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Shen, L.

Publications and source records attributed to Shen, L..

At least 73 records · Page 4Linked to original sources

Transcriptomic and spatial GABAergic neuron subtypes in zona incerta mediate distinct innate behaviors

Understanding the anatomical connection and behaviors of transcriptomic neuron subtypes is critical to delineating cell type-specific functions in the brain. Here we integrated single-nucleus transcriptomic sequencing, in vivo circuit mapping, optogenetic and chemogenetic approaches to dissect the molecular identity and function of heterogeneous GABAergic neuron populations in the zona incerta (ZI) in mice, a region involved in modulating various behaviors. By microdissecting ZI for transcriptomic and spatial gene expression analyses, our results revealed two non-overlapping Ecel1- and Pde11a-expressing GABAergic neurons with dominant expression in the rostral and medial zona incerta (ZIrEcel1 and ZImPde11a), respectively. The GABAergic projection from ZIrEcel1 to periaqueductal gray mediates self-grooming, while the GABAergic projection from ZImPde11a to the oral part of pontine reticular formation promotes transition from sleep to wakefulness. Together, our results revealed the molecular markers, spatial organization and specific neuronal circuits of two discrete GABAergic projection neuron populations in segregated subregions of the ZI that mediate distinct innate behaviors, advancing our understanding of the functional organization of the brain.

neuroscience↗

Histopathologic Evaluation and Single-Cell Spatial Transcriptomics of the Colon Reveal Cellular and Molecular Abnormalities Linked to J-Pouch Failure in Patients with Inflammatory Bowel Disease.

Background and AimsTotal abdominal colectomy (TAC) with a staged ileal pouch-anal anastomosis (IPAA) is a common surgical treatment for ulcerative colitis (UC). However, a significant percentage of patients experience pouch failure, leading to morbidity. This retrospective case-control study identified histopathological features of the TAC specimen associated with pouch failure and investigated the molecular mechanisms of this susceptibility using single-cell spatial transcriptomics. MethodsWe analyzed a cohort of 417 patients who underwent IPAA between 2000-2010 at the University of Chicago Medical Center for up to 18 years. Histological examination of TAC specimens focused on disease activity, depth of inflammation, and specific features, including granulomas and deep ulcers. A subset of patients was profiled using single-cell spatial transcriptomics to map gene expression and immune cell interactions in relation to the risk of pouch failure. ResultsThe 18-year pouch failure risk was 23%, with post-procedure diagnosis of CD as a major risk factor (HR = 4.3, 95% CI: 2.3-8.1) as well as high-risk histologic features, including deep chronic inflammation (HR = 21, 95% CI: 11-41) and severe disease activity (HR = 14, 95% CI: 5.7-32) in TAC specimens. Spatial transcriptomics showed immune infiltration of T and myeloid cells, reduced myocyte-glial interactions, and cytokine signaling pathways such as IL-10, IL-1{beta}, and type I/II interferons, associated with an increased risk of pouch failure. ConclusionHistological features and spatial molecular profiling are predictive of IPAA failure. These findings support the use of histologic evaluation and targeted molecular analysis of the TAC specimen to identify high-risk patients and improve IPAA outcomes.

pathology↗

Multimodal single-cell analyses reveal molecular markers of neuronal senescence in human drug-resistant epilepsy

The histopathological neurons in the brain tissue of drug-resistant epilepsy exhibit aberrant cytoarchitecture and imbalanced synaptic circuit function. However, the gene expression changes of these neurons remain unknown, making it difficult for the diagnosis or to dissect the mechanism of drug-resistant epilepsy. By integrating whole-cell patch clamp recording and single-cell RNA sequencing approaches, we identified a transcriptionally distinct subset of cortical pyramidal neurons. These neurons highly expressed genes CDKN1A (P21), CCL2 and NFKBIA that associated with mTOR pathway, inflammatory response and cellular senescence. We confirmed the expression of senescent marker genes in a subpopulation of cortical pyramidal neurons with enlarged soma size in the brain tissue of drug-resistant epilepsy. We further revealed the expression of senescent cell markers P21, P53, COX2, {gamma}-H2AX, {beta}-Gal and reduction of nuclear integrity marker Lamin B1 in histopathological neurons in the brain tissue of drug-resistant epilepsy patients with different pathologies, but not in control brain tissue with no history of epilepsy. Additionally, chronic, but not acute, epileptic seizures induced senescent markers expression in cortical neurons in mouse models of drug-resistant epilepsy. These results provide important molecular markers for histopathological neurons and new insights into the pathophysiological mechanisms of drug-resistant epilepsy.

neuroscience↗

The SWIB domain-containing DNA topoisomerase I of Chlamydia trachomatis mediates DNA relaxation

The obligate intracellular bacterial pathogen, Chlamydia trachomatis (Ct), has a distinct DNA topoisomerase I (TopA) with a C-terminal domain (CTD) homologous to eukaryotic SWIB domains. Despite the lack of sequence similarity at the CTDs between C. trachomatis TopA (CtTopA) and Escherichia coli TopA (EcTopA), full-length CtTopA removed negative DNA supercoils in vitro and complemented the growth defect of an E. coli topA mutant. We demonstrated that CtTopA is less processive in DNA relaxation than EcTopA in dose-response and time course studies. An antibody generated against the SWIB domain of CtTopA specifically recognized CtTopA but not EcTopA or Mycobacterium tuberculosis TopA (MtTopA), consistent with the sequence differences in their CTDs. The endogenous CtTopA protein is expressed at a relatively high level during the middle and late developmental stages of C. trachomatis. Conditional knockdown of topA expression using CRISPRi in C. trachomatis resulted in not only a developmental defect but also in the downregulation of genes linked to nucleotide acquisition from the host cells. Because SWIB-containing proteins are not found in prokaryotes beyond Chlamydia spp., these results imply a significant function for the SWIB-containing CtTopA in facilitating the energy metabolism of C. trachomatis for its unique intracellular growth. ImportanceC. trachomatis (Ct) is a medically important bacterial pathogen that is responsible for the most prevalent sexually transmitted bacterial infection. Bioinformatics, genetics, and biochemical analyses have established that the presence of a SWIB domain in CtTopA, a DNA topoisomerase I, is relevant to chlamydial physiology. Further defining the mechanisms of the C-terminal SWIB domain on the catalytic function of CtTopA in an intracellular pathogen is warranted for a more complete understanding of the interactions between C. trachomatis and its host cells.

molecular biology↗

Delineation of Single-cell Altas Provides New Insights for Development of Coronary Artery Lesions in Kawasaki Disease: Bad and Good Signaling Molecules

BackgroundKawasaki Disease (KD) is a vasculitis syndrome featured with a high and persistent fever and mainly affects children under 5 years of age. It is the leading cause of acquired heart disease in the form of coronary artery lesions (CALs) for children in developed countries. Most KD can be relieved with the high-dosage Intravenous immunoglobulin (IVIG) therapy, but a small proportion develop CALs after IVIG treatment. MethodsWe performed the single-cell RNA sequencing for the peripheral blood mononuclear cells (PBMCs) from three KD non-CAL patients whose samples were acquired before and after IVIG treatment and three KD CAL patients whose samples were acquired only after IVIG treatment. Cell-to-cell communication patterns were also analyzed in KD CAL and non-CAL patients ResultsOverall cell expression feature analyses show immunoglobulin and adaptive immunity related genes are upregulated in KD CAL patients while B cell activation related genes are downregulated in them. Pseudo-time analyses demonstrate that both KD non-CAL patients before treatment and KD CAL patients after treatment have a dysregulated B cell developmental trajectory while the former has a mixed T and B lineage and the latter has a mixed monocyte and B lineage. The early elevated expression of SPI1 could partly explain the dysregulated B cell development in KD CAL patients. Cell communication analyses propose a disorder cell communication pattern in KD non-CAL patients before treatment and some persistent bad cell-to-cell signals in KD CAL patients after treatment. There are four signaling molecules, APP, CCL, and MCH-II, whose expression is significantly increased in the CD14 and CD16 monocytes of KD CAL patients, where the expression of RESISTIN is significantly increased in those KD non-CAL patients. ConclusionsOur results suggest that APP, CCL, and MCH-II might be the bad signals for indicating the possible development of CAL while RESISTIN is a good one for protecting from CAL.

immunology↗

Targeting synthetic lethality between non-homologous end joining and radiation in very high-risk SHH medulloblastoma

Specific and biologically informed treatments for medulloblastoma, especially the highly lethal TP53 mutant SHH subgroup, remain elusive, where radiotherapy is the primary treatment option. Applying genome-wide CRISPR-Cas9 screening in combination with lethal doses of radiotherapy, we identified the main driver of radiation resistance in SHH medulloblastoma is loss of p53. A negative selection CRISPR-Cas9 screen across multiple models of Trp53-deficient SHH medulloblastoma revealed a strong synthetic lethal interaction between components of the non-homologous end-joining pathway and radiation, particularly DNA protein kinase (DNA-PK) and its binding partners. Both genetic and pharmacological perturbation of DNA-PK enhanced radiosensitivity in TP53-deficient SHH medulloblastoma, leading to cell death. In vivo treatment of somatic and germline TP53-mutant SHH medulloblastoma models with peposertib, a small-molecule inhibitor of DNA-PK, significantly improved survival when combined with radiotherapy, strongly supporting further clinical investigation.

cancer biology↗

Graph-Regularized Optimal Transport for Single-Cell Data Integration

BackgroundRecent advancements in single-cell omics technologies have enabled detailed characterization of cellular processes. However, coassay sequencing technologies remain limited, resulting in un-paired single-cell omics datasets with differing feature dimensions; Findingwe present GROTIA (Graph-Regularized Optimal Transport Framework for Diagonal Single-Cell Integrative Analysis), a computational method to align multi-omics datasets without requiring any prior correspondence information. GROTIA achieves global alignment through optimal transport while preserving local relationships via graph regularization. Additionally, our approach provides interpretability by deriving domain-specific feature importance from partial derivatives, highlighting key biological markers. Moreover, the transport plan between modalities can be leveraged for post-integration clustering, enabling a data-driven approach to discover novel cell subpopulations; ConclusionsWe demonstrate GROTIAs superior performance on four simulated and four real-world datasets, surpassing state-of-the-art unsupervised alignment methods and confirming the biological significance of the top features identified in each domain. The software is available at https://github.com/PennShenLab/GROTIA.

bioinformatics↗

PSKH1 kinase activity is differentially modulated via allosteric binding of Ca2+ sensor proteins

Protein Serine Kinase H1 (PSKH1) was recently identified as a crucial factor in kidney development and is overexpressed in prostate, lung and kidney cancers. However, little is known about PSKH1 regulatory mechanisms, leading to its classification as a "dark" kinase. Here, we used biochemistry and mass spectrometry to define PSKH1s consensus substrate motif, protein interactors, and how interactors, including Ca2+ sensor proteins, promote or suppress activity. Intriguingly, despite the absence of a canonical Calmodulin binding motif, Ca2+-Calmodulin activated PSKH1 while, in contrast, the ER-resident Ca2+ sensor of the CREC family, Reticulocalbin-3, suppressed PSKH1 catalytic activity. In addition to antagonistic regulation of the PSKH1 kinase domain by Ca2+ sensing proteins, we identified UNC119B as a protein interactor that activates PSKH1 via direct engagement of the kinase domain. Our findings identify complementary allosteric mechanisms by which regulatory proteins tune PSKH1s catalytic activity, and raise the possibility that different Ca2+ sensors may act more broadly to tune kinase activities by detecting and decoding extremes of intracellular Ca2+ concentrations.

biochemistry↗

Connectomic Organization of the Suprachiasmatic Nucleus

The suprachiasmatic nucleus (SCN), the mammalian master clock, is a special structure dedicated to the time computation. However, a connectomic understanding of the nucleus as a whole is lacking. Using serial section electron microscopy, we reconstructed multiscale and multimodal SCN communication networks. Intra-SCN synaptic network consists of 9,566 morphologically similar neurons and 4.3 million synapses, organized into multiscale circuitries that interact with SCN-traversing axon fascicles. Strikingly, SCN neurons engage in unique soma-soma ephaptic interaction, forming 2,038 electrotonic integrative units with the largest overlapping the light-responsive area (LRA). SCNs paracrine modality contains 47,396 m3 dense core vesicles, with notable scarcity in the LRA, suggesting cross-modal coordination and functional integration. These distinct network features provide comprehensive insights into the system architecture of the mammalian circadian clock.

neuroscience↗

CXXC-finger protein 1 associates with FOXP3 to stabilize homeostasis and suppressive functions of regulatory T cells

FOXP3-expressing regulatory T (Treg) cells play a pivotal role in maintaining immune homeostasis and tolerance, with their activation being crucial for preventing various inflammatory responses. However, the mechanisms governing the epigenetic program in Treg cells during their dynamic activation remain unclear. In this study, we demonstrate that CXXC finger protein 1 (CXXC1) interacts with the transcription factor FOXP3 and facilitates the regulation of target genes by modulating H3K4me3 deposition. Cxxc1 deletion in Treg cells leads to severe inflammatory disease and spontaneous T-cell activation, with impaired immunosuppressive function. As a transcriptional regulator, CXXC1 promotes the expression of key Treg functional markers under steady-state conditions, which are essential for the maintenance of Treg cell homeostasis and their suppressive functions. Epigenetically, CXXC1 binds to the genomic regulatory regions of Treg program genes in mouse Treg cells, overlapping with FOXP3 binding sites. Given its critical role in Treg cell homeostasis, CXXC1 presents itself as a promising therapeutic target for autoimmune diseases.

immunology↗

Low-cost and highly efficient generation of near-complete bacterial pathogen genomes by TELL-Seq

Recent evidences suggest that de novo genome assembly can provide additional insights into genomic variation landscape beyond short-read NGS analyses. Despite the advent of longread sequencing technologies, generating high-quality bacterial genome assemblies remains expensive and requires high-quality and large quantities of DNA. TELL-Seq, an emerging linked-read technology, has been reported as a low-cost alternative for producing nearcomplete genome assembly in certain bacterial species. However, a systematic assessment of its performance and characteristics in de novo bacterial genome assembly has not yet been conducted. To address this, we benchmarked TELL-Seq using a set of clinical and standard bacterial pathogens with a wide range of genome size (2.0 6.4 Mbp), GC-content (32% - 68%), genome complexity (mappability from 0.15 to 0.60) and Gram types. Our findings indicate that, with 1/6 cost and 1/15,000 of DNA compared to PacBio HiFi, TELL-Seq could generate as high quality near-complete bacterial genome assemblies. The optimal depth for assembly is around 200x, as increased depth improves contiguity and completeness, though quality plateaus at 250x. In general, genome complexity was significantly correlated with assembly quality, but GC-content was not. Nevertheless, genomes with extreme GC-content may require higher depths for accurate assembly. Our study suggests that TELL-Seq could be a scalable method for large-scale bacterial genomic surveys. The data generated from this study could serve as a benchmark dataset for further algorithm development. Impact StatementAn increasing body of literature have shown that de novo genome assembles could provide additional insights into genomic variation beyond standard short-read technologies. Its particularly useful in clinical and epidemiological studies of bacteria, due to high variable nature of their genomes. Although great advances have been made in long-read sequencing technology, its still expensive with high requirement over sample DNAs quality and quantity, limiting its adoption in large-scale studies or surveys. Linked-read technology is an inexpensive alternative which used single molecule barcoding to mark origin of reads for better scaffolding of contigs assembled from normal short reads. TELL-Seq, as one of these promising technologies, was reported to be able to inexpensively and efficiently generate near-complete bacterial de novo genomic assemblies with low DNA inputs. Theres not yet a systematic benchmarking of this technology in bacterial pathogens. In this study, a set of clinically important bacterial pathogens with a wide spectrum of GC-content, genome size, genome complexity, and Gram Type were used to investigate the performance of TELL-Seq technology in de novo genome assembly. We found that, with about 1/6 of cost and 1/15000 of DNA quantity, it could generate comparable de novo assemblies compared to standard reference genomes or PacBio HiFi assemblies, while beating conventional short-read assemblies. We found several key factors, such as genome complexity, and sequencing depth, which would impact the quality of the assembly. Our study suggests that a sequencing depth of 200x is sufficient to achieve satisfactory results. Our study has revealed characteristics of this technology in bacterial genome assembly and paved the way for its large-scale application in clinical or epidemiological surveys. Data SummaryO_LIRaw sequencing data for all isolates have been deposited to SRA, accessible through these NCBI BioProject PRJNA1133244. C_LIO_LIA full list of SRA BioSample accession numbers are available in Tab S5. C_LIO_LIAssemblies and analyses companion this paper is available at: https://github.com/x-lab/tellseq_bacteria C_LI

bioinformatics↗

3D Brain Vascular Niche Model Captures Invasive Behavior and Gene Signatures of Glioblastoma

Glioblastoma (GBM) is a lethal brain cancer with no effective treatment; understanding how GBM cells respond to tumor microenvironment remains challenging as conventional cell cultures lack proper cytoarchitecture while in vivo animal models present complexity all at once. Developing a culture system to bridge the gap is thus crucial. Here, we employed a multicellular approach using human glia and vascular cells to optimize a 3-dimensional (3D) brain vascular niche model that enabled not only long-term culture of patient derived GBM cells but also recapitulation of key features of GBM heterogeneity, in particular invasion behavior and vascular association. Comparative transcriptomics of identical patient derived GBM cells in 3D and in vivo xenotransplants models revealed that glia-vascular contact induced genes concerning neural/glia development, synaptic regulation, as well as immune suppression. This gene signature displayed region specific enrichment in the leading edge and microvascular proliferation zones in human GBM and predicted poor prognosis. Gene variance analysis also uncovered histone demethylation and xylosyltransferase activity as main themes for gene adaption of GBM cells in vivo. Furthermore, our 3D model also demonstrated the capacity to provide a quiescence and a protective niche against chemotherapy. In summary, an advanced 3D brain vascular model can bridge the gap between 2D cultures and in vivo models in capturing key features of GBM heterogeneity and unveil previously unrecognized influence of glia-vascular contact for transcriptional adaption in GBM cells featuring neural/synaptic interaction and immunosuppression.

bioengineering↗

Ultra-resolution Deconvolution of Spatial Transcriptomics Unveils Spatiotemporal Cellular Dynamics in Complex Microenvironments

Immune cells infiltrate tissues in response to exogenous pathogens or spontaneous tumors, generating protective immunity to safeguard tissues. Despite advancements in spatial transcriptomics (ST), the precise spatial distribution and functional specialization of immune cells within tissue microenvironments remain elusive. Here, we introduce an ultra-precision ST deconvolution algorithm (UCASpatial) that enhances the mapping of cell subpopulations to spatial locations by leveraging the contribution of genes indicative of cell identity through entropy-based weighting. Using both in silico and real ST datasets, we demonstrate that UCASpatial improves the robustness and accuracy in identifying low-abundant cell subpopulations and distinguishing transcriptionally heterogeneous cell subpopulations. Applying UCASpatial to human colorectal cancer (CRC), we link genomic alterations in individual cancer clones to multi-cellular characteristics of the tumor immune microenvironment (TIME) and reveal the co-evolution of tumor cells and TIME at a clonal resolution. We show that the copy number gain on chromosome 20q (chr20q-gain) in tumor cells orchestrates a T cell-excluded TIME, indicative of resistance to immunotherapy in CRC, and is associated with tumor-intrinsic human endogenous retrovirus subfamily H (HERV-H) silencing and impaired type I interferon response. In murine wound healing models, we illuminate the spatiotemporal dynamics of individual cell subsets across various stages of the healing process. We discovered that the scarring-healing mice (C57BL/6) exhibited a replacement of Prg4+ chondrogenic progenitors to Igfbp5+ chondrocytes in the wound bed at the regeneration stage, a change not observed in the regenerative strain (MRL/MpJ). The Igfbp5+ chondrocyte, spatially coordinating with Cd36+ Gpnmb+ Il1b- macrophage and Fmod+ fibroblast, forms a pro-fibrotic community associated with regeneration failure. The cell-cell interactions within this three-cell cluster, mediated by the IL11-IL11RA axis, drive the pro-fibrotic community formation and limit regeneration in C57BL/6 mice. Our findings present UCASpatial as a versatile tool for deciphering fine-grained cellular landscapes in ST and exploring intercellular mechanisms in complex and dynamic microenvironments.

bioinformatics↗

Quantifying Contributions from TopologicalCycles in the Brain Network towards Cognition

This study proposes a novel metric called Homological Vertex Importance Profile (H-VIP), utilizing topological data analysis tool persistent homology, to analyze human brain structural and functional connectomes. Persistent homology is a useful tool for identifying topological features such as cycles and cavities within a network. The salience of persistent homology lies in the fact that it offers a global view of the network as a whole. However, it falls short in precisely determining the relative relevance of the vertices of the network that contribute to these topological features. Our aim is to quantify the contribution of each individual vertex in the formation of homological cycles and provide insight into local connectivity. Our proposed H-VIP metric captures, quantifies, and compresses connectivity information from vertices even at multiple degrees of separation and projects back onto each vertex. Using this metric, we analyze two independent datasets: structural connectomes from the Human Connectome Project and functional connectomes from the Alzheimers Disease Neuroimaging Initiative. Our findings indicate a positive correlation between various cognitive measures and H-VIP, in both anatomical and functional brain networks. Our study also demonstrates that the connectivity in the frontal lobe has a higher correlation with cognitive performance compared to the whole brain network. Furthermore, the H-VIP provides us with a metric to easily locate, quantify, and visualize potentially impaired connectivity for each subject and may have applications in the context of personalized medicine for neurological diseases and disorders.

bioinformatics↗

Structures of PSI-FCPI from Thalassiosira pseudonana in high light provide convergent evolution and light-adaptive strategies in diatom FCPIs

Diatoms achieve great survival success in the fluctuating oceanic environment, rely on fucoxanthin chlorophyll a/c-binding proteins (FCPs) to complete light harvesting and quenching, which provide about 20% primary productivity on earth. We report two cryo-electron microscopic structures of photosystem I (PSI) with 13 or 5 FCPIs respectively at 2.78 [A] and 3.20 [A] resolution from Thalassiosira pseudonana under high light conditions. 8 Lhcr FCPIs are found detached from the PSI-13FCPI supercomplex under high light conditions, remaining 5 FCPIs are stably combined with the PSI core including Lhcr3, RedCAP, Lhcq8, Lhcf10, and FCP3 subunits. The specific pigment network in this centric diatom T. pseudonana demonstrates a higher proportion of Chlorophylls a, diadinoxanthins, and diatoxanthins but fewer fucoxanthins compared with the huge PSI-FCPI from another centric diatom Chaetoceros gracilis, thus exhibiting more efficiency in energy transfer and dissipation among FCPI antennas. These results reveal the assembly mechanism of several types of peripheral FCPIs and corresponding light-adaptive strategies in T. pseudonana, as well as the convergent evolution of the diatoms PSI-FCPI structures.

plant biology↗

Automated Cytometric Gating with Human-Level Performance Using Bivariate Segmentation

Recent advances in cytometry technology have enabled high-throughput data collection with multiple single-cell protein expression measurements. The significant biological and technical variance between samples in cytometry has long posed a formidable challenge during the gating process, especially for the initial gates which deal with unpredictable events, such as debris and technical artifacts. Even with the same experimental machine and protocol, the target population, as well as the cell population that needs to be excluded, may vary across different measurements. To address this challenge and mitigate the labor-intensive manual gating process, we propose a deep learning framework UNITO to rigorously identify the hierarchical cytometric subpopulations. The UNITO framework transformed a cell-level classification task into an image-based semantic segmentation problem. For reproducibility purposes, the framework was applied to three independent cohorts and successfully detected initial gates that were required to identify single cellular events as well as subsequent cell gates. We validated the UNITO framework by comparing its results with previous automated methods and the consensus of at least four experienced immunologists. UNITO outperformed existing automated methods and differed from human consensus by no more than each individual human. Most critically, UNITO framework functions as a fully automated pipeline after training and does not require human hints or prior knowledge. Unlike existing multi-channel classification or clustering pipelines, UNITO can reproduce a similar contour compared to manual gating for each intermediate gating to achieve better interpretability and provide post hoc visual inspection. Beyond acting as a pioneering framework that uses image segmentation to do auto-gating, UNITO gives a fast and interpretable way to assign the cell subtype membership, and the speed of UNITO will not be impacted by the number of cells from each sample. The pre-gating and gating inference takes approximately 2 minutes for each sample using our pre-defined 9 gates system, and it can also adapt to any sequential prediction with different configurations.

immunology↗

Coxsackievirus group B3 regulates ASS1-mediated metabolic reprogramming and promotes macrophage inflammatory polarization in viral myocarditis

Coxsackievirus group B3 (CVB3) belongs to the genus Enteroviruses of the family Picornaviridae and is the main pathogen underlying viral myocarditis (VMC). No specific therapeutic is available for this condition. Argininosuccinate synthase 1 (ASS1) is a key enzyme in the urea cycle that converts citrulline and aspartic acid to argininosuccinate. Here, we found that CVB3 and its capsid protein VP2 inhibit the autophagic degradation of ASS1 and that CVB3 consumes citrulline to upregulate ASS1, triggers urea cycle metabolic reprogramming, then activates macrophages to develop pro-inflammatory polarization, thereby promoting the occurrence and development of VMC. Conversely, citrulline supplementation to prevent depletion can downregulate ASS1, rescue macrophage polarization, and alleviate the pathogenicity of VMC. These findings provide a new perspective on the occurrence and development of VMC, revealing ASS1 as a potential new target for the treatment of this disease. IMPORTANCEViral myocarditis (VMC) is a common and potentially life-threatening myocardial inflammatory disease, most commonly caused by CVB3 infection. So far, the pathogenesis of VMC caused by CVB3 is mainly focused on two aspects: one is the direct myocardial injury caused by a large number of viral replication in the early stage of infection, and the other is the local immune cell infiltration and inflammatory damage of the myocardium in the adaptive immune response stage. There are few studies on the early innate immunity of CVB3 infection in myocardial tissue, but the appearance of macrophages in the early stage of CVB3 infection suggests that they can play a regulatory role as early innate immune response cells in myocardial tissue. Here, we discovered a possible new mechanism of VMC caused by CVB3, revealed new drug targets for anti-CVB3 and discovered the therapeutic potential of citrulline for VMC.

microbiology↗

Hierarchical cortical entrainment orchestrates the multisensory processing of biological motion

When observing others behaviors, we continuously integrate their movements with the corresponding sounds to enhance perception and develop adaptive responses. However, how the human brain integrates these complex audiovisual cues based on their natural temporal correspondence remains unclear. Using electroencephalogram (EEG), we demonstrated that rhythmic cortical activity tracked the hierarchical rhythmic structures in audiovisually congruent human walking movements and footstep sounds. Remarkably, the cortical tracking effects exhibit distinct multisensory integration modes at two temporal scales: an additive mode in a lower-order, narrower temporal integration window (step-cycle) and a super-additive enhancement in a higher-order, broader temporal window (gait-cycle). Furthermore, while neural responses at the lower-order timescale reflect a domain-general audiovisual integration process, cortical tracking at the higher-order timescale is exclusively engaged in the integration of biological motion cues. In addition, only this higher-order, domain-specific cortical tracking effect correlates with individuals autistic traits, highlighting its potential as a neural marker for autism spectrum disorder. These findings unveil the multifaceted mechanism whereby rhythmic cortical activity supports the multisensory integration of human motion, shedding light on how neural coding of hierarchical temporal structures orchestrates the processing of complex, natural stimuli across multiple timescales.

neuroscience↗