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Biology subjects

Lin, Z.

Publications and source records attributed to Lin, Z..

At least 19 recordsLinked to original sources

Representation learning of somatic missense mutation landscapes across cancer types

Somatic missense mutations are pervasive in cancer genomes, yet existing studies have largely compressed them into mutation burden, mutation signatures, or driver gene annotations. Such representations obscure mutation-specific context and higher-order dependencies, leaving the latent biological structure of somatic mutation landscapes insufficiently characterized by systematic, data-driven approaches. Here we present MMRL, a pan-cancer Missense Mutation Representation Learning framework that learns the representations directly from somatic missense mutation profiles. By integrating mutation-associated features including gene identity, trinucleotide context, AlphaMissense pathogenicity, amino acid substitution and protein positional information, MMRL uses self-supervised learning to capture higher-order patterns among missense mutations across ~50,000 tumor samples from diverse cancer types. Across three pan-cancer cohorts, MMRL embeddings consistently achieved higher cross-validated prognostic discrimination than TMB and remained significantly associated with overall survival after adjustment for cancer type and TMB, as well as age where available. This prognostic value was also observed among patients treated with immune checkpoint inhibitors. Unsupervised clustering analysis of MMRL embeddings identified nine mutation subtypes in the TCGA pan-cancer cohort, with distinct survival outcomes, cancer-type compositions and mutational signature profiles, indicating that the learned embedding space captured clinically and biologically meaningful structure. Attention-based analyses further indicated that MMRL captured context-dependent mutation patterns beyond mutation frequency and predicted pathogenicity. Together, MMRL provides a data-driven strategy for decoding somatic missense mutation landscape and may facilitate precision oncology.

bioinformatics↗

Spatialsnake: a flexible workflow for spatial transcriptomics analysis across platforms

Background: Spatial transcriptomics technologies measure gene expression at different spatial resolutions and generate diverse data outputs. Existing workflows support a range of platforms and analyses, but combining methods and extending analyses to selected populations or tissue regions can require additional scripts and repeated data preparation. Findings: We developed Spatialsnake, a flexible workflow built on SpatialData and Snakemake for analysing processed outputs from Visium, Visium HD, Stereo-seq, Xenium and MERFISH. A common command-line interface supports single- and multi-sample analysis, with adjustable parameters and saved intermediate results. Users can select populations, tissue regions or distance-based neighborhoods, repeat clustering and annotation, and map refined labels back to the full dataset. Additional modules support cell-type composition estimation, spatial-domain identification, cell-cell communication inference, regulon analysis and sample-level comparisons. We demonstrate these functions using mouse-brain Visium and colorectal cancer Visium HD datasets. Joint analysis of three colorectal cancer sections retained 1,527,987 bins and enabled further analysis of 223,632 epithelial bins, linking epithelial subpopulation annotations to their locations within the complete tissue. Conclusions: Spatialsnake provides a unified workflow for spatial transcriptomics analysis across sequencing- and imaging-based platforms. Its flexible analysis modules support both whole-tissue analysis and further investigation of selected cell populations and tissue regions.

bioinformatics↗

Epstein-Barr Virus in HIV-Associated Conjunctival Squamous Cell Carcinoma and Transcriptional Reprogramming of Conjunctival Epithelial Cells

The involvement of Epstein-Barr virus (EBV) in conjunctival squamous cell carcinoma (cSCC) remains incompletely defined. This study integrated analyses of primary tumors with an experimental model of the conjunctival epithelium. Five Nigerian tumors from patients with HIV and three Japanese tumors from patients without HIV were examined by EBV-encoded RNA in situ hybridization (EBER-ISH), EBV DNA PCR, and virome analysis of RNA sequencing data. EBER localized to epithelial tumor cells in four Nigerian specimens and none of the Japanese specimens. EBV DNA and RNA were each detected in three Nigerian tumors, with every EBER-positive tumor supported by at least one additional assay. Human telomerase reverse transcriptase-immortalized conjunctival epithelial cells infected with Akata-GFP-EBV expressed latency-associated and lytic viral genes. Comparison of three infected and three control cultures identified 96 differentially expressed host genes and 23 enriched Hallmark gene sets at a false discovery rate below 0.05. RT-qPCR confirmed increased HES1, CXCL8, CXCL2, and LOX and decreased FGFBP1, CSTA, SAPCD2, and TMEM40 expression. Prominent responses involved inflammatory signaling, epithelial remodeling, metabolism, and cell-cycle regulation. These findings identify tumor-cell-associated EBV in a subset of HIV-associated cSCC and establish an epithelial model for investigating infection-associated host responses.

microbiology↗

Cortex-wide single-cell activity mapping in freely moving mice

How the cortex supports complex, naturalistic behavior can be revealed only in freely moving animals. Although head-mounted microscopes promise access to the neural dynamics underlying such behavior, fundamental trade-offs among field of view, spatial resolution, device weight, and background contamination have prevented cortex-wide single-neuron recording, leaving distributed cortical coordination largely inaccessible. To meet these challenges, we introduce COMET (Cortex-wide Observational Miniature Epifluorescence Technique), a 3.75-g head-mounted mesoscope that integrates an aberration-controlled wide-field optical design, uniform high-efficiency excitation and single-coaxial power-and-data transmission with an end-to-end denoising and signal-extraction pipeline. This enables cortex-wide calcium imaging at single-cell resolution in freely moving mice. COMET captures activity from >15,000 layer 2/3 neurons per 5-min recording over fields of view up to 10 mm in diameter while preserving natural behavior. Benchmarking against benchtop two-photon microscopy demonstrates high spatial concordance of detected neurons and matched event-level calcium dynamics. We apply COMET to social interaction to quantify region-specific engagement and to an auditory trace fear-conditioning task that requires natural movement and behavioral expression, revealing time-ordered changes in regional firing-rate structure and functional connectivity preceding a global conditioned response. COMET provides an open, lightweight hardware-software framework for linking single-neuron activity to cortex-scale network dynamics during freely expressed behaviors under changing internal or external conditions.

neuroscience↗

High-throughput in vivo DNA data encoding by multiplexed conjugationand orthogonal base editing

Bacterial conjugation and CRISPR base editing offer complementary routes for programmable DNA transfer and heritable genomic writing, but their combined potential for information encoding in living cells remains unexplored. Here, we introduce CONCORD, a bacterial encoding platform that couples multiplexed bacterial conjugation to genomic base editing for synthesis-free in vivo DNA data writing. A recipient Writer strain expresses the base-editing machinery and is equipped with a writing template, whereas reusable donor Guide strains deliver the encoding sgRNA signals by conjugation. Using this setup, we encode binary information into genomic DNA in a high-throughput manner. Moreover, we systematically evaluated multiple orthogonal base editors for an expanded encoding repertoire and improved data recovery through redundancy encoding. We deploy the system to encode 45,689 bits into DNA including two culturally and historically significant artifacts: a greeting from NASA's Voyager Golden Record and a photograph of Navajo petroglyphs and recovered these datasets with 100% and 99.5% accuracy, respectively, without computational error correction. Connecting and engineering the unique mating and immune system of microbial cells we have established a framework for programmable information writing in bacterial populations, with applications for biological event recording and sustainable DNA data storage.

synthetic biology↗

Stress-recovery dynamics reveal a separatrix in transcriptomic landscapes across organs and aging

Aging is often characterized statically as molecular profiles, but how these profiles may affect the capacity of systems to respond to the external environment remains elusive. We perturbed young and aged mice via transient sleep deprivation and profiled transcriptomes from six organs immediately after stress and following recovery. The same perturbation induced complex temporal dynamics for each gene in an organ- and age- dependent manner. A shape parameter distinguished genes that recovered toward control expression from those that continued to drift away during recovery. Transcriptomic vector fields were inferred from these transitions using neural ordinary differential equations, revealing distinct stability regimes across organ systems. Interestingly, that of testis from the young mice contained a separatrix bounding the region within which perturbed state can return toward control. These findings establish transient perturbation and recovery as a framework for probing age-dependent transcriptomic stability and identifying boundaries that determine whether a perturbed system can return.

systems biology↗

OmicsResonance: An LLM-assisted cloud ecosystem for interactiveand reproducible single-cell transcriptomic analysis

While single-cell RNA sequencing (scRNA-seq) is indispensable, existing analytical tools impose high computational barriers, requiring complex environment configurations and programming proficiency. To democratize single-cell analysis, we developed OmicsResonance, a code-free, web-based platform that eliminates local installations and empowers researchers to execute end-to-end analyses directly within a browser. The platform integrates standard processing pipelines and Large Language Model (LLM)-assisted cell annotation with a suite of advanced modules, including pseudo-time inference, CNV profiling, and virtual knockout simulations. Built on a scalable architecture, OmicsResonance champions "justified analysis" by avoiding black-box defaults. Its interactive interface allows users to dynamically adjust parameters and instantly visualize biological impacts, ensuring transparent and biologically sound analytical decisions. Validation across three public datasets successfully reproduced established findings and facilitated further interpretation of the data. Ultimately, OmicsResonance bridges the gap between complex computational pipelines and bench research, providing an accessible yet powerful environment for scRNA-seq data exploration. The platform is available at https://cloud.rnastar.com/.

bioinformatics↗

Regulatory-scale stripe analysis from single-cell Hi-C with scStripe

Chromatin stripes are a directional architectural feature of three-dimensional genome organization, but their analysis in single-cell Hi-C (scHi-C) at regulatory resolution is hindered by extreme sparsity. We developed scStripe, an imputation-free two-stage statistical framework that detects stripes from sparse cell-type--aggregated scHi-C maps and directly quantifies the resulting aggregate-defined stripes in raw individual-cell contact maps using per-cell stripe scores. Across three complementary benchmark settings, scStripe achieved the highest F1 scores and showed strong aggregate stripe enrichment, while the detected stripes recapitulated characteristic structural and regulatory features reported in bulk data. Per-cell stripe scores resolved recurrent configurations of the EBF1-anchored stripe, captured genome-wide variation associated with cell type, cell-cycle phase, and developmental stage, and identified positively associated gene--stripe pairs with pronounced cell-type specificity using matched scRNA-seq. Together, scStripe provides a practical, scalable framework for regulatory-scale stripe analysis across single cells without requiring single-cell enhancement or 3D reconstruction.

genetics↗

Exploratory profiling of defense system signatures in Klebsiella pneumoniae clonal populations

Bacterial defense systems against bacteriophages are critical for bacterial genome stability and fitness, yet their distribution and epidemiological relevance in Klebsiella pneumoniae remain unexplored. We aimed to characterize defense system signatures across major K. pneumoniae clonal lineages and evaluate their utility as genomic signatures for tracking clonal dissemination. Here, we analyzed 6,346 genomes to characterize population structure, defense system signatures, and their coevolution with resistance determinants and plasmid backbones. PopPUNK clustering resolved 146 lineages that stratified into major clonal lineages (G-ST-KL combinations) with distinct resistance and virulence profiles. DefenseFinder and PADLOC identified 320 distinct defense systems, revealing that each clonal lineage harbors a unique defensotype characterized by systematic module replacement rather than stochastic gene loss. Co-occurrence networks further showed that these systems are organized into lineage-specific functional modules, with contrasting architectures even among lineages sharing the same sequence type. Integration of defense, resistance, and plasmid data uncovered strong lineage-specific associations, whereby broad-host-range plasmid backbones acquired distinct defense-resistance payloads in different clonal backgrounds. Geographic and host-niche analyses demonstrated that defense system distribution reflects clonal lineage expansion rather than independent geographic selection, and analysis of 689 Chinese genomes confirmed vertical inheritance of lineage-specific signatures along transmission chains. Collectively, defense systems in K. pneumoniae are organized into lineage-specific defensotypes shaped by synergistic modules and clonal evolutionary dynamics. Defense system profiling provides an additional layer of epidemiological resolution beyond conventional typing and offers practical utility for genomic surveillance, particularly in resource-limited settings where PCR-based detection of conserved systems could serve as a rapid proxy for identifying high-risk K. pneumoniae clones.

bioinformatics↗

Protein Phosphatase 2A Activation Attenuates Acute Myocardial Injury in Takotsubo Syndrome by Modulating Ferroptosis and Mitochondrial Injury in Cardiomyocytes

BackgroundTakotsubo syndrome (TTS) is an acute stress-induced cardiomyopathy characterized by transient left ventricular dysfunction. Despite its reversible nature, TTS is associated with substantial morbidity and mortality in the acute phase, and no specific treatments are available. The precise molecular mechanisms that connect catecholamine stress to reversible myocardial injury are not fully understood. PP2A, a holoenzyme with serine/threonine phosphatase activity, plays a vital role in normal cardiac development, and its dysregulation has been associated with heart disease. Its role in TTS and its potential as a therapeutic target remain completely unknown. MethodsAnalysis of public multi-omics datasets from stress cardiomyopathy (SCM) and experimental models of TTS, along with treatment of cardiomyocytes with human TTS plasma, was used to investigate a potential role for protein phosphatase 2A (PP2A) in stress-induced myocardial injury. To clarify the functional impact of manipulating PP2A activity in TTS, we used a series of disease relevant cell based and in vivo models, leveraging both genetic and pharmacological approaches to modulate PP2A activity in cardiomyocytes and in mice. To gain mechanistic insights into how PP2A influences TTS pathology and downstream signaling pathways, RNA sequencing, stress-responsive iron handling, mitochondrial function, and cardiac phenotypes were thoroughly evaluated in both in vivo and in vitro studies. ResultsPP2A activity was markedly reduced in cardiac tissues from mice with isoprenaline-induced TTS, as well as in isoprenaline-treated cardiomyocytes. Genetic or pharmacological inhibition of PP2A worsened catecholamine-induced cardiac dysfunction and myocardial injury. Most notably, pharmacological activation of PP2A using an orally bioavailable small-molecule activator strongly mitigated myocardial damage and enhanced cardiac function in TTS models. Mechanistically, PP2A inactivation promoted JNK-MAPK signaling and dysregulated stress-responsive iron-handling pathways, leading to ferritinophagy-mediated ferroptosis and mitochondrial dysfunction. Pharmacological JNK inhibition effectively rescued myocardial injury caused by PP2A deficiency in two TTS animal models and in cardiomyocytes. ConclusionsPP2A inactivation is a key molecular event linking catecholamine stress to myocardial injury in TTS. Restoring PP2A activity or inhibiting downstream JNK attenuates ferritinophagy-dependent stress responses and mitochondrial dysfunction, providing a unifying mechanistic framework and highlighting the PP2A-JNK axis as a potential target for short-term intervention during the acute phase of TTS. CLINICAL PERSPECTIVEO_ST_ABSWhat Is New?C_ST_ABS* Protein phosphatase 2A (PP2A) activity is acutely suppressed during the early phase of Takotsubo syndrome (TTS), with preferential involvement of the apical myocardium, closely mirroring the diseases characteristic clinical phenotype. * Downstream of PP2A inactivation, catecholamine stress triggers JNK-MAPK signaling activation and dysregulated stress-responsive iron handling, including ferritinophagy-mediated ferroptosis and mitochondrial dysfunction in cardiomyocytes. * Pharmacological restoration of PP2A activity or downstream inhibition of JNK mitigates acute myocardial injury and preserves cardiac function, thereby establishing the PP2A-JNK axis as a central stress-responsive pathway in TTS. What Are the Clinical Implications?* Identification of PP2A inactivation as a key molecular event highlights a novel opportunity for targeted intervention during the acute phase. * Studies in preclinical animal TTS models provide the first evidence that illuminates the therapeutic potential of a small-molecule PP2A activator as a strategy for acute TTS and may serve as a broad cardioprotective strategy in settings where cardiac dysfunction is implicated. * Targeting downstream JNK signaling, which is activated by PP2A inactivation, emerges as an additional mechanism-based strategy for attenuating acute myocardial injury in TTS.

molecular biology↗

Targeting NAT10 suppresses TFH responses and alleviates allergic asthma via an ac4C-TOX2 axis

Chemical modifications of RNA, such as N4-acetylcytidine (acC), fine-tune gene expression, but their roles in cell fate determination within the immune system remain poorly understood. Here, we identify the RNA cytidine acetyltransferase NAT10 as a pivotal regulator of T follicular helper (TFH) cell differentiation and the germinal centre response. T cell-specific ablation of Nat10 in mice severely impaired TFH cell development, germinal centre formation, and antibody production following viral infection. Integrated epitranscriptomic and transcriptional profiling revealed that NAT10 deposits acC modifications on a cohort of mRNAs critical for immune function. We pinpointed the transcription factor TOX2 as a key downstream target, showing that acC modification within its mRNA coding sequence enhances both transcript stability and translation efficiency, thereby promoting TOX2 protein expression. Enforced TOX2 expression fully rescued the TFH differentiation defect in NAT10-deficient cells. This NAT10-acC-TOX2 axis is conserved in humans, where its activity correlates with the magnitude of vaccine-elicited TFH responses. Furthermore, we identified R428 as a potent NAT10 inhibitor and demonstrated that its administration could suppress pathogenic TFH responses and alleviate symptoms in a mouse model of allergic asthma. Our work elucidates a central epitranscriptomic mechanism controlling T helper cell fate and humoral immunity, and nominates NAT10 as a potential therapeutic target for TFH-driven diseases.

immunology↗

A de novo designed enzyme for photo-proximity labeling of E3 ligase neighborhoods in live cells

Photocatalytic proximity labeling proteomics (photo-PLP) has emerged as a powerful technology for rapid capture of protein interactomes in situ. Typically, photo-PLP relies on chemical conjugation of the photocatalyst to the target of interest which creates practical challenges for derivatized photocatalyst synthesis and bioconjugation specificity. Integrating the precision of genetically encodable enzymes with the versatility of chemically defined photocatalysts provides a modular approach to further expand the scope of neighborhood mapping. Here, we present EYClamp, a de novo designed proximity labeling enzyme harnessing the off-the-shelf photocatalyst Eosin Y (EY) as a cofactor. Using a domain-swapped dimer architecture, we designed a scaffold that binds EY with high affinity (Kd = 10 nM) and lengthens its triplet excited-state lifetime by 29-fold. EYClamp enables efficient, multi-scale photocatalytic proximity labeling in live cells with aryl-diazirine-, aryl-azide- and phenol-biotin. We genetically fused EYClamp to a panel of six important E3 ligases. Using EYClamp, we identified over 1,500 candidate neighbors for KEAP1, MDM2, ASB7 and STUB1, providing a broad and unbiased view of these important neighborhoods. Critical functional networks were revealed including ASB7 engagement with HP1a/CUL5 complex for heterochromatin remodeling. Our EYClamp provides a genetically encodable "plug-and-play" solution for photo-PLP interactome discovery of the large family of E3 ligases and establishes domain-swapping as a promising strategy for de novo photoenzyme design.

biochemistry↗

FoxO3a and miR-34a-3p Are Involved in Oxidative Stress-Induced Dysfunction of Human Endothelial Progenitor Cells

BackgroundEndothelial progenitor cells (EPCs) contribute to endothelial repair and neovascularization, and EPC dysfunction is closely associated with oxidative stress-related vascular injury. Forkhead box O3a (FoxO3a) regulates cellular stress responses, whereas miR-34a has been implicated in endothelial dysfunction, senescence, and apoptosis. However, the relationship between FoxO3a and miR-34a-3p in oxidatively injured EPCs remains incompletely defined. ObjectiveThis study investigated the role of FoxO3a in H2O2-induced EPC dysfunction and examined whether miR-34a-3p directly interacts with the FoxO3a 3' untranslated region (3'UTR). MethodsHuman umbilical cord blood-derived EPCs were identified by DiI-ac-LDL uptake, FITC-UEA-1 binding, and the expression of EPC-related markers. Oxidative stress was induced by H2O2. Cell viability, apoptosis, and angiogenic capacity were evaluated using CCK-8 assay, Annexin V/7-AAD flow cytometry, and Matrigel tube formation assay, respectively. FoxO3a expression was modulated using adenoviral overexpression or knockdown vectors, and miR-34a was modulated using mimics or antagomir. FoxO3a and miR-34a expression levels were detected by Western blot and qPCR. A dual-luciferase reporter assay was used to verify the interaction between hsa-miR-34a-3p and the FoxO3a 3'UTR. ResultsH2O2 reduced EPC viability, increased apoptosis, and impaired tube formation in a concentration-dependent manner. H2O2 increased FoxO3a protein abundance and miR-34a expression, whereas FoxO3a mRNA did not change markedly. FoxO3a overexpression aggravated, whereas FoxO3a knockdown partially alleviated, H2O2-induced EPC dysfunction. Similarly, miR-34a mimics further suppressed EPC viability and tube formation, while miR-34a antagomir exerted a protective effect. Dual-luciferase reporter analysis showed that hsa-miR-34a-3p significantly reduced the activity of the wild-type FoxO3a 3'UTR reporter, while mutation of the predicted binding site abolished this suppression. ConclusionFoxO3a and miR-34a participate in oxidative stress-induced EPC dysfunction. The dual-luciferase data demonstrate that hsa-miR-34a-3p directly targets the FoxO3a 3'UTR, suggesting the presence of miR-34a-3p-mediated post-transcriptional feedback within the FoxO3a-related stress-response network in EPCs.

biochemistry↗

Paralogous lncRNAs CYTOR and MORRBID share a conserved trans acting function in MEK ERK signaling

Background: Long non-coding RNAs (lncRNAs) exhibit rapid evolutionary turnover, often driven by genomic duplication. How paralogous lncRNAs maintain, partition, or diverge in function across distinct genomic contexts remains poorly understood. The evolutionarily conserved lncRNA MORRBID and its primate-specific paralog CYTOR provide a natural framework to interrogate the functional consequences of lncRNA duplication. Results: Although CYTOR and MORRBID have acquired distinct transcript variants influenced by their divergent genomic environments, we demonstrate that they maintain a robust, shared core function encoded by near-identical dominant two-exon transcripts. Using SNP-based paralog-specific quantification, we found that CYTOR contributes more strongly to the shared transcript pool, while both transcripts localize predominantly to the cytoplasm, consistent with a shared trans-acting function. Simultaneous repression of CYTOR and MORRBID consistently impairs cell adhesion and migration across multiple cancer models. Mechanistically, the shared CYTOR/MORRBID transcript pool associates with MEK2 and sustains MEK-ERK signaling. This signaling axis promotes FOSL1 expression and AP-1-linked transcriptional output, including expression of the downstream effector EPHA4, whose role was supported by rescue experiments. Patient tumor transcriptomes and healthy single-cell datasets further supported the associated mesenchymal, adhesion, and epithelial-mesenchymal transition program. Conclusions: Our findings establish that paralogous lncRNAs can retain a conserved mechanistic core despite context-dependent transcriptional divergence. The CYTOR/MORRBID transcript pool defines a shared lncRNA signaling module that supports MAPK-ERK signaling and adhesion-migration programs across cancer and mesenchymal-like cellular contexts. This defines a unified mechanistic framework for the shared core function of these widely studied paralogous lncRNAs.

genetics↗

Symptomatic human norovirus infection in zebrafish embryos uncovers neural infection and extracellular vesicle-mediated transmission dynamics

Human norovirus (hNoV) is the leading global cause of acute gastroenteritis, imposing a substantial health and economic burden worldwide. Progress in understanding hNoV pathogenesis has been hindered by the lack of tractable small-animal models that recapitulate symptomatic infection. Although zebrafish larvae support hNoV replication, infection remains asymptomatic, limiting their utility for studying disease mechanisms and host-pathogen interactions. In this study, we report that the zebrafish embryo infection model, in which microinjection of hNoV at the early cell stage, resulted in robust systemic viral replication accompanied by overt pathological manifestations, including pericardial and renal edema, yolk and cranial opacity, and mortality by 3 days post-infection. Disease severity displayed marked individual variability and correlated closely with viral burden. Integrated multi-omics analyses, including bulk transcriptomics, untargeted metabolomics, and single-cell RNA sequencing, demonstrated that embryonic infection elicits a stronger and more coordinated antiviral response than larval-stage infection, while enabling widespread viral dissemination across diverse cell lineages. Approximately two-thirds of infected cells were derived from the nervous system or neural crest lineages, providing a potential mechanistic basis for the neurological complications occasionally reported in hNoV-infected patients. Furthermore, we identified a developmental stage-dependent role for extracellular vesicle (EV)-associated hNoV transmission: free virions mediated more efficient infection and higher symptomatic incidence in immunologically immature embryos, whereas EV-associated virions exhibited enhanced infectivity in more immunocompetent larvae. Together, these findings establish the zebrafish embryo as a versatile and accessible in vivo platform for studying symptomatic hNoV infection, reveal host maturity-dependent viral transmission strategies, and provide new opportunities for mechanistic studies and high-throughput evaluation of antiviral and vaccine candidates. Author summaryHuman norovirus is the leading cause of stomach flu worldwide but studying it has been difficult because the lack of a simple, small-animal model that actually gets sick from the virus. While older zebrafish larvae can harbor the virus, they do not show symptoms. In this study, we successfully created a new model by injecting human norovirus into zebrafish embryos at their early cell stage. Unlike the older larvae, these embryos developed clear symptoms, including fluid buildup around the heart and kidneys, tissue cloudiness, and death within three days. Using advanced genetic and metabolic tracking, we discovered that the virus spreads widely throughout the embryos body, particularly targeting cells in the nervous system. This link might explain why human patients occasionally suffer from neurological symptoms. Additionally, our study revealed that the virus changes its transmission strategy based on the animals age: it travels freely to infect vulnerable embryos but hides inside lipid vesicles to infect older, more immune-developed larvae. Ultimately, these findings provide a practical, efficient animal model to better understand norovirus sickness and rapidly test new vaccines and treatments.

microbiology↗

OmicOS: A Comprehensive Omics Ecosystem Infrastructure and Agent System for the AI Era

Biology has accumulated a vast ecosystem of omics methods, but much of this ecosystem remains built for expert humans rather than scientific agents. Methods are scattered across Python packages, R/Bioconductor and CRAN workflows, command-line tools, incompatible data containers and implicit object states, making even routine analyses difficult for an AI system to choose, execute and verify reliably. Here we introduce OmicOS, a comprehensive omics ecosystem infrastructure and agent system that turns OmicVerse V2, an open-source omics community, into an executable foundation for agentic biology. OmicVerse V2 provides the community substrate: scalable AnnDataOOM-compatible rust backends, agent-friendly Python algorithms for single-cell, spatial, bulk and multi-omics analysis, interfaces to single-cell foundation models, and Python-native reconstructions of historically R-centred Bioconductor/CRAN-style workflows. OmicOS makes this substrate actionable by registering analytical functions as state-aware capability contracts, allowing agents to inspect live data objects, select valid methods, execute controlled workflows and record provenance. The result is not a fixed pipeline, but a programmable omics environment in which agents compose real analyses from verified community methods rather than inventing tools. Across external and purpose-built benchmarks, OmicOS ranked first among the evaluated systems, reaching 81.2% on BiomniBench. Adding OmicVerse to a minimal agent improved task completion by up to 34.2 percentage points with qwen-3.6-35b, and controlled ablations showed that the gains came from registry-grounded execution rather than from larger models, documentation retrieval or unrestricted tool exposure. The same infrastructure scaled to atlas-sized data, reproduced R-centred workflows in Python and converted external pathology software into agent-usable skills. In a discovery task starting from a whole-body spatial map and the term "Alzheimers disease", OmicOS composed a non-canonical workflow that integrated spatial expression, genetic association, eQTL and colocalization evidence to nominate a colon epithelial risk axis centred on PICALM, CD2AP and CR1. Together, OmicVerse and OmicOS define an open foundation for AI-era omics, showing how a community of biological methods can be transformed into a reliable, extensible and agent-operable system for discovery. HighlightO_LIOmicVerse 2.0 consolidates 694 methods spanning 11 omics domains into agent-callable high-level APIs. C_LIO_LIRebuildR automatically reconstructs and evolves R/Bioconductor methods as Python-native implementations under output-equivalence gates. C_LIO_LIOmicOS establishes a state-of-the-art omics agent harness, ranking first on general omics benchmarks across models and substantially improving the analytical capability of local open-source models. C_LIO_LICompositional use of ecosystem modules nominates a colon epithelial axis associated with Alzheimers disease risk. C_LIO_LIExternal algorithm packages supporting automatic iterative evolution can be integrated into the OmicOS ecosystem. C_LI

bioinformatics↗

PRC2 complex subunit JARID2 regulates embryonic pituitary stem cell differentiation to the POMC lineage

The pituitary is essential for growth, fertility, and stress response. Pituitary development is defined by transcription factor cascades, but how chromatin landscapes influence it remains elusive. JARID2 is a subunit of polycomb repressive complex 2 repressing transcription by depositing trimethylation on histone 3 lysine 27 (H3K27me3). Here, we established that H3K27me3 levels increase with differentiation in anterior pituitary from embryonic day (E) 10.5 to E14.5 despite ubiquitous Jarid2 mRNA expression. Germline loss of Jarid2 causes pituitary stem cell (PSC) hyperplasia and corticotrope hypoplasia without changing H3K27me3 bulk levels at E14.5. Pituitary-specific loss of Jarid2 with Prop1T2AiCre (Jarid2Pitko/Pitko) exhibits POMC lineage hypoplasia and PSC hyperplasia at E16.5. Pou1f1 or Nr5a1 lineages are not affected by Jarid2 mutation. To determine gene expression and chromatin accessibility changes in Jarid2Pitko/Pitko, we performed single nucleus (sn) multi-omics on E14.5 pituitaries. SnRNAseq revealed potential targets of Jarid2, including Meis2. SnATACseq revealed chromatin reprograming towards PSC retention rather than differentiation. Pax7 is reduced in both modalities in PSC. Together, we show that Jarid2 promotes stemness exit and POMC lineage differentiation, uncovering novel epigenetic regulation of pituitary development. SUMMARY STATEMENTExpanding the repertoire of the regulation of pituitary development, chromatin modifier also help stem cells in this essential gland to differentiate and choose hormone-secreting fate.

Developmental Biology↗

Dehydration/1,6-addition-based Site-specific Bioconjugation Unveils Norepinephrinylation as a Widespread Post-translational Modification in the Cellular Proteome

Norepinephrine (NE) is a key neurotransmitter and hormone involved in diverse physiological and pathological processes. Beyond its canonical non-covalent signaling through binding adrenergic receptors, NE also induces protein post-translational modifications (PTMs), representing an emerging regulatory mechanism. Two major forms of NE-derived PTMs have been proposed: non-enzymatic norepinephrinylation (NEylation) of cysteine residues mediated by NE quinone and transglutaminase 2 (TG2)-catalyzed NEylation of glutamine residues. However, the cellular abundance, biochemical basis, and pathophysiological roles of NEylation remain poorly understood due to limited detection tools. Here, we report a novel bioconjugation chemistry for selective labeling and enrichment of the endogenous NEylation proteome in cell lines and tissues, which is based on acid-catalyzed dehydration and 1,6-addition to thiol probes. This strategy enables fluorescence imaging and chemical proteomic profiling, revealing NEylation as a widespread PTM that affects enzymatic activities of modified proteins, including protein tyrosine-protein phosphatase non-receptor type 11 (PTPN11). Visual Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=75 SRC="FIGDIR/small/731782v3_ufig1.gif" ALT="Figure 1"> View larger version (21K): org.highwire.dtl.DTLVardef@406ac5org.highwire.dtl.DTLVardef@121d6b9org.highwire.dtl.DTLVardef@98354corg.highwire.dtl.DTLVardef@d312ef_HPS_FORMAT_FIGEXP M_FIG C_FIG

biochemistry↗