Biology subjects

Xie, H.

Publications and source records attributed to Xie, H..

At least 37 records · Page 2Linked to original sources

bioRxiv2025

Dorsal Attention Network as a Convergent Hub of Diverse Non-pharmacological Interventions Preserving Functional Gradients and Cognition in Aging

Non-pharmacological interventions (NPIs) in aging neuroscience have largely focused on intervention-specific regional effects, with limited understanding of generalizable network-level mechanisms. Here, adopting a previously unexplored gradient-based perspective of functional brain organization, we analyzed an NPI dataset involving four interventions in older adults (training/control group: n = 112/59). NPIs led to strengthened intra-network functional integration and maintained macroscale gradient architecture. Virtual lesion analyses identified the dorsal attention network (DAN) as a key contributor to gradient maintenance. Critically, enhanced post-intervention DAN connectivity was associated with maintained gradient structure and improved global cognition. These findings establish a unifying framework in which the DAN acts as a convergent hub through which diverse NPIs preserve functional brain organization and attenuate cognitive aging.

neuroscience↗

bioRxiv2025

Arf GTPases Define BST-2-Independent Pathways for HIV-1 Assembly and Release

ADP-ribosylation factor (Arf) proteins are small GTPases that regulate intracellular membrane trafficking and actin cytoskeleton remodeling through cycles of GTP binding and hydrolysis. Arf1, a central regulator of Golgi and endosomal trafficking, and Arf6, which controls plasma membranes and endosomal dynamics, have both been implicated in late stages of the HIV-1 life cycle. However, the precise mechanisms by which these GTPases support HIV-1 assembly and release remain incompletely understood. Here, we provide direct evidence that Arf1 and Arf6 are required for efficient trafficking of the HIV-1 Gag polyprotein, assembly, and virion release. Perturbation of Arf1 function with either a GTP-locked (Q71L) or GDP-locked (T31N) mutant significantly reduced virus release, impaired Gag association with membrane compartments, and blocked Gag targeting to the plasma membrane. Manipulation of Arf1 activity via the GTPase-activating protein AGAP1 further demonstrated that dynamic cycling of Arf1 between GTP- and GDP-bound states is essential for productive Gag trafficking. Similarly, expression of a constitutively active Arf6 mutant (Q67L) misdirected Gag to intracellular membranes and markedly decreased virion production. Importantly, disruption of Arf1 or Arf6 function did not affect the total expression, surface levels, or intracellular distribution of the host restriction factor BST-2. Together, these findings establish that Arf1- and Arf6-mediated trafficking pathways are critical host determinants of HIV-1 assembly and release, functioning independently of BST-2 antagonism. IMPORTANCEThe small GTPases Arf1 and Arf6 control fundamental processes in membrane trafficking and cytoskeletal dynamics, yet their roles in HIV-1 replication are not well defined. We show that both proteins are required for efficient trafficking of HIV-1 Gag polyprotein to the plasma membrane and for subsequent virus release. Disrupting either GTPase reroutes Gag to intracellular membranes and reduces virion production, independently of the antiviral host factor BST-2. These results identify Arf1- and Arf6-dependent trafficking as critical host pathways for HIV-1 assembly and egress, expanding our understanding of the cellular machinery hijacked by retroviruses to support infections.

microbiology↗

bioRxiv2025

Functional Connectome of Superagers Reveals Early Markers of Resilience and Vulnerability to Alzheimers Disease

As populations age, identifying the neurobiological basis of cognitive resilience is critical for delaying or preventing Alzheimers disease (AD). While most older adults experience memory decline, a subset known as superagers (SA) maintains youthful memory into late life, offering a unique window into protective mechanisms against neurodegeneration. Here, we identified a functional connectivity (FC) signature, termed Alzheimers-resilient connectome (ARC), that robustly differentiates SA from age-matched patients with AD. Using resting-state fMRI in a discovery cohort (N = 290), we identified ARC derived from machine learning classifiers that distinguished SA from AD with high accuracy (AUC = 0.85), and validated the replicability of the ARC in an independent replication cohort (N = 143). ARC involved prefrontal, temporal and insular networks and was strongly associated with brain age. When applied to cognitively unimpaired (CU) adults (discovery cohort: N = 818 and replication cohort: N = 497), ARC-based subtyping revealed SA-like and AD-like subgroups with similar baseline cognitive performance but markedly divergent longitudinal trajectories. SA-like CU individuals showed slower cognitive decline, reduced amyloid-{beta} accumulation, and lower risk of conversion to mild cognitive impairment and AD, reinforcing the ARC signature as a potential early indicator of resilience. Genome-wide association analysis identified CLYBL and FRMD6 as novel genetic modulators associated with these divergent aging phenotypes. Together, our findings position ARC as a sensitive and generalizable biomarker of resilience, enabling early risk stratification and precision prevention for AD.

neuroscience↗

bioRxiv2025

Identification of senescence-related hub genes and potential therapeutic agents for chronic heart failure

BackgroundChronic heart failure (CHF), the terminal phase of cardiovascular disease progression, has emerged as an increasingly severe global public health concern. Despite current therapeutic approaches aimed at symptom relief, their long-term effectiveness remains limited, urgently necessitating the exploration of novel treatment strategies. This study endeavored to explore the role of cellular senescence in CHF, identify the characteristic genes linked to cellular senescence, and predict potential therapeutic agents. MethodsWe acquired CHF-related datasets from the Gene Expression Omnibus database and cell senescence-related genes from the CellAge database to identify differentially expressed cell senescence-related genes. We then conducted Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses to elucidate the functions of these differentially expressed genes, constructed a protein-protein interaction network, and screened hub genes. Using receiver operating curve (ROC) analysis, we developed a diagnostic model based on these hub genes. Furthermore, we constructed networks for the hub genes involving miRNAs, lncRNAs, transcription factors, and drugs. Subsequently, we explored the potential mechanism of action of metformin in the treatment of CHF through molecular docking studies. Lastly, we verified the expression of the hub genes in a doxorubicin-induced CHF model in rats. Results We ultimately identified nine hub genes associated with cellular senescence: STAT1, MMP9, MAP2K1, SOCS1, SDC1, MET, EIF4EBP1, ATF3, and NAMPT. These genes exhibited significant differential expression between CHF and normal tissues. The constructed diagnostic model demonstrated robust diagnostic performance in ROC curve analysis, with an area under the curve exceeding 0.7, thereby providing biomarker support for early CHF diagnosis. Furthermore, we identified a regulatory network comprising 94 lncRNAs, 63 miRNAs, and 11 transcription factors and screened 42 potential therapeutic drugs. Subsequent molecular docking simulations revealed that metformin could effectively bind to the hub genes. Finally, we validated the expression of some hub genes in a rodent CHF model, in which gene expression regulation varied across diverse experimental settings. ConclusionsOur research identified nine genes cellular senescence-related genes with potential roles in CHF pathogenesis, offering fresh perspectives concerning the diagnosis and treatment of CHF.

bioinformatics↗

bioRxiv2025

Herpes simplex virus 1 strain 17+ with R2 mutation in UL37 has residual retrograde transport

Herpes simplex virus 1 (HSV-1) causes lifelong recurrent infections. Following primary infection of the oral or genital mucosa, HSV-1 travels retrogradely through axons and establishes latency in the cell body of ganglionic neurons of the peripheral nervous system. Periodic reactivation in neurons and anterograde transport of virions back to peripheral regions causes oral or genital ulcerations. Many host and viral factors implicated in retrograde and anterograde transport of HSV-1 have been identified. In particular, studies reported that introducing five amino acid substitutions in the R2 region of the viral tegument protein UL37 was sufficient to completely eliminate retrograde transport of HSV-1 strain F. Here, we introduced the same R2 mutations in the highly neurovirulent HSV-1 strain 17+. We report that this R217 virus has residual retrograde travel. We show that R217 can establish latency in mouse models of ocular and vaginal infection and reactivate. These results contradict published evidence and show that the R2 mutation is not sufficient to fully prevent retrograde transport of HSV-1.

microbiology↗

bioRxiv2025

THA_1941 from Thermosipho africanus: A Thermostable β-1,3-Glucan Phosphorylase for Efficient β-1,3-Glucan Synthesis

{beta}-1,3-Glucan phosphorylases capable of utilizing glucose as a priming substrate are key biocatalysts for the synthesis of functional {beta}-1,3-glucan. In this study, we identified THA_1941 from Thermosipho africanus (Ta{beta}GP) as a GH161 {beta}-1,3-glucan phosphorylase exhibiting robust synthetic activity towards glucose, as confirmed by 13C nuclear magnetic resonance, liquid chromatography-mass spectrometry, and sequence and structural analyses. Ta{beta}GP displayed exceptional thermostability, retaining 93% of its activity at 60 {degrees}C for 180 h, and showed broad pH tolerance ranging from pH 5.0 to 10.0, surpassing the performance of previously reported homologs. In addition, Ta{beta}GP exhibited broad substrate flexibility, accepting both - and {beta}-linked disaccharides, and demonstrated strong resistance to metal ions and lignocellulose-derived inhibitors. In the presence of 150 mM glucose 1-phosphate as the donor substrate, Ta{beta}GP synthesized {beta}-1,3-glucan with a tunable average degree of polymerization (10-32), depending on the concentration of glucose used as the primer. The combination of thermostability, inhibitor resistance, and substrate versatility makes Ta{beta}GP a promising biocatalyst for the economically viable and environmentally sustainable synthesis of {beta}-1,3-glucan from non-food biomass sources.

biochemistry↗

bioRxiv2025

Immune-mediated indirect interaction between gut microbiota and bacterial pathogens

BackgroundOrganism survival depends on the ability to orchestrate interactions between the host immune system and gut microbiota in response to pathogenic infections. These tripartite interactions shape pathogen virulence evolution. A key regulator of the immune system and, hence, bipartite interactions (in insects) is the immune deficiency (Imd) pathway, which modulates gut microbiota and pathogens by synthesizing antimicrobial peptides (AMPs). However, whether Imd-dependent AMPs mediate indirect interactions between gut microbiota and pathogens in a tripartite context remains unclear. Using RNAi-mediated knockdown of Tenebrio molitor Relish (TmRelish), we hypothesized that Imd-dependent AMPs influence indirect interaction between Providencia burhodogranaria_B infection and the gut microbiota. ResultsWhile TmRelish-knockdown altered bipartite interactions, disrupting gut microbiota load and composition and increasing pathogen load and virulence through higher host mortality, it did not support our tripartite hypothesis. Instead of Imd-dependent AMPs, gut microbiota and pathogen were influenced by Imd-independent AMPs expression, suggesting alternative regulatory pathways. Nevertheless, our investigations of tripartite interactions showed a positive effect of P. b_B infection on gut microbiota load, while survival analysis further revealed a negative effect of gut microbiota on pathogens infection, suggesting microbiota- mediated immune priming. ConclusionsThese findings suggest that while Imd-dependent AMPs may not mediate tripartite interactions, microbiota-host interactions, such as microbiota-mediated immune priming and changes in microbiota load, can shape infection outcomes. These effects on infection outcomes almost certainly exert important selective pressures on the evolution of bacterial virulence.

immunology↗

bioRxiv2025

Tie2-Dependent Mechanisms Promote Leptomeningeal Collateral Remodeling and Reperfusion Following Stroke

Leptomeningeal collaterals are distal pial arterial anastomotic vessels that provide an alternative route for redistributing cerebral blood flow following arterial obstruction, thereby limiting tissue damage. However, the regulatory mechanisms and strategies to enhance this adaptive response remain under investigation. This study explored the pharmacological effects of Tie2 receptor activation, using the peptide agonist Vasculotide, following permanent middle cerebral artery occlusion (pMCAO). Vasculotide improved collateral growth and remodeling, which correlated with reduced infarct volume, enhanced blood flow, and functional recovery within 24hrs post-pMCAO. In contrast, collateral growth was attenuated in Tie2 and EphA4/Tie2 double knockdown mice, while the loss of EphA4 increased Tie2 and Ang-1 expression and mimicked the positive effects of Vasculotide following stroke. Furthermore, bulk RNA sequencing of meningeal tissue identified key transcriptomic changes, including alterations in AJ-associated transcripts, such as Krt5, Krt14, and Col17a1, in the ipsilateral meninges of both endothelial cell-specific EphA4 knockout and Vasculotide-treated mice. Krt5 expression was found upregulated on meningeal arterial vascular network in injured KO mice, highlighting a potential new mediator of meningeal vascular remodeling. These findings illustrate that EphA4 and Tie2 play opposing roles in collateral remodeling, including the regulation of Krt5. Modulating their activity could potentially enhance the collateral response to stroke.

neuroscience↗

bioRxiv2025

Glycogen Engineering Improves the Starvation Resistance of Mesenchymal stem cells and their Therapeutic Efficacy in Pulmonary Fibrosis

Mesenchymal stem cells (MSCs) are widely used in regenerative medicine, including the treatment of pulmonary fibrosis. However, implanted MSCs disappear within days, constraining therapeutic efficacy, which is largely attributed to nutrient deprivation. In this study, we established glycogen metabolism engineering strategies in mammalian cells. By expressing a functionally optimized glycogen synthase (GYSmut), MSCs could accumulate large amounts of glycogen rapidly as a reserve substance. Glycogen engineering significantly improved the survival of MSCs during starvation both in vitro and in vivo, enhancing cell viability post-implantation and their therapeutic efficacy in pulmonary fibrosis. Glycogen-engineered MSCs may serve as chassis cells for further applications. Our research highlights the importance of glucose metabolism regulation in cell-based therapy and demonstrates the great potential for the metabolic engineering of MSCs and other therapeutic cells.

bioengineering↗

bioRxiv2025

Virus-host interactome reveals host cellular pathways perturbed by tick-borne encephalitis virus infection

Tick-borne encephalitis virus (TBEV) poses an increasingly significant threat to public health. Here, we delved into the virus-host interactome and discovered that TBEV has a profound impact on multiple host cellular pathways. Viral pre-membrane protein (prM), non-structural proteins NS1, NS2B3, NS4A, and NS5 remodel the hosts innate immune responses. PrM and NS2B3 are involved in autophagy, NS4A is associated with neurodegenerative diseases, and NS5 participates in spliceosome dynamics, ribosomal biogenesis, cell cycle regulation, and DNA damage response. Notably, TBEV infection causes G0/G1 cell cycle arrest in host cells. NS5 interacts with histone acetyltransferase P300 to upregulate P16 expression, suppressing CDK4 and resulting in cell cycle arrest. Elevated P16 and reduced CDK4 levels were observed in TBEV-infected brain organoids. The P300 inhibitors and CDK4 agonist can reverse virus-induced cell cycle arrest and inhibit viral replication. Further analysis uncovered potential antiviral targets like KAT6A, XIAP, and RIOK1/BRD9. These findings provide valuable insights into TBEV pathogenicity and hold promise for antiviral drug development.

microbiology↗

bioRxiv2025

Clinical performance evaluation of a tiling amplicon panel for whole genome sequencing of respiratory syncytial virus

Accurate genomic characterization of respiratory syncytial virus (RSV) is crucial for studies of epidemiology and viral evolution, and monitoring potential escape from newly authorized vaccines and antivirals. We adapted a viral whole genome tiling amplicon panel (UW-ARTIC) and developed a custom bioinformatic pipeline for high-throughput, cost-effective sequencing of RSV-A and RSV-B. We established genome acceptability criteria and determined the performance characteristics of the panel including assay sensitivity, specificity, breadth of genome recovery, accuracy, and precision using contrived and remnant clinical specimens. High-quality genomes (>95% genome completeness; >500X and >1000X average depth for whole genome and fusion gene respectively) were recovered from samples with Ct [≤] 30 ([~]594 and 2,004 copies per reaction for RSV-A and RSV-B respectively). Minor variants were accurately identified in sample mixtures of 5:95 and higher. The assay showed high accuracy when compared against Sanger, shotgun metagenomic, and hybridization capture-based sequencing; and high repeatability and reproducibility. The UW-ARTIC RSV panel has utility in genomic surveillance, clinical and research applications. It has been used to generate FDA-reportable data for clinical trials of RSV antiviral products, with robust performance characteristics in samples from around the globe from as recently as the 2023/24 season. Continued genomic surveillance and future updates to primer sets will be essential for continued recovery of genomes as RSV continues to evolve.

genomics↗

bioRxiv2025

Minimization of gene editing off-target effects by tissue restriction of expression

Therapeutic in vivo gene editing with highly specific nucleases has the potential to revolutionize treatment for a wide range of human diseases, including genetic disorders and latent viral infections like herpes simplex virus (HSV). However, challenges regarding specificity, efficiency, delivery, and safety must be addressed before its clinical application. A key concern is the risk of off-target effects, which can cause unintended and potentially harmful genetic changes. We previously developed a curative in vivo gene editing approach to eliminate latent HSV using HSV-specific meganuclease delivered by an AAV vector. In this study, we investigate off-target effects of meganuclease by identifying potential off-target sites through GUIDE-tag analysis and assessing genetic alterations using amplicon deep sequencing in tissues from meganuclease treated mice. Our results show that meganuclease expression driven by a ubiquitous promoter leads to high off-target gene editing in the mouse liver, a non-relevant target tissue. However, restricting the meganuclease expression with a neuron-specific promoter and/or a liver-specific miRNA target sequence efficiently reduces off-target effects in both liver and trigeminal ganglia. These findings suggest that incorporation of regulatory DNA elements for tissue-specific expression in viral vectors can reduce off-target effects and improve the safety of therapeutic in vivo gene editing.

molecular biology↗

bioRxiv2025

Autoimmune regulator deficiency causes sterile epididymitis and impacts male fertility through disruption of inorganic physiology

Autoimmune regulator (AIRE), a transcription factor expressed by medullary thymic epithelial cells, is required for shaping the self-antigen tolerant T cell receptor repertoire. Humans with mutations in AIRE suffer from Autoimmune Polyglandular Syndrome Type 1 (APS-1). Among many symptoms, men with APS-1 commonly experience testicular insufficiency and infertility, but the mechanisms causing infertility are unknown. Using an Aire-deficient mouse model, we demonstrate that male subfertility is caused by sterile epididymitis characterized by immune cell infiltration and extensive fibrosis. In addition, we reveal that the presence of autoreactive immune cells and inflammation in epididymides of Aire-deficient mice are required for iron (Fe) deposition in the interstitium, which is brought on by macrophages. We further demonstrate that male subfertility is associated with a decrease in metals zinc (Zn), copper (Cu), and selenium (Se) which serve as cofactors in several antioxidant enzymes. We also show increase in DNA damage of epididymal sperm of Aire-/- animals as a key contributing factor to subfertility. The absence of Aire results in autoimmune attack of the epididymis leading to fibrosis, Fe deposition, and Cu, Zn and Se imbalance, ultimately resulting in sperm DNA damage and subfertility. These results highlight the requirement of Aire to promote immune tolerance throughout the epididymis, disruption of which causes an imbalance of inorganic elements with resulting consequence on male fertility. Key pointsBreakdown of epididymal self-tolerance promotes disruption of inorganic elements. Autoimmunity causes interstitial fibrosis resulting in sperm DNA damage and subfertility. Elevated interstitial iron and macrophages contribute to fibrosis.

pathology↗

bioRxiv2024

Optimizing femtosecond laser fabricating strategy of Nitinol hypotube for vascular interventional surgery

Guidewires and catheters are essential in minimally invasive procedures, particularly in accessing targets within the vascular system for neuron surgery. Femtosecond lasers can precisely cut nickel-titanium micro tubes, known as Nitinol hypotubes, serving as the heads of micro guidewires while protecting their core tips. The quality and geometry of these hypotubes depend on the focus of the laser cutting system. We evaluated the cutting efficiency and quality of Nitinol hypotubes using objective lenses with three numerical apertures (NA). Quantitative analysis indicated that higher NA objectives yield better surface quality, resulting in lower debris. Additionally, cutting with high NA objectives produced significantly lower arithmetic mean surface roughness and enhanced mechanical properties. Using a two-temperature model, we simulated the interaction between femtosecond lasers and Nitinol, showing that higher NA objectives increase electron temperatures, thus improving material removal efficiency. This study also tested the optimized Nitinol hypotube prformance in simulations of invasive neuron surgery.

neuroscience↗

bioRxiv2024

Polarized ATP synthase in synaptic mitochondria induced by learning and plasticity signals

MINFLUX represents a state-of-the-art single-molecule localization microscopy technology that surpasses the conventional diffraction limit, enabling the visualization and analysis of nanostructures with exceptional precision. Despite its potential, the utilization of MINFLUX has been primarily confined to in vitro cultured cell environments. In this research, we have refined the sample preparation protocols to facilitate 3D MINFLUX imaging in fixed brain tissue sections, focusing on the mitochondrial distribution within dendritic spines and engram cells of the dentate gyrus. Probing single molecules in vivo reveals an interesting finding: the reorganization of mitochondrial inner membrane proteins during synaptic plasticity within dendritic spines of engram cells. Utilizing 3D MINFLUX nanoscopy, we identified a significant redistribution of -F1-ATP synthase, which correlates with learning related activities. This redistribution implies a pivotal function for polarized ATP synthesis in the vicinity of the postsynaptic zone, which may modulate both short-term and long-term synaptic modifications, thereby influencing synaptic plasticity and memory consolidation. Furthermore, dual-color 3D MINFLUX imaging has uncovered distinct patterns of mitochondrial reorganization involving both the inner and outer membranes within dendritic spines. These patterns, induced by plasticity signals, persist for up to 12 hours in neuronal cultures. This distinction highlights the presence of distinct regulatory mechanisms governing mitochondrial proteins during synaptic plasticity. These results offer new insights into the molecular mechanisms underlying synaptic plasticity and underscore the transformative potential of 3D MINFLUX imaging for studying neuronal processes in the brain.

neuroscience↗

bioRxiv2024

Machine Learning Identifies Genes Linked to Neurological Disorders Induced by Equine Encephalitis viruses (EEV), Traumatic Brain Injuries (TBI), and Organophosphorus nerve agents (OPNA)

Venezuelan, eastern, and western equine encephalitis viruses (collectively referred to as equine encephalitis viruses---EEV) cause serious neurological diseases and are a significant threat to the civilian population and the warfighter. Likewise, organophosphorus nerve agents (OPNA) are highly toxic chemicals that pose serious health threats of neurological deficits to both military and civilian personnel around the world. Consequently, only a select few approved research groups are permitted to study these dangerous chemical and biological warfare agents. This has created a significant gap in our scientific understanding of the mechanisms underlying neurological diseases. Valuable insights may be gleaned by drawing parallels to other extensively researched neuropathologies, such as traumatic brain injuries (TBI). By examining combined gene expression profiles, common and unique molecular characteristics may be discovered, providing new insights into medical countermeasures (MCMs) for TBI, EEV infection and OPNA neuropathologies and sequelae. In this study, we collected transcriptomic datasets for neurological disorders caused by TBI, EEV, and OPNA injury, and implemented a framework to normalize and integrate gene expression datasets derived from various platforms. Effective machine learning approaches were developed to identify critical genes that are associated, either shared among the three neuropathologies or to either TBI, EEV, and OPNA. With the aid of deep neural networks, we were able to extract important association signals for accurate prediction of different neurological disorders by using integrated gene expression datasets of VEEV, OPNA, and TBI samples. Gene ontology and pathway analyses further identified neuropathologic features with specific gene product attributes and functions, shedding light on the fundamental biology of these neurological disorders. Collectively, we highlight a workflow to analyze published transcriptomic data using machine learning, which can be used for both identification of gene biomarkers that are unique to specific neurological conditions, as well as genes shared across multiple neuropathologies. These shared genes could serve as potential neuroprotective drug targets for conditions like EEV, TBI, and OPNA.

neuroscience↗

bioRxiv2024

Elevated EGR1 Binding at Enhancers in Excitatory Neurons Correlates with Neuronal Subtype-Specific Epigenetic Regulation

Brain development and neuronal cell specification are accompanied with epigenetic changes to achieve diverse gene expression regulation. Interacting with cell-type specific epigenetic marks, transcription factors bind to different sets of cis-regulatory elements in different types of cells. Currently, it remains largely unclear how cell-type specific gene regulation is achieved for neurons. In this study, we generated epigenetic maps to perform comparative histone modification analysis between excitatory and inhibitory neurons. We found that neuronal cell-type specific histone modifications are enriched in super enhancer regions containing abundant EGR1 motifs. Further CUT&RUN data validated that more EGR1 binding sites can be detected in excitatory neurons and primarily located in enhancers. Integrative analysis revealed that EGR1 binding is strongly correlated with various epigenetic markers for open chromatin regions and associated with distinct gene pathways with neuronal subtype-specific functions. In inhibitory neurons, the majority of genomic regions hosting EGR1 binding sites become accessible at early embryonic stages. In contrast, the super enhancers in excitatory neurons hosting EGR1 binding sites gained their accessibility during postnatal stages. This study highlights the significance of transcription factor binding to enhancer regions, which may play a crucial role in establishing cell-type specific gene regulation in neurons.

neuroscience↗

bioRxiv2024

scCompass: An integrated cross-species scRNA-seq database for AI-ready

Emerging single-cell sequencing technology has generated large amounts of data, allowing analysis of cellular dynamics and gene regulation at the single-cell resolution. Advances in artificial intelligence enhance life sciences research by delivering critical insights and optimizing data analysis processes. However, inconsistent data processing quality and standards remain to be a major challenge. Here we propose scCompass, which provides a data quality solution to build a large-scale, cross-species and model-friendly single-cell data collection. By applying standardized data pre-processing, scCompass integrates and curates transcriptomic data from 13 species and nearly 105 million single cells. Using this extensive dataset, we are able to archieve stable expression genes (SEGs) and organ-specific expression genes (OSGs) in human and mouse. We provide different scalable datasets that can be easily adapted for AI model training and the pretrained checkpoints with state-of-the-art (SOTA) single-cell foundataion models. In summary, the AI-readiness of scCompass, which combined with user-friendly data sharing, visualization and online analysis, greatly simplifies data access and exploitation for researchers in single cell biology(http://www.bdbe.cn/kun).

bioinformatics↗