

neuroscience↗

bioRxiv2026

Genomic insights into rapid diversification and adaptive introgression in the earthworm Amynthas aspergillum

How species diversify in highly fragmented landscapes while maintaining genetic connectivity remains a central question in evolutionary biology. The megascolecid earthworm Amynthas aspergillum exemplifies this paradox, showing deeply divergent mitochondrial lineages despite extensive nuclear gene flow across southern China. We conducted whole-genome resequencing across its core distribution in the Guangxi karst region to elucidate the population structure and processes underlying this cytonuclear discordance. Genome-wide analyses identified three genetically distinct groups shaped by fine-scale karst isolation, alongside pervasive historical and contemporary introgression. Demographic modeling revealed rapid diversification during the Late Pleistocene ([~]0.14LJMa) with pronounced fluctuations in effective population size. Although isolation increased inbreeding and mutational load in some lineages, introgression persisted even among deeply divergent mitochondrial clades. Notably, several introgressed regions showed strong signatures of positive selection, including genes involved in mitochondrial function and metabolism.Together, these results demonstrate that gene flow can simultaneously mitigate the genomic costs of isolation and promote functional innovation via adaptive introgression, providing a genomic framework for diversification with gene flow in subterranean invertebrates inhabiting fragmented karst landscapes.

genomics↗

bioRxiv2026

A novel uN2CpolyG Transgenic Mouse Model Recapitulates Multisystemic polyG Proteinopathy Pathology of Neuronal Intranuclear Inclusion Disease

Neuronal intranuclear inclusion disease (NIID) is a polyglycine disease that primarily affects the neuronal and neuromuscular systems. Here, we developed a novel transgenic mouse model that faithfully recapitulates the multisystemic impairments associated with polyG intranuclear inclusions. Our findings demonstrate that polyG expression induces neurodegeneration, behavioral deficits, and age-dependent accumulation of uN2CpolyG aggregates across multiple tissues.

animal behavior and cognition↗

bioRxiv2026

Ancient DNA reveals early use of melons in China's Song Dynasty

Melon (Cucumis melo L.) domestication is thought to have occurred independently once in Northeast Africa and twice in India, but archaeobotanical seed remains point to a possible additional domestication in China. Because Cucumis seeds are difficult to diagnose morphologically, genomic data from archaeological material are needed to evaluate these scenarios and reconstruct ancient melon traits. We sequenced two Song Dynasty melon seeds from Shuomen Gugang (China), recovering 4.6x and 1.7x nuclear genome coverage. Nuclear and chloroplast analyses place both seeds within cultivated C. melo from China, supporting introduction from the broader Asian domestication pool rather than independent Chinese domestication. To assess whether these seeds carried traits associated with sweet dessert melons, we examined loci underlying fruit phenotypes. Neither seed carried alleles for orange flesh; one harbored an allele linked to yellow/orange peel, the other possessed alleles associated with green flesh and reduced acidity. Since wild melons are monoecious, the presence of the derived andromonoecy allele in one seed, associated with rounder fruit shape, suggests early selection on fruit morphology. Together, these findings indicate that Song Dynasty melons were likely consumed as fresh or culinary fruits rather than as sweet dessert melons. Their flesh coloration resonates with Song-period aesthetic sensibilities, exemplified by jade-green celadon ceramics frequently crafted in melon-shaped forms. By anchoring East Asian archaeobotanical remains within modern melon genomic variation, this study provides a temporal framework for melon dispersal into China and shows how ancient genomics can illuminate past crop use.

evolutionary biology↗