Biology subjects

Zhang, L.

Publications and source records attributed to Zhang, L..

At least 253 records · Page 14Linked to original sources

bioRxiv2025

IgG-Bridging-Seeded Synergistic Aggregation of SARS-CoV-2 Spikes Underlies Potent Neutralization by A Low-Affinity Antibody

Mechanistic studies of viral neutralization typically prioritize high-affinity antibodies, relegating low-affinity binders to the sidelines. We report P5-1C8, a Class 1 SARS-CoV-2 antibody that exemplifies this underexplored "low-affinity yet high-potency" phenotype, retaining strong neutralization of Omicron JN.1 despite markedly weakened trimer binding (KD = 225 nM; IC50 = 0.06 nM). Structural and biophysical analyses reveal that P5-1C8 engages WT and BA.1 spikes through canonical intra-spike bivalency, but with JN.1 it induces aggregation. Using virion-like nanoparticles displaying multiple spikes, we show that IgG remains bound with no detectable dissociation and triggers pronounced aggregation. Coarse-grained molecular dynamics delineate the stepwise pathway in which weak IgG-spike contacts seed aggregation via transient inter-spike bridging. Together, these findings establish the first mechanistic framework demonstrating how weak-binding antibodies can nonetheless achieve potent neutralization through higher-order aggregation, thereby expanding the conceptual landscape of antibody function and opening new directions for antibody evaluation and design. Graphical AbstractLow-affinity antibodies are frequently disregarded in discovery pipelines. This work reports P5-1C8, a Class 1 SARS-CoV-2 antibody with weak trimer binding (KD-to-IC50 > 3,700-fold) yet potent neutralization of Omicron JN.1. Structural, biophysical, functional and coarse-grained simulations collectively demonstrate that transient inter-spike IgG bridging seeds higher-order aggregation, which in turn drives neutralization and provides a mechanistic framework. O_FIG O_LINKSMALLFIG WIDTH=199 HEIGHT=200 SRC="FIGDIR/small/691454v1_ufig1.gif" ALT="Figure 1000"> View larger version (79K): org.highwire.dtl.DTLVardef@1d4f132org.highwire.dtl.DTLVardef@1274400org.highwire.dtl.DTLVardef@e186a6org.highwire.dtl.DTLVardef@4f1870_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

bioRxiv2025

Engineering an Anaerobic Microenvironment to Empower Hydrogenase-Catalyzed Hydrogen Therapy for Diabetic Wound Healing

The inherent oxygen sensitivity of hydrogenases has long restricted their applications to anaerobic systems. Here, we present a hybrid peptide-nanocluster hydrogel that establishes a self-sustaining anaerobic microenvironment to enable hydrogenase-catalyzed hydrogen therapy under aerobic conditions. This system integrates a custom-designed Fmoc-KYF peptide hydrogel with integrated silver nanoclusters (AgNCs), which host an engineered [NiFe]-hydrogenase (3S1C-Hyd-2). Mechanistic studies combining molecular dynamics simulations and spectroscopic analysis revealed that hydrophobic pockets within the peptide network trap oxygen molecules, while photoexcited AgNCs rapidly deplete invasive O2. Our design ensures stable hydrogen evolution, effectively overcoming the oxygen sensitivity that has long restricted hydrogenase applications in biomedical contexts. In vitro, the in-situ-generated hydrogen effectively scavenges reactive oxygen species, suppresses pro-inflammatory cytokine production. In a diabetic mouse model, this light-activated system markedly accelerates wound closure (87% by day 11), reduces oxidative stress, promotes macrophage polarization toward a reparative phenotype, enhances angiogenesis, and upregulates tissue repair pathways, as confirmed by transcriptomic profiling. Our work establishes a new bioengineering paradigm for constructing anaerobic microenvironments through synergistic material-enzyme-light interactions, offering a versatile platform for hydrogenase-enabled therapeutic interventions in oxidative stress-related diseases.

biochemistry↗

bioRxiv2025

Ethylene signal-driven plant-multitrophic synergy boosts crop performance

Efficient nutrient use in agriculture depends on the dynamic interplay between plant roots, soil, and microbial communities. The root-rhizosphere interface is central to nutrient uptake and serves as a key hub for interactions with beneficial microbes. Arbuscular mycorrhizal (AM) fungi, positioned at the nexus between plant roots and soil microbiota, play a critical role in enhancing crop performance under nutrient-limited conditions. In this study, we dissected the genetic and molecular basis of AM fungi-induced lateral root development in maize (Zea mays), focusing on the role of ethylene-responsive transcription factors (ERFs). We identified ERF genes as essential regulators of pericycle cell division, acting downstream of ethylene biosynthesis genes (ACS6 and ACS7) and AM fungal signaling. Our findings reveal that AM fungi promote lateral root initiation by activating ERF expression and reprogramming flavonoid metabolism, particularly reducing the accumulation of flavonols such as kaempferol and quercetin, which otherwise inhibit root development when over-accumulated. Furthermore, we demonstrated that Massilia, a beneficial rhizobacterium, synergizes with AM fungi to enhance lateral root formation by colonizing fungal hyphae, degrading flavonoids, and contributing to auxin production. Together, our results uncover a tripartite signaling network linking ethylene signaling, flavonoid-mediated microbial recruitment, and AM symbiosis. This study highlights ERFs as central integrators of plant-microbe interactions and provides a molecular framework for engineering root architecture and microbiome assembly to improve nutrient acquisition and support sustainable crop productivity.

plant biology↗

bioRxiv2025

Process optimization for enhanced enzymatic nylon deconstruction

Plastics such as polyamides (PAs) possess unique physicochemical properties that make them indispensable in modern society. However, their energy-intensive production and challenging end-of-life management highlight the urgent need for efficient recycling or remanufacturing solutions. Enzymatic depolymerization offers a promising route toward circular recycling, yet remains constrained by limited enzyme characterization, lack of validation under industrially relevant conditions, and overall performance. Here we optimized the reaction conditions for three recently discovered nylon-degrading enzymes. One of them, Nyl12, achieved product titers with PA6 and PA66 that exceed previously reported values, without enzyme engineering or substrate pretreatment. We further demonstrated the scalability of the process and its application to complex PA-based materials used in microelectronic components. Analysis of substrate features, including surface area and particle size, revealed key parameters governing enzymatic activity and provided a framework for future pretreatment and process optimization efforts. In combination, these efforts provide a new benchmark for enzymatic nylon recycling.

biochemistry↗

bioRxiv2025

Ferrapoptosis: Discovery of a Hybrid Programmed Cell Death

Traditional taxonomies classify ferroptosis and apoptosis as distinct forms of regulated cell death. Here, we challenge this view by defining and validating a previously unrecognized neuronal death entity in traumatic brain injury (TBI), which we term "Ferrapoptosis". This hybrid mode of death is characterized by the coexistence of ferroptotic and apoptotic molecular and ultrastructural features within the same neuron-- ultrastructural alterations that cannot be fully characterized by any known cell death modalities. By integrating single-cell transcriptomics with multi-layered functional assays, we show that Ferrapoptosis dominates in severe injury and the acute phase, and is critically driven by mitochondrial oxidative stress. Over time, its predominance is gradually replaced by death modes in which either ferroptosis or apoptosis alone becomes the major pathway. Genome-wide CRISPR screening further identifies Smg7 as a key regulator that synchronously activates both death programs to drive the hybrid phenotype, whereas genetic or viral inhibition of Smg7 reduces Ferrapoptosis and promotes neurological recovery after TBI in mice. Our work systematically delineates a previously unrecognized form of cell death and its pathogenetic mechanisms, providing experimental evidence to refine cell death classification, and suggesting a conceptual strategy for treating complex diseases such as TBI by targeting shared regulatory nodes. HIGHLIGHTSO_LIDefined and validated a previously unrecognized cell death modality, termed "Ferrapoptosis". C_LIO_LIElucidated the ordered pattern of Ferrapoptosis across key stages of TBI pathogenesis. C_LIO_LIRevealed mitochondrial oxidative stress as the pivotal hub integrating ferroptosis and apoptosis. C_LIO_LIIdentify Smg7 as a core driver of Ferrapoptosis and a promising neuroprotective target. C_LI

cell biology↗

bioRxiv2025

Improved spike-in normalization clarifies the relationship between active histone modifications and transcription

Spike-in normalization enables quantitative analysis of ChIP-sequencing (ChIP-seq) signal. Here we introduce a novel robust dual-spike-in normalization approach for ChIP-seq (ChIP-wrangler). We identify optimal conditions, such as the ratio between the spike-in species and the target, demonstrate the ability of this approach to detect technical artefacts, and use ChIP-wrangler to revisit recent claims that active histone marks are dependent on transcription. Concerned that previous studies improperly used spike-in normalization to arrive at their conclusions, we used ChIP-wrangler to show that acute depletion of RNA polymerase II (RNAPII) has only a modest impact on the levels of H3K4me3 and H3K27ac. In line with other studies, our results provide proof that the maintenance of histone acetylation is not merely a consequence of ongoing transcription. Further, we show that promoters and enhancers are differentially impacted by inhibiting transcription. Specifically, of the 5.9% peaks that showed a decrease in H3K27ac following depletion of RNAPII, 82% are promoter-distal and contain enhancer-related DNA binding motifs. Further, the small subset of regions that gain acetylation (0.35%) were enriched for stress response motifs. Our innovative ChIP-seq normalization approach provides increased rigor and "guardrails" for successful spike-in normalization, and as applied here refines the understanding of the intricate crosstalk between RNAPII activity and histone marks associated with transcription.

genomics↗

bioRxiv2025

GPR17 structure and agonism with small molecules and oxysterols

GPR17 is a class A orphan GPCR that regulates myelination in the central nervous system. Inhibiting GPR17 is a potential therapeutic mechanism to induce remyelination. The limited understanding of the structural basis of GPR17 agonism and antagonism is a challenge for GPR17 drug discovery. We present novel cryo-EM structures of GPR17 with bound orthosteric antagonist or agonist/G protein heterotrimer with biophysical and cellular characterization to inform rational drug discovery. Both ligands bind towards a lateral edge of the orthosteric pocket, while an exceptionally long extracellular loop 2 occupies and limits access to this site. In contrast, pharmacological and photoaffinity studies indicate that endogenous oxysterol agonists of GPR17 bind allosterically. Characterization of oxysterol agonism versus a known orthosteric ligand in oligodendrocytes further supports an allosteric mechanism. Therefore, the design of more potent orthosteric ligands is limited by pocket size and accessibility. Targeting allosteric binding offers an alternative approach to GPR17 antagonism.

biochemistry↗

bioRxiv2025

DNA Motors Powered by Exonuclease III for Autonomous Rolling Motion and Biosensing Applications

Nucleic acid-based synthetic motors emulate key behaviors of biological machines, enabling applications in biosensing and nanoscale actuation. Among the reported synthetic motors, RNase H-powered motors offer high speed and processivity with demonstrated applications in computation and viral sensing. However, these motors rely on RNA as "fuel" source, limiting their stability. Here, we report the development of a robust, RNA-free DNA motor powered by Exonuclease III. These motors exhibit self-avoiding rolling motion driven by enzymatic hydrolysis of surface-bound DNA fuel strands, consistent with a burnt-bridge Brownian ratchet mechanism of translocation. We systematically optimized motor performance by chemically tuning the fluorescence reporter, DNA sequence composition, and surface fuel density. Fluorescence and brightfield microscopy revealed super-diffusive and Levy-like stop-and-go dynamics under optimized conditions. Importantly, the established DNA-only architecture confers resistance to RNase degradation, and the system can be configured for motion-based biosensing via aptamer-functionalized components that selectively stall in response to viral targets. Beyond the significance of creating a chemically stable, tunable, and biosensing-compatible DNA motor platform, the work also establishes the modularity of the rolling motor platform and highlights how enzymatic diversity can expand their chemical and functional scope.

biophysics↗

bioRxiv2025

Nuclear factor kappa B subunits and IkappaB family are modulated in the ovine endometrium during early pregnancy

Pregnancy modulates the endometrial immune responses to establish maternal immune tolerance, and nuclear factor kappa B (NF-{kappa}B) subunits and I{kappa}B family are involved in the maternal innate and adaptive immune responses. It, nevertheless, is unclear if early pregnancy regulates the expression of NF-{kappa}B subunits and inhibitor of NF-{kappa}B (I{kappa}B) family in the ovine endometrium. In this study, ovine endometria were sampled at day 16 of the estrous cycle (N16), and at days 13, 16, and 25 of pregnancy (P13, P16, and P25), and mRNA and protein expression of NF-{kappa}B subunits and I{kappa}B family was analyzed by RT-qPCR, western blot, and immunohistochemistry. The results revealed that the expression of all NF-{kappa}B subunits was decreased at P25 compared with N16 both in mRNA and protein expression, but the expression of B cell leukemia-3, I{kappa}B, I{kappa}B kinase {gamma}, and I{kappa}B{delta} was increased at P25 compared with N16 both in mRNA and protein expression. I{kappa}B{beta}, however, was downregulated during early pregnancy, and the expression of I{kappa}B{varepsilon} and I{kappa}B{zeta} was decreased at P13 and P16 compared with N16 and P25 both in mRNA and protein expression. In summary, early pregnancy changed the expression of NF-{kappa}B subunits and I{kappa}B family in the ovine endometrium both in mRNA and protein expression, which may be essential for maternal immune tolerance and embryo implantation.

immunology↗

bioRxiv2025

Life-long behavioral screen reveals an architecture of vertebrate aging

Mapping behavior of individual vertebrate animals across lifespan is challenging, but if achieved, could provide an unprecedented view into the life-long process of aging. We created the first platform for high-resolution continuous behavioral tracking of a vertebrate animal across natural lifespan from adolescence to death--here, of the African killifish. This behavioral screen revealed that animals follow distinct individual aging trajectories. The behaviors of long-lived animals differed markedly from those of short-lived animals, even relatively early in life, and were linked to organ-specific transcriptomic shifts. Machine learning models accurately predicted age and even forecasted an individuals future lifespan, given only behavior at a young age. Finally, we found that animals progressed through adulthood in a sequence of stable and stereotyped behavioral stages with abrupt transitions suggesting a novel structure for the architecture of vertebrate aging.

animal behavior and cognition↗

bioRxiv2025

A SARS-CoV-2 entry inhibitor trimerizes to lock the spike protein in a closed conformation

The SARS-CoV-2 spike protein binds its receptor ACE2 to initiate target-cell infection. To engage ACE2, at least one of the three receptor-binding domains (RBDs) of the spike must adopt the up orientation. Here we describe S22, a potent, bioavailable, and non-toxic inhibitor of BA.2 and all subsequent Omicron variants. Cryo-EM analyses showed that S22 assembled as a trimer in a previously uncharacterized pocket of the spike apex, stabilizing all three RBDs in the down orientation, thereby preventing ACE2 association. Binding studies, especially those using mixed S22-sensitive and -resistant spikes, imply a cooperative assembly of three S22 molecules with three RBDs, resulting in an unusually slow S22 off-rate. Consistent with its slow dissociation and favorable pharmacokinetics, S22 suppressed viral replication 100-fold in the lungs of XBB.1.5-infected mice. Thus, S22 potently inhibits Omicron entry through a distinct mechanism whereby a small compound assembles cooperatively as a trimer to stabilize spike in an inactive conformation.

microbiology↗

bioRxiv2025

Gut metabolite IPA alleviates white matter injury post-ICH by enhancing myelin debris phagocytosis via Stap1 inhibition

BackgroundIntracerebral hemorrhage (ICH) causes neurological dysfunction and white matter injury (WMI) characterized by myelin loss, axonal injury and myelin debris accumulation. Microglia-mediated debris clearance is critical for WMI repair. The microbiota-gut-brain axis plays an essential role in the central nervous system diseases, one of the ways in which gut microbiota affects brain is via producing metabolites. Indole-3-proprionic acid (IPA), a tryptophan-derived metabolite that mainly produced by Clostridium sporogenes, exhibits anti-inflammatory and neuroprotective properties. However, its effect on ICH remains unclear. This study aims to investigate the IPA level after ICH and the therapeutic effects of IPA on neurological deficits and WMI, as well as the potential mechanisms underlying IPA-mediated neuroprotection. MethodsAn ICH model was established using C57BL/6 mice, which then received intragastric IPA (20 mg/kg/day). Fecal abundance of IPA-related genes and IPA levels in feces and plasma were measured by qPCR and UPLC-MS/MS. Behavioral tests, qPCR, and immunofluorescence staining were used to assess neurological function, myelin integrity, and axonal injury. In vitro, BV2 microglia, with or without Stap1 knockdown, were co-cultured with myelin debris to assess IPAs effects on phagocytosis. Additionally, targeted plasma IPA profiling was performed in 30 ICH patients and 30 matched healthy controls. ResultsThe relative abundance of IPA production-related genes and IPA levels in feces and plasma were significantly decreased after ICH and remained low into the chronical phase. After IPA administration, the neurological deficits, myelin loss and axonal injury of mice with ICH were significantly improved. In vitro, IPA increased BV2 microglia myelin debris phagocytosis by inhibiting Stap1 expression. IPA levels were significantly reduced in ICH patients, consistent with ICH mouse model. ConclusionsOur findings demonstrated that the gut microbiota-derived metabolite IPA could facilitate neurological deficits recovery and alleviate WMI, which could be a promising therapeutic strategy to improve ICH prognosis.

neuroscience↗

bioRxiv2025

OSM-11 modulates salinity-stress tolerance in Caenorhabditis elegans

Most terrestrial animals exhibit narrow salinity tolerance compared to their marine counterparts. Previous studies identified osm-11 (which encodes a Notch co-ligand) mutations as a driver of hyper-saline tolerance in Caenorhabditis elegans, but mechanistic insights remained unclear. This study employs RNA sequencing and CRISPR/Cas-9 genome editing to demonstrate that osm-11 mutations enhance salinity stress resistance through up-regulation of fatty acid metabolism (acdh-12, acs-17) and cytochrome P450 pathways (ugt-15), while suppressing calcium signaling. Furthermore, we demonstrated that acdh-12 mutation impairs salinity-stress tolerance by activating ferroptosis and mitophagy, accompanied by down-regulated oxidative phosphorylation and up-regulated autophagic pathways. Morphological observations show that mitochondrial fragmentation contributes to wild-type nematode mortality under high salinity, while enlarged lipid droplets in wild-types correlate with reduced {beta}-oxidation gene expression (dhs-28, daf-22), whose knockout disrupts tolerance in mutants. These findings unravel the multi-pathway regulatory network of osm-11-mediated salinity tolerance, providing mechanistic insights for developing protective strategies against environmental salinity stressors impacting animal survival.

genetics↗

bioRxiv2025

De Novo Design of a Protein Binder to Probe Gas Channel and Enhance the Oxygen Tolerance of Hydrogenase

[NiFe]-hydrogenases exhibit outstanding catalytic performance for H2 production and oxidation but suffer from extreme O2 sensitivity, limiting their biotechnological potential. The identity and functional roles of gas channels that connect to the buried [NiFe] active site have remained unclear, impeding the rational engineering of O2-tolerant enzyme variants. In this study, we present an artificial intelligence-guided de novo protein binder design strategy, utilizing compact protein binders as selective molecular probes to map hydrophobic O2 diffusion pathways in Escherichia coli hydrogenase-2 (Hyd-2). By integrating RFdiffusion, ProteinMPNN, and AlphaFold, approximately 100,000 candidate binders were computationally screened, leading to the identification of two high-affinity binders, L1 and L2. Structural, biophysical, and electrochemical analyses reveal that L1 specifically occludes the primary O2 ingress channel, thereby enhancing the enzymes oxygen tolerance by more than threefold, whereas L2, which targets a putative secondary channel, exerts a negligible effect, demonstrating the nonfunctionality of this pathway. These results provide the first direct experimental evidence for a hierarchical organization of O2 diffusion channels in [NiFe]-hydrogenases and establish binder-mediated channel occlusion as a generalizable, mutation-free approach for probing gas transport mechanisms and selectivity in metalloenzymes.

biochemistry↗

bioRxiv2025

SpaTranslator: A deep generative framework for universal spatial multi-omics cross-modality translation

Recent advances in spatial omics technologies have enabled the simultaneous analysis of multiple molecular patterns in tissue sections, offering unprecedented insights into cellular microenvironments. However, the high cost of measurements and the sparsity of data restrict the availability of paired spatial multi-omics datasets. Here, we present SpaTranslator, a deep generative framework that integrates graph neural networks with an adversarial variational generative model to fully capture spatial characteristics and enable effective cross-modality translation of spatial omics data, enabling simulation of paired spatial multi-omics data from single-omics measurements. Extensive experiments demonstrate that SpaTranslator consistently outperforms baseline methods in both clustering accuracy and biological coherence across various real-world scenarios, including spatial transcriptomics-epigenomics and spatial transcriptomics-proteomics translation tasks. Furthermore, SpaTranslator provides biologically meaningful insights through marker genes and proteins recovery, motif enrichment analysis, and gene regulation inference. Our work offers an effective and adaptable solution for spatial multi-omics cross-modality translation, supporting a broad range of biological and biomedical research.

bioinformatics↗

bioRxiv2025

Modular mRNA lipid nanoparticle platform rescues diverse genetic male infertility

Genetic male infertility arises from diverse mutations that disrupt spermatogenesis, yet therapeutic strategies capable of restoring germ-cell function remain limited. Messenger RNA (mRNA) therapeutics offer a programmable and non-integrating approach, but their functional compatibility in structured and immune-privileged tissues remains unclear. Here we identify a temporal mismatch between mRNA delivery kinetics and the progression of spermatogenesis as a key barrier to functional rescue. We show that delivery efficiency does not predict outcome: formulations with high peak expression but short duration fail to support spermiogenesis, whereas sustained expression aligned with developmental timing enables recovery. Guided by this principle, we establish a testis-targeted mRNA delivery platform that restores spermatogenesis across multiple genetic models and generates functional sperm capable of supporting embryo development and multigenerational inheritance. The approach is modular, extends to human seminiferous tubules ex vivo, and is supported by comprehensive safety analyses. Together, these findings define a design constraint for RNA therapeutics in structured tissues: functional rescue requires temporal alignment between delivery kinetics and the therapeutic window defined by tissue-specific biological programs.

bioengineering↗

bioRxiv2025

Reprogramming the Immune Suppressive Tumor Microenvironment in Glioma Enhances the Efficacy of Immune-Mediated Gene Therapy

Gliomas account for ~80% of primary malignant brain tumors. Many CNS WHO grade 2-3 and some grade 4 gliomas harbor mutant isocitrate dehydrogenase 1 (mIDH1), which causes a gain of function mutation (IDH1 R132H) leading to the production of 2-hydroxyglutarate (2HG). Mutant IDH1-induced 2HG, through epigenetic reprogramming elicits an immune-permissive tumor microenvironment (TME). An immunosuppressive mechanism in the glioma TME involves adenosine production via the ectoenzyme CD73. This study investigates mIDH1s influence on CD73 expression and adenosine levels. We demonstrate that mIDH1 glioma cells exhibit reduced CD73 expression, driven by DNA hypermethylation, leading to reduced adenosine levels. Since wtIDH1 gliomas have high CD73 expression, we evaluated CD73 blockade as an immunotherapy target. We show that CD73 inhibition used as monotherapy, did not improve survival in wtIDH1 glioma-bearing mice. However, when combined with immune-stimulatory Ad-TK (adenoviral vectors encoding herpes simplex virus thymidine kinase) and Ad-Flt3L (adenoviral vectors encoding FMS-like tyrosine kinase 3 ligand) gene therapy, CD73 blockade significantly enhanced therapeutic efficacy and increased anti-glioma effector T cell activity. These findings reveal that CD73 inhibition used in combination with immune stimulatory Ad-TK/Ad-Flt3L gene therapy may be an effective treatment for wtIDH1 gliomas, which could be readily translated to the clinical arena.

cancer biology↗

bioRxiv2025

Can Lightweight LLM Agents Improve Spatial TranscriptomicsAnnotation?

Spatial transcriptomics (ST) links gene expression to tissue organization, yet automated annotation of spatial regions remains a persistent challenge. Recent studies have explored large language models (LLMs) for biological reasoning, but their applicability in low-compute, freetier settings is largely unexplored. We investigate whether lightweight LLM agents can improve ST annotation by integrating rule-based heuristics, prototype discovery, and multirole reasoning (Analyst-Consensus-Reviewer) within a unified agentic framework. Across six STARmap and MERFISH datasets, we benchmark single- and multi-agent variants using standard clustering and spatial coherence metrics (NMI, ARI, CHAOS, ASW). Our results show that small open-weight models such as llama3.2 and qwen3 match or slightly exceed deterministic baselines in cluster recovery, while producing more spatially consistent and interpretable predictions. These findings high-light the potential of modular LLM agents as resource-efficient components in future spatial omics annotation pipelines.

genomics↗