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Li, G.

Publications and source records attributed to Li, G..

At least 109 records · Page 6Linked to original sources

Memory traces bias new learning for hippocampal generalization

The ability to use generalized prior experience to guide behavior in novel situations is a fundamental cognitive function1. While recent evidence suggests that the hippocampus supports generalization how this is accomplished is poorly understood2-9. Here we combined longitudinal optical imaging in head-fixed mice with computational modeling to examine generalization in hippocampal area CA1. We found that prior training accelerated behavioral adaptation to a novel environment and that this was accompanied by highly stable hippocampal representations. We identified putative memory traces from prior experience that enabled this generalization at multiple levels. At the population level, novel-context network dynamics rapidly aligned with low-dimensional neural subspaces10 established during prior experience. At the cellular level, spatially-informative weak "residual" activity reflecting generalizable information about the task structure appeared to bias which neurons form place fields (PFs) and where via behavioral timescale synaptic plasticity (BTSP)11,12. Finally, this was an active process as many PFs changed their reference frame in the novel environment to reflect the consistent task structure. In sum, the influence of memory traces on new PF formation may allow past experience to guide new learning such that representations are based on generalizable features, thus enabling rapid adaptive behavior in new contexts.

neuroscience↗

Rapid neocortical network modifications via dendritic plateau potential induced plasticity

Learning in brains is associated with changes in neuronal network activity thought to be driven by synaptic plasticity. While recent work in the hippocampus has revealed some of the mechanisms involved there, less is known about how neocortical circuits adapt, especially during behavior. Here to determine if neocortical areas possess rapid plasticity mechanisms that could support online adaptations we used optical imaging and intracellular membrane potential (Vm) recordings to examine the activity of layer V neurons in a higher visual area of mice learning a task. The introduction of a novel rewarded stimulus resulted in a rapid modification of population activity that featured abrupt alterations in single neuron selectivity. Vm recordings revealed that both naturally occurring and experimentally-induced dendritic calcium plateau potentials (plateaus) rapidly alter the action potential (APs) output and Vm dynamics of neurons over many seconds of time around the plateau, in some cases from one trial to the next. Trains of high frequency APs had no effect. Finally, experimental inhibition during learning of the distal dendritic region responsible for initiating plateaus reduced the rate of population level adaptation. Our findings suggest that the deep layers of higher order visual cortex possess a rapid learning mechanism mediated by plateau-induced synaptic plasticity.

neuroscience↗

AA-ending codon-based computational analyses uncover novel cytoplasmic effectors in the Magnaporthe oryzae secretome

Phytopathogens secrete diverse, sequence-unrelated effector proteins outside (apoplastic) or into (cytoplasmic) plant cells to suppress host defenses and cause devastating diseases. Effectors rapidly evolve to avoid counter-detection by the host, and fungal cytoplasmic effectors lack recognizable host cell-targeting motifs, impeding cataloguing of the full suite of host-deployed effectors encoded in pathogen genomes. In the devastating rice blast fungus Magnaporthe oryzae, cytoplasmic and apoplastic effectors are secreted by different routes, but candidates must be confirmed by fluorescent labelling, consequently few are known. AA-ending codon usage rates are the fraction of AA-ending codons as a percentage of the total number of AA- and synonymous AG-ending codons in an mRNA. In M. oryzae, high AA % rates of the corresponding mRNAs distinguished seven experimentally confirmed cytoplasmic effectors from four experimentally confirmed apoplastic effectors, but whether AA % rates can identify new effectors is unknown. Here, using computational analyses and live-cell imaging confirmation, we successfully predicted, based on AA % rates, two new cytoplasmic effectors and two apoplastic effectors in the M. oryzae secretome. Our findings support the notion that cytoplasmic effector mRNAs are globally enriched for AA-ending codons, aiding effector discovery and the search for novel sources of durable crop resistance.

plant biology↗

Cross-Species Transcriptomic Integration Reveals a Conserved, MIRO1-Mediated Macrophage-to-T Cell Signaling Axis Driving Immunosuppression in Glioma

Mitochondrial regulators are increasingly recognized for their influence on immune signaling within the tumor microenvironment (TME). In glioma, where immunosuppression limits therapeutic efficacy, we investigate how targeting the mitochondrial protein MIRO1 alters the TME. We combine single-nucleus RNA sequencing of murine gliomas treated in vivo with a MIRO1-binding compound and bulk RNA sequencing of human glioma resections treated with the same compound ex vivo. Cross-species transcriptomic integration reveals a MIRO1-responsive program in the TME. Among shared targets, we identify PARP11/Parp11 as a consistently upregulated gene in glioma that is downregulated following MIRO1-binding compound treatment in both human and mouse gliomas. Cell-cell communication analysis shows that a specific cluster of macrophages (MAC1), which exhibits robust Parp11 and Pdl1 (encoding PD-L1) expression, sends immunosuppressive signals to CD8+ cytotoxic T cells, and may receive prostaglandin E{square} signals from another cluster of macrophages (MAC4). Targeting MIRO1 eliminates this cell circuitry and reduces the tumor cell population. Our study provides a transcriptomic framework for understanding mitochondria-immune crosstalk and nominates MIRO1-PARP11 as a potential effector axis of brain immune dysfunction. Summary BlurbTranscriptomic integration of single-nucleus RNA sequencing of murine gliomas and bulk RNA sequencing of human gliomas reveals an immunosuppressive signaling axis in the glioma TME, mediated by MIRO1.

cancer biology↗

Neural manifolds that orchestrate walking and stopping

Walking, stopping and maintaining posture are essential motor behaviors, yet the underlying neural processes remain poorly understood. Here, we investigate neural activity behind locomotion and its walk-to-stop transition. Based on a new theory of the lumbar spinal cord1, 2 we propose and predict that spinal population activity contains limit cycle dynamics to drive walking and fixed-point attractors for stopping. To test these predictions we record neural activity in lumbar cord of freely moving rats using Neuropixels probes3. To control stopping, we stimulate a brainstem nucleus, known to induce motor arrest4-7. We find: During locomotion, the population activity of lumbar spinal neurons exhibits rotational dynamics8-10. These dynamics unfold within a low-dimensional locomotor manifold11, 12, a looping set of trajectories that serves as the repeating signature of locomotion, that also behaves as a limit-cycle attractor. Shortly before stopping, the neural state rapidly changes from the locomotor manifold to a postural fixed point attractor. When kicking the state out of the fixed point using perturbations it shifts to a nearby albeit different fixed point. Repeated stoppings form a local quasi-continuum of fixed points representing various poses - i.e. a postural manifold. These observations are in agreement with our theory, which further indicates the mechanistic roles for subpopulations of spinal interneurons for controlling walking and stopping. Besides explaining the data, our theory makes further predictions to be tested in future experiments.

neuroscience↗

Multi-Dimensional Spatiotemporal Attention Neural Network for Next Generation Sequencing Basecalling

Next-generation sequencing (NGS) remains the most used sequencing technique in the field of genomics. Traditional basecall methods face significant challenges in decoding high density sequencing data due to inherent noise in biochemical reactions and limitations of instruments. Here, we present a multi-dimensional deep learning neural network based on spatiotemporal attention mechanism named AICall. The network skips computationally heavy but less effective steps of peak finding and brightness extraction/correction, and directly basecalls from the time sequence of multi-dimensional image stacks obtained in real time. By introducing attention mechanism, it effectively extracts spatial and time-related key information including spatial crosstalk, spectral crosstalk, phasing, base-quenching, and intensity decay, and significantly improves basecall accuracy. We demonstrate that AICall achieves an average error rate less than 0.01% and provides more reliable sequencing results for downstream analysis.

bioinformatics↗

BMP-Smad1/9 signaling is required for PGC proliferation in zebrafish

The specification and maintenance of germ cell lineage are vital for reproductive development and heredity. The germ cell fate in some species, such as zebrafish and Xenopus, is determined by maternally supplied germ plasm, whereas in mammals it is induced by bone morphogenetic protein (BMP) signaling after implantation. It remains elusive whether BMP signaling is implicated in zebrafish germ cell development. Here, we demonstrate that, in zebrafish, BMP-Smad1/9 signaling is required for primordial germ cell (PGC) maintenance but not for PGC fate determination or migration. BMP inhibitor treatment or whole-embryo smad1/9 knockdown reduces the number of PGCs. To investigate cell-autonomous roles of BMP-Smad1/9 in PGCs, we generated PGC-specific smad1/9 knockouts using a double-transgenic approach with PGC-specific expression of Cas9 and ubiquitous expression of guide RNAs (gRNAs). Loss of Smad1/9 in PGCs leads to impaired PGC proliferation and increased apoptosis, resulting in reduced PGC numbers and adult sex bias. Moreover, transcriptome analysis of smad1-deficient PGCs revealed no significant changes in the expression of PGC-specific genes, but a marked upregulation of genes involved in cell cycle checkpoints and DNA damage repair. Notably, ectopic ATR-pChk1 activation in smad1-cKO PGCs validates cell cycle defects and DNA replication stress. ATR inhibition restores PGC numbers in mutant embryos. Collectively, these findings underscore a critical role of BMP-Smad1/9 signaling in zebrafish PGC population maintenance, while it is dispensable for PGC fate determination and migration.

developmental biology↗

Machine Vision Enabled Lateral Flow Immunoassay Using Functionalized Gold Nanoparticles for Point-of-Care Cardiac Biomarker Detection

Acute myocardial infarction (AMI) remains one of the most prevalent and fatal cardiovascular disease. Given the critical diagnostic significance of cardiac troponin I (cTnI) and myoglobin (Myo) in AMI, there is an urgent clinical demand for rapid and accurate detection methods to improve patient outcomes and reduce mortality. To meet this need, we developed a sensing platform that integrates functionalized gold nanoparticle-based lateral flow immunoassay (AuNPs-LFIA) with a machine vision model, enabling rapid quantitative detection of cTnI and Myo. By covalently conjugating antibodies to gold nanoparticles (AuNPs@Ab), we achieved greater probe specificity and stability. The integration of machine vision algorithms allowed quantitative readouts within 8 minutes, a 46.7% improvement of the detection time compared to conventional methods (15 minutes). The platform achieved limits of detection of 0.224 ng/mL for Myo and 0.071 ng/mL for cTnI, with excellent correlation to commercial kits (R2 > 0.99). Overall, these results demonstrate that machine vision-enhanced AuNPs-LFIA offers an efficient, sensitive and reliable strategy for point-of- care testing (POCT) in cardiovascular diagnostics, particularly in resource-limited settings.

bioengineering↗

Paw switching with lateralized cholinergic modulation

Motor preferences, such as handedness, reflect fundamental asymmetries in brain function and behavior across vertebrate species, including humans and rodents1. Although individual hand or paw preferences are typically stable, they can be reshaped through experience or training, underscoring the plasticity of lateralized motor circuits2. However, the neural mechanisms that enable this behavioral switching remain unclear. Here we show that experience-driven shifts in paw preference in mice arise from asymmetric cholinergic modulation between the two hemispheres. Using a behavioral paradigm designed to induce paw switching, we found that a subset of animals developed a stable change in preference following training. Selective activation or inhibition of cholinergic neurons on one side of the brain was sufficient to bias this switching behavior. During lateralized movements, an endogenous imbalance in cholinergic activity emerges between the hemispheres, suggesting that interhemispheric cholinergic asymmetry enables motor flexibility. These findings identify a previously unrecognized mechanism by which cholinergic signaling dynamically regulates lateralized motor control, providing insight into how hemispheric imbalances may shape persistent individual motor preferences.

neuroscience↗

Effective repurposed antivirals against an emerging virus

The ongoing global monkeypox virus (MPXV) outbreak urgently needs effective medications, which be accelerated through drug repurposing. However, it is challenging to poinpoint protein targets. Here we introduce a novel method rooted in molecular evolutionary theory for quick drug target identification for MPXV. It identifies drug targets as positively selected genes of viral proteins which bind host proteins. From the identified targets, we select a top gene product OPG021 for virtural drug screening. One top-ranked drug nilotinib is experimentally shown to have a significant 69% of antiviral efficacy of the FDA-approved antiviral tecovirimat (TPOXX(R) or ST-246). Higher binding affinity but not antiviral efficacy of repursposed drugs than FDA-approved drugs suggests the complexity of drug repurposing and underscores the importance of experimental validation. This innovative drug target identification strategy will contribute to combating the ongoing MPXV outbreak and other viral acute and chronic viral diseases.

pathology↗

Species-specific basal fluidization shapes early forebrain development

The human forebrain exhibits an expanded surface area compared with other great apes. Despite progress in dissecting species-specific gene expression programs and cell lineages, the tissue-level physical mechanisms underlying human-specific neurodevelopment remain unclear. Here, by quantifying tissue dynamics and mechanics using oil microdroplets in cerebral organoids from humans, gorillas, chimpanzees, and mice, we uncover a transient tissue fluidization occurring exclusively in the basal region of human neuroepithelia. Enhanced droplet motility and frequent cell rearrangements reveal this basal fluidization, which gradually diminishes at the onset of neurogenesis in humans. By contrast, such basal fluidization is not detected in non-human neuroepithelia examined here. Mechanistically, basal fluidization is driven by basal nuclear fluctuations and facilitated by expanded intercellular spaces. Increasing N-cadherin expression in human neuroepithelia to gorilla levels suppresses both nuclear fluctuations and basal fluidization. Integrating simulations of neuroepithelial dynamics with experimental data, we further find that nuclear fluctuations underlying basal fluidization promote the insertion of newly divided nuclei into the basal side to support tangential surface expansion, a hallmark of human forebrain development.

developmental biology↗

De Novo Design of Anti-Aging Peptides

Aging, a universal biological process in complex organisms, is increasingly recognized to be driven by progressive loss of epigenetic information, as proposed in the Information Theory of Aging (ITOA). However, research on anti-aging peptides remains scarce, with most existing efforts confined to derivatives of natural proteins, while systematic design attempts are virtually absent. This limitation not only restricts discovery within the evolutionary sequence space but also hampers the identification of candidates with novel mechanisms and improved efficacy. Here, we present ElixirSeeker2, the first computational framework for de novo design of anti-aging peptides. By integrating modeling of known anti-aging peptides, activity scoring from the IC50 database, and penalty constraints from toxic peptides, ElixirSeeker2 enables large-scale virtual screening and identification of novel peptide candidates. Several lead peptides demonstrated significant effects in delaying cellular senescence, restoring cellular functions in vitro and in enhancing locomotor activity of aged Caenorhabditis elegans. This study not only validates the feasibility of de novo design in anti-aging interventions but also establishes a strategy for the development of next-generation biologics.

bioinformatics↗

Suppressing cortical glutamatergic neurons produces paradoxical interictal discharges and seizures

IntroductionSeizures are traditionally attributed to excessive excitation or deficient inhibition, yet recent clinical and slice data show they can also paradoxically arise when inhibition outweighs excitation. We chemogenetically suppressed neocortical glutamatergic neurons to test whether such suppression elicits epileptic activity in vivo. MethodsCaMKII-driven Gi-coupled hM4Di or Gq-coupled hM3Dq Designer Receptor Exclusively Activated by Designer Drug (DREADDs) were expressed in cortical glutamatergic neurons of Rasgrf2-jGCaMP8m and wildtype C57BL/6J mice. Widefield calcium imaging and 32-channel transparent electrocorticography were performed before and after systemic clozapine-N-oxide (CNO; 1.25-5 mg kg {superscript 1}). ResultsDREADD activation induced intermittent, large-amplitude, synchronized calcium transients confined to the CaMKII-hM4Di focus, accompanied by focal ECoG spikes that persisted for >3 h and sometimes evolved into seizures. By contrast, CNO activation of excitatory neurons via CaMKII-hM3Dq DREADDs desynchronized activity without epileptiform discharges. The same process duplicated in wild-type animals provoked similar epileptiform discharges. ConclusionSelective suppression of excitation can paradoxically drive cortical networks into hypersynchronous, epileptic states, challenging the simple excess-excitation model of ictogenesis. These findings highlight that seizures may result from relative inhibitory dominance, and that considering this excess inhibition mechanism could inspire new therapeutic approaches.

neuroscience↗

Microbes suppress genetic disorders of hyper-activated Ras by inhibiting iron-mediated growth factor modulation in C. elegans

Gut bacteria play crucial roles in promoting host health, but their ability to suppress the effects of genetic defects remains unclear. Ras(gain-of-function, gf) mutations are involved in various developmental disorders, thus identifying bacterial-activity changes capable of repressing the effects of hyper-activated Ras is important. Here, we screened mutations of all non-essential E. coli genes and identified 151 E. coli mutants that mitigate let-60/Ras(gf)-induced vulval developmental abnormalities in C. elegans. Interestingly, bacteria with mutations in genes involved in iron acquisition suppress host Ras(gf)-induced vulval defects through elevating 2,3-dihydroxybenzoic acid, a bacterial siderophore that sequesters iron. Consequently, host mitochondrial iron availability is decreased, which prompts the nuclear accumulation of the chromatin modifier LIN-65 and then downregulates lin-3/EGF transcription to repress Ras(gf)-induced vulval defects. Our findings identify a mechanism for coordinating Ras growth signaling with iron availability, through which gut bacteria suppress host Ras(gf)-induced defects and exemplify the potential of modifying gut bacterial activity to improve genetic diseases.

developmental biology↗

scPhoenix: A Contrastive Learning-based Framework with Aux-Core Feature Disentanglement Enhances Sparse Cellular Multi-omics Translation

Recent advances in single-cell multi-omics co-assays and spatiotemporal sequencing technologies have provided unprecedented opportunities for systematically characterizing cellular heterogeneity. However, severe sparsity and pronounced spatial heterogeneity--hallmark features of complex diseases and tumor microenvironment--remain major obstacles in deciphering cellular multi-omics data. Here, we present scPhoenix, a contrastive learning-based framework for single-cell cross-modality translation. scPhoenix adopts a two-stage Aux-Core strategy to disentangle modality-specific feature extraction from cross-modality feature interaction. Across diverse datasets, it preserves cellular heterogeneity during translation and demonstrates significant advantages for data with high sparsity. In addition, the framework integrates a contrastive learning framework with five effective data augmentation methods tailored to single-cell data. Moreover, scPhoenixs design supports extensions to unpaired data training and spatial multi-omics translation, enabling robust performance in scenarios with high spatial heterogeneity. scPhoenix is freely available at https://github.com/liwz-lab/scPhoenix.

bioinformatics↗

XomicsDB: a database of paired multi-omics datasets for systems biology

Life science research is primarily driven by data integration on the basis of theoretical development. Broad applications of multiomics (xomics) data calls for efficient integration of xomics data to infer cellular operation and regulation. To that end, it is urgently needed good-quality xomics data should be curated and shared for the community. Here we present XomicsDB, a database curating paired xomics datasets at both bulk and single-cell levels in model organisms. It contains 183 datasets from 13 model organisms, with a total of seven xomics data types. Users can download these datasets individually or in a batch from the ftp server provided. Users can also upload their paired xomics datasets for sharing. Incoporation of xomics data intom GSMs are demonstrated in model organisms Escherichia coli and human. Future efforts will be on collecting more single-cell xomics data and curating non-model oragnisms. The XomicsDB can be found at: http://xomicsdb.com.

systems biology↗

PRIME: A Multi-Agent Environment for Orchestrating Dynamic Computational Workflows in Protein Engineering

Artificial intelligence (AI) is revolutionizing protein engineering, yet its practical application is often hindered by a fragmented toolchain and the specialized expertise required to orchestrate complex computational workflows. To address these challenges, we have developed PRIME, an autonomous protein engineering multi-agent system. The core innovation of PRIME is dynamic workflow synthesis: it interprets high-level engineering objectives, reasons over a curated library of more than 65 validated protein tools, and autonomously constructs custom computational pathways. Crucially, by grounding every step in verifiable tool execution, PRIME mitigates the risk of model hallucination. It also automates the complete pipeline for developing specialized AI models, from data acquisition through training. In a benchmark of 213 multi-step protein engineering tasks, PRIME exhibited superior performance, successfully completing the majority of tasks where state-of-the-art, general-purpose AI agents fail. We validated its capabilities in demanding real-world applications, including the fully autonomous training of a machine learning classifier and the de novo design of a therapeutic antibody against SARS-CoV-2. By abstracting technical complexity, PRIME empowers scientists to execute sophisticated computational experiments with unprecedented flexibility, establishing a new paradigm for autonomous scientific discovery. The PRIME agent and source code will be made publicly available.

bioinformatics↗

RhoGAP54D promotes cell size asymmetry and inhibits pulsatile Myosin activity in Drosophila neural stem cells

The Actomyosin cortex is a highly dynamic part of the cytoskeleton and cells can modulate its properties. This is important for essential cellular functions including migration, cell shape control and cleavage furrow positioning during cell division. Asymmetrically dividing Drosophila neural stem cells, called neuroblasts, exhibit stereotypic patterns of Myosin dynamics along the cell cycle. Some of the Myosin dynamics manifest as flows and are important to asymmetrically position the cleavage furrow which establishes the cell size-difference between the neuroblast and its daughter cell. Myosin can be regulated by small GTPases and their GAPs and GEFs, providing spatio-temporal control. Rho kinase downstream of the small GTPase Rho regulates Myosin activity, yet the regulation and contribution of its GEFs and GAPs to asymmetric neuroblast division are not resolved. Here, we systematically analysed the localization of RhoGAPs and RhoGEFs expressed in neuroblasts and identified the ARHGAP19 homolog RhoGAP54D as a regulator of Myosin dynamics. A cytoplasmic pool of RhoGAP54D suppresses pulsatile Myosin activity during interphase and metaphase, regulated by the nucleoporin Members Only via slow nuclear import. In anaphase RhoGAP54D is recruited to the apical cortex and constitutes the trigger that initiates the directional Myosin flow that positions the cleavage furrow. This depends on PsGEF which is itself recruited downstream of Par3/Baz and Pins, linking cell polarity to RhoGAP54D activity to promote daughter cell size asymmetry during neuroblast division.

cell biology↗