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Lyu, J.

Publications and source records attributed to Lyu, J..

At least 19 recordsLinked to original sources

Intelligent SEEQPI enables reconstruction of inhibitory neuronal nuclei and dry-mass mapping deep in the living mouse brain

Multiphoton fluorescence microscopy enables deep brain imaging with subcellular resolution and molecular specificity, but limited photon budgets constrained by tissue heating and nonlinear damage restrict temporal resolution of structural imaging in deeper regions. Moreover, imaging multiple molecularly defined cell populations requires additional fluorescent labels, while spectral bandwidth and crosstalk constrain multiplexed detection. Here we develop an intelligent imaging framework that uses label-free Scattering-Enabled Epi-Quantitative Phase Imaging (SEEQPI) to infer molecularly specific information deep in vivo. Using paired SEEQPI and three-photon fluorescence images, we developed a Feature-wise Linear Modulation U-Net with generative adversarial learning to reconstruct inhibitory-neuron nuclei. The network accurately predicts nuclear distributions and maintains performance when training and validation volumes are separated axially by up to 6 m, enabling sparse fluorescence supervision. Cross-animal training further improves predictions in sparsely sampled target animals. Inferred nuclear maps enable dry-mass density estimation, demonstrating molecularly specific, label-free quantitative imaging deep within the living brain.

bioengineering↗

Astrocytes in the Dentate Gyrus Shift the Equilibrium from Pattern Separation to Pattern Completion and Inhibit Fear Extinction

Pattern separation and pattern completion are core hippocampal computations linked to memory interference and overgeneralization in many neuropsychiatric disorders and to mnemonic discrimination deficits in neurodegenerative conditions. Astrocytes are increasingly recognized as important integrators and modulators of neuronal activity as many studies have shown changes in animal behavior and neural circuits induced by manipulation of astrocytic activity. The role of astrocytes in the dentate gyrus for learning and memory is, however, largely unknown. To investigate the functional significance of astrocytic activity in the dentate gyrus, we expressed the calcium extruding pump hPMCA2w/b (CalEx), resulting in inhibition of astrocytic calcium activity, the Gq-coupled receptor hM3Dq, or the Gi-coupled receptor hM4Di, allowing chronic activation of Gq- and Gi-dependent pathways by a designer drug, in dentate gyrus astrocytes. Our main finding is that inhibition of astrocytic calcium activity by CalEx resulted in improved pattern separation and impaired pattern completion. In -vivo calcium imaging revealed that CalEx expression in astrocytes altered the neuronal activity pattern in dentate gyrus neurons with an overall inhibitory effect. This suggests that in the dentate gyrus astrocytes promote the activity of these neurons. Furthermore, chronic activation of hM4Di resulted in impaired between-session fear extinction while chronic activation of hM3Dq resulted in impaired within-session fear extinction and improved pattern separation learning over multiple days, suggesting that activation of astrocytic activity enhances mechanistically separable forms of fear extinction in a Gq- or Gi-pathway-specific manner. Our findings reveal that dentate gyrus astrocytic calcium shifts the balance between pattern separation and pattern completion towards pattern completion and thus modulates an essential neuronal functional output of the dentate gyrus. Chronic activation of astrocytes inhibits fear extinction, and thus also affects management of memory interference. Our findings imply that astrocytic modulation may be beneficial to treat cognitive deficits in disorders in which overgeneralization is a problem.

neuroscience↗

Spontaneous behavior predicts colony membership, individual identity, and rank in naked mole-rat societies

Animal societies are organized across scales, from moment-to-moment actions of individuals to dynamic group structure. A central challenge in sociobiology is to understand how behaviors of individuals shape group structure. Here, using machine vision to map recurrent fine-scale behavioral modules in the eusocial naked mole-rat (Heterocephalus glaber), we show that spontaneous behavior in isolation predicts group-level social organization, including colony membership and individual identity. We determined dominance relationships and found highly linear hierarchies, with ranks stable over months to years. Remarkably, fine-scale behavioral profiles in isolation correctly predicted pairwise dominance relationships, allowing reconstruction of rank order within each colony. Models trained within one colony predicted rank poorly in others, suggesting that naked mole-rats express social position through behavioral patterns specific to each colony. Together, our results connect fine-scale behavior to social structure maintained over years and show that, even when an animal is alone, its behavior carries signatures of its identity, colony, and place within that society.

animal behavior and cognition↗

Topoisomerase-mediated resolution of negative DNA supercoiling sustains human transcription and gene activation

Transcription generates DNA supercoiling that can influence gene expression, but how transcription-associated supercoiling shapes RNA polymerase II (RNAPII) dynamics in human cells remain poorly understood. Here, we show that topoisomerase-mediated resolution of negative DNA supercoiling is required for productive transcription. Acute topoisomerase perturbation causes negative supercoiling to accumulate around transcription start sites (TSS), with greater negative supercoiling accumulation associated with stronger transcription reduction. Elevated negative supercoiling behind the elongating RNAPII, but not positive supercoiling ahead, is associated with reduced RNAPII elongation rates. Using NOTE-seq2 to simultaneously profile newly synthesized and total RNA in single cells, we further demonstrate that acute TOP1 depletion increases gene expression noise by reducing both transcriptional burst size and frequency. Mechanistically, negative supercoiling accumulation at TSS increases RNAPII promoter occupancy and promoter-proximal pausing, providing a potential basis for reduced burst size. Micro-C analysis shows that TOP1 depletion largely preserves chromatin compartments and TADs but weakens short-range chromatin loops, including enhancer-promoter interactions, likely contributing to reduced burst frequency. Finally, during T-cell activation, impaired resolution of negative supercoiling compromises rapid gene upregulation and attenuates the transcriptional activation program. Together, these findings establish topoisomerase-mediated resolution of negative DNA supercoiling as a key mechanism linking DNA topological homeostasis to RNAPII dynamics, chromatin looping, and rapid gene activation.

genomics↗

A Single-cell Spatiotemporal Atlas Encoding Age-dependent Evolution of the Ischemic Penumbra

Aging is the predominant risk factor for stroke and a major driver of poor neurological recovery. Although the ischemic penumbra represents a key therapeutic target, its age-dependent molecular landscape remains poorly understood. Here, we generated a spatiotemporal transcriptomic atlas of the post-stroke penumbra in young (3-4 months) and aged (19-20 months) mice at acute (day 3) and chronic (day 14) stages following transient focal cerebral ischemia. Integrating spatial transcriptomics with dissociated single-cell RNA sequencing revealed a persistent transcriptomic penumbra (TP) that remains detectable for at least 14 days after stroke in both age groups, far beyond the window suggested by conventional imaging modalities. Aging profoundly altered TP organization, resulting in dysregulated energy metabolism, impaired neurovascular repair, diminished pro-reparative cell-cell communication, and extensive remodeling of transcriptional regulatory networks. Using this atlas, we further identified regulatory hub genes whose predicted perturbation could simultaneously counteract multiple age-associated pathological pathways. These data define the molecular architecture of the aging post-stroke penumbra and provide a publicly accessible framework for mechanistic discovery and therapeutic target prioritization aimed at improving recovery after stroke.

neuroscience↗

The mitochondrial RNA extrusion-induced innate immunity is regulated by N6-methyladenosine machinery

Mitochondrial RNA (mtRNA) released into the cytosol functions as a damage associated molecular pattern that activates pattern-recognition receptor (PRR)-mediated inflammation, yet its release mechanisms and cytoplasmic fate remain poorly understood. Here we report that chemical Abt-373-treatment and Vesicular stomatitis virus (VSV) infection induce mtRNA extrusion through Bax/Bak and VDAC1 channels, accompanied by mtDNA release. Extruded mtRNA in A549 cells activates multiple cytosolic PRRs, including RIG-I, MDA5, TLR3/7/8, and PKR, each contributing differentially to the innate immune signaling. Analysis of GEO datasets and methylated RNA immunoprecipitation (MeRIP) assays further reveals that mtRNA carries methyladenosine (m6A) modification. m6A machinery proteins are involved in the cytoplasmic retention time of mtRNA and its interaction with RIG-I, thereby modulating mtRNA-induced innate immunity. Thus, our work establishes in vitro models of mtRNA extrusion, and highlights m6A-dependent modulation as a potential therapeutic target for mtRNA-driven inflammation.

immunology↗

Visualizing immunoreceptor forces and their effects in vivo

Immunoreceptors experience forces that modulate their activities; however, demonstrating this in vivo has been limited by technical challenges. As a first step toward meeting this challenge, we adapted a synthetic Notch (SynNotch) receptor system to report force transmission through immunoreceptors in vivo by replacing the native ligand-binding domain with a receptor-specific antibody and rewiring Notch signaling to drive EGFP or luciferase expression. We expressed SynNotch on Jurkat cells targeting CD40 or T cell receptor (TCR) and characterized their activation in coculture with B or T cells, defining the requirements, optimal conditions, and kinetics of activation. Using complementary mechanobiology approaches, we quantified the exogenous force required for reporter activation and verified that activation depends on forces generated by receptor-expressing sender cells rather than SynNotch-expressing receiver cells. By implanting sensors and targets into immunocompromised mice, we visualized mechanically activated reporter expression on CD40 and TCR-targeting SynNotch cells in vivo. Furthermore, CD40 and TCR signaling was amplified when the receptor bore force against mechanical support from immobilized ligand, indicating that force functions as biologically relevant co-stimulus. Together, our results establish mechanically activated SynNotch reporters as a useful strategy for detecting receptor-associated mechanical signaling across 2D coculture, 3D organoid, and in vivo systems.

bioengineering↗

Combinatorial docking and molecular generation to navigate over 100-billion molecules for prospective ligand discovery

Commercially available make-on-demand libraries now exceed 100 billion compounds, requiring over 50 years to screen on 2,000 CPU cores using conventional docking. We present two complementary approaches to address this challenge. CombiDOCK, a combinatorial docking framework, enables exhaustive screening at the 100-billion scale within 40 days. MINT-Dock, a generative framework, accelerates navigation of this space by integrating CombiDOCK with Monte Carlo Tree Search. Benchmarked on 46 diverse targets, CombiDOCK matched full-molecule docking accuracy, and MINT-Dock achieved a 4,800-fold enrichment over random selection. Compared with prior billion-scale brute-force campaigns against {sigma}2, VMAT2, and VAChT, prospective CombiDOCK screens of the 100-billion-molecule library yielded higher hit rates and more potent ligands, while MINT-Dock achieved comparable outcomes across single- and multi-target objectives with >20-fold computational cost reductions. Docking-predicted poses of the best VAChT-binding compounds were confirmed by cryo-EM structures. These methods provide exhaustive and generative paths for navigating the trillion-molecule frontier of drug discovery.

bioinformatics↗

A Small-Molecule Mitochondrial Complex I Modulator Improves Behavioral and Mitochondrial Dysfunction in Schizophrenia

Weak inhibition of mitochondrial complex I (mtCI) has been shown to have neuroprotective effects in cellular and animal models of Alzheimers and Huntingtons diseases, at least in part by enhancing mitochondrial biogenesis and function. Mitochondrial dysfunction has also been demonstrated in schizophrenia patients and mouse models of schizophrenia. We tested whether weak inhibition of mtCI would ameliorate mitochondrial and behavioral phenotypes in a mouse model of schizophrenia. In mice with four copies of the Gldc gene, 8 weeks of treatment with the weak mtCI inhibitor, the small-molecule tricyclic pyrone compound CP2, reversed spontaneous alternation deficits in the Y maze, startle habituation deficits, and social novelty deficits in the three-chamber social interaction test. Consistent with the mechanism of action, Western blots revealed that CP2 reverses the reduced expression of PGC-1, a master regulator of mitochondrial biogenesis, and of the VDAC1, a primary gatekeeper for the exchange of metabolites, ions, and ATP between mitochondria and the cytosol. These findings suggest that the improvement of mitochondrial function may represent a novel strategy to reverse pathophysiological and behavioral deficits in schizophrenia.

neuroscience↗

The Impact of Dysregulated Lipid Metabolism on the Gut-Brain Axis in Patients with Intracerebral Hemorrhage

BACKGROUNGBisphenol A (BPA) has been linked to hypertension and disturbances in lipid metabolism; however, limited evidence is available regarding its association with hypertensive intracerebral hemorrhage (ICH). METHODSA multicenter, retrospective case-control study was conducted involving 129 participants, including individuals from an ICH group and healthy controls. Standard assays were employed to assess serum thyroid function, lipid profiles, serum fatty acid-binding [x]protein 4 (FABP4), oxidative stress markers, gap junction proteins, Wnt/{beta}-catenin signaling pathway activity, and expression changes of S100A8-mediated inflammatory cytokines involved in gut-brain interactions. Correlation analyses using Pearson and Spearman methods revealed that both BPA exposure and low T3 levels were significantly associated with elevated diastolic blood pressure, altered lipid metabolism, gut microbiota composition, and microglial activation. RESULTSGender-based disparities in lipid metabolism were identified. Changes in {beta}3-adrenergic receptor and neuromodulin-1 expression appear to influence fat regulation and attenuate oxidative stress responses. Subsequently, increased expression of gap junction proteins and activation of the Wnt/{beta}-catenin signaling pathway contribute to metabolic reprogramming and alterations in biochemical kinetics. Gut microbiota analysis demonstrated that, compared to controls, the ICH group exhibited significant dysbiosis and reduced alpha diversity. Further correlation analyses indicated that BPA levels were positively associated with FABP4 and oxidative stress markers, while S100A8 showed a strong dependence on microglial expression. CONCLUSIONThe interplay between lipid metabolism dysfunction and pro-inflammatory cytokines enhances vascular vulnerability. Collectively, BPA exposure, oxidative stress, and microglia-mediated neuroinflammation are significantly associated with an elevated risk of hypertensive ICH. China Clinical Trial Registry registration noticeFrom: China Clinical Trials Registry +To:guopingwang60a yunyanshuangfei FUNDINGThis work was supported by the Natural Science Foundation of Shanxi Province (grant no. 201701D121177) Key informationGender-specific differences were observed in lipid metabolism and oxidative stress parameters; BPA exposure was shown to induce lipid metabolic disturbances, promote excessive production of oxidative stress byproducts, and consequently elevate oxidative stress responses; BPA was associated with stress-induced alterations in thyroid hormone function, further exacerbating dysregulation of lipid metabolism and oxidative stress; Fatty acid binding protein 4 (FABP4), a key adipokine implicated in metabolic disorders and adipose tissue inflammation, exhibited a significant positive correlation with serum BPA levels, whereas low levels of triiodothyronine (T3) were negatively correlated with FABP4. These findings suggest that serum FABP4 may serve as a biochemical marker for chronic low-grade adipose tissue inflammation and metabolic dysfunction; Gap junction proteins and the Wnt/{beta}-catenin signaling pathway may contribute to microglial activation and mediate neuroinflammatory responses, nerve injury, and secondary pathological processes in obesity-related cerebral hemorrhage.

biochemistry↗

A post-translational regulatory map of chronic antigen-driven human T cell dysfunction.

T cells exposed to persistent antigen in the context of chronic viral infections or cancer lose self-renewal and cytotoxic capacity. Several transcriptional, epigenetic, and metabolic drivers of this process have been identified. However, the post-transcriptional regulatory mechanisms influencing the proteome of dysfunctional T cells are not well understood. Here we present a time-resolved molecular landscape of human T cells during the development of chronic antigen-driven dysfunction. Persistent T cell receptor stimulation significantly remodeled the proteome, including changes in canonical T cell exhaustion-associated proteins and proteins related to mitochondrial function, redox homeostasis, nucleotide metabolism, and cell-cycle progression. Dysfunctional T cells displayed activation of stress response pathways that were recapitulated in vivo; targeting these pathways altered the cytotoxic capacity of T cells during persistent tumor exposure. Our comprehensive proteomic resource reveals unique post-transcriptional changes in dysfunctional T cells and lays the groundwork for novel cysteine-directed therapeutics to enhance cancer immunotherapy.

immunology↗

Inhibition of Endocannabinoid Degradation in Astrocytes Reprograms Glial Reactivity and Prevents Seizure Sequelae

BackgroundTemporal lobe epilepsy (TLE) is the most common form of focal epilepsy and is characterized by a pathological cascade of excitotoxicity that leads to neuroinflammation, progressive neuronal loss, and subsequent cognitive decline. Despite its prevalence, effective disease-modifying therapies remain lacking. Previous studies have demonstrated that the endocannabinoid system contributes to epileptic activity. In particular, inactivation of monoacylglycerol lipase (MAGL), the key rate-limiting enzyme responsible for the degradation of the endocannabinoid 2-arachidonoylglycerol (2-AG), an endogenous lipid mediator with anti-inflammatory and neuroprotective properties, suppresses seizures and reduces neuroinflammation. However, the cellular and molecular mechanisms underlying these protective effects remain unclear. MethodsTo dissect the cellular mechanisms underlying MAGL-mediated neuroprotection, we employed a kainic acid (KA)-induced status epilepticus model in mice with global, astrocyte-specific (aKO), and neuron-specific (nKO) deletion of mgll. We combined single-nucleus RNA sequencing (snRNA-seq) to map the transcriptomic landscape of glial responses with pharmacological interventions to validate key signaling pathways, as well as behavioral assays to assess functional recovery. ResultsWe demonstrated that astrocyte-specific, but not neuron-specific, mgll deletion was sufficient to attenuate seizure susceptibility and hippocampal neurodegeneration, thereby recapitulating the protective phenotype observed in global knockouts. Transcriptomic profiling revealed that astrocytic MAGL deficiency fundamentally reshaped the glial response to injury by preventing the transition to pro-inflammatory reactive astrocyte states and suppressing the activation of disease-associated microglia (DAM). Mechanistically, we identified a signaling pathway in which the neuroprotective effects of MAGL inhibition depend on cannabinoid receptor 1 (CB1) activation and are mediated by downstream peroxisome proliferator-activated receptor {gamma} (PPAR-{gamma}) signaling. Either genetic deletion of CB1 or pharmacological blockade of PPAR-{gamma} abolished the protective effects. Furthermore, aKO mice exhibited reduced neuronal loss, preserved synaptic structural integrity and protection against post-seizure cognitive deficits. ConclusionThese findings reveal astrocytic MAGL as a crucial regulatory node in the epileptic brain and demonstrated that enhancing 2-AG signaling in astrocytes orchestrates neuroprotection via CB1-PPAR-{gamma} signaling pathways, thereby attenuating neuroinflammation, preserving synaptic function, and preventing the cognitive comorbidities associated with epilepsy.

neuroscience↗

The Red Rice Bran Extract (RRBE) Mitigates Photoaging by Targeting Mitochondrial Oxidative Stress and Regulating Thermal Damage Responses

The photoprotective efficacy of natural skin-active complexes is well recognized, yet their ap-plication is often hindered by the challenge of deciphering their complex, multi-component, and multi-target mechanisms. To bridge the gap between established phenotypes and molecular mechanisms, we developed an AI-driven integrated platform that combines phytochemical profiling, network pharmacology, and deep learning-based target prediction with rigorous biophysical validation. We applied this platform to investigate RRBE, a bioactive complex refined from red rice bran extract. In vivo clinical studies confirmed that RRBE significantly accelerates the resolution of UV-induced erythema, while cellular and 3D tissue models demonstrated robust suppression of oxidative stress and DNA damage responses. To decode its material basis, the platform deconstructed RRBE into 10 distinct chemical modules. Leveraging our SCOPE-DTI deep learning model for global target prediction, we identified flavonoids (Module 1) and phenolic acids (Module 10) as the primary bioactive drivers relevant to photoprotection. These computational predictions were structurally supported by molecular docking and definitively validated in a physiological environment via Cellular Thermal Shift Assay-Mass Spectrometry (CETSA-MS). Mechanistically, RRBE functions through a synergistic polypharmacology: (1) Module 1 components, represented by procyanidin B2, target NDUFA7 to stabilize mitochondrial function and mitigate ROS; (2) Module 10 components, exemplified by caffeic acid, ferulic acid, and p-coumaric acid, engage FKBP11 and HSP90AA1 to regulate protein homeostasis and stress responses. This work not only deciphers the polypharmacological basis of RRBEs photoprotective action but also validates a scalable "AI-guided, cell-validated" discovery pipeline, offering a rational paradigm for uncovering the protective benefits of complex natural extracts.

systems biology↗

Selective Inactivation of Astrocytic Monoacylglycerol Lipase for Alzheimer Disease Therapy

Alzheimers disease (AD) is the leading cause of dementia in the elderly, yet effective therapies remain lacking. Here, we identify monoacylglycerol lipase (MAGL), the principal enzyme that degrades the endocannabinoid 2-arachidonoylglycerol (2-AG) in the brain, specifically in astrocytes as a promising therapeutic target for AD. APP transgenic (TG) mice with astrocyte-specific MAGL deletion (TG-aKO), but not neuron-specific deletion (TG-nKO), exhibit markedly reduced A{beta} pathology, neurodegeneration, and neuroinflammation, along with preserved synaptic structure and function and improved cognition. These benefits are recapitulated in TG mice by AAV-mediated silencing of astrocytic MAGL, whereas MAGL overexpression exacerbates neuropathology and accelerates synaptic and cognitive decline. Transcriptomic analyses reveal that dysregulated synapse-, inflammation-, and AD-related gene expression profiles are reversed in TG-aKO mice. MAGL expression is elevated in astrocytes from both AD patients and TG mice. Remarkably, a single intracerebroventricular (ICV) injection of AAV-MAGL-shRNA administered at either presymptomatic or postsymptomatic stages prevents or reverses neuropathology and synaptic and cognitive impairments in TG mice, providing preclinical evidence that astrocytic MAGL silencing represents an effective therapeutic strategy for AD.

neuroscience↗

AlphaFold3 for Structure-guided Ligand Discovery

Deep-learning methods for protein structure prediction, such as AlphaFold2 (AF2) and RosettaFold (RF), have transformed structural biology and accelerated downstream biological discovery. More recent models, including AlphaFold3 (AF3) and RosettaFold All-Atom (RFAA), extend this capability to protein-ligand co-folding, enabling direct prediction of bound complexes from sequence and ligand inputs. This advance has raised the possibility that such models could function not only as structure predictors but also as AI-based molecular docking engines for virtual screening. Yet their true impact on ligand discovery remains unclear and, in many cases, controversial. Here, we systematically assess AF3 co-folding across tasks central to small-molecule discovery compared to conventional molecular docking. First, retrospective enrichment of actives over decoys showed that AF3 outperforms the physics-based docking program DOCK3 across 43 drug targets in DUDE-Z; however, this advantage is largely driven by hidden ligand-only biases inherent to computational decoy sets. In contrast, in three large experimental datasets (the sigma-2 receptor ({sigma}2), the D4 dopamine receptor (D4), AmpC {beta}-lactamase (AmpC)) with over 2,500 tested molecules that lack such biases, DOCK3 achieved stronger overall enrichment, while AF3 contributed mainly to early enrichment. Second, out-of-sample pose reproduction on >8,000 protein-ligand complexes deposited after the AF3 training and validation cutoff showed that AF3 accuracy is strongly dependent on training-set similarity, indicating that the model memorizes atomic positions more than learning general principles of molecular recognition. Finally, in the first prospective head-to-head screen against the {sigma}2 receptor, novel to AF3s training set, AF3 achieved a 13% hit rate and identified a 13 nM binder directly from the screen. However, compared with the parallel DOCK3 campaign, AF3 delivered a two-fold lower hit rate, despite yielding a similar affinity distribution among the top five hits. A crystal structure of the {sigma}2 receptor bound to the most potent AF3-derived hit confirmed that AF3 produced a near-native ligand pose. AF3 therefore represents the beginning of deep-learning-based structure-guided ligand discovery: a complementary tool rather than a replacement for conventional docking, with practical applications both as a screening engine and as a post-docking filter that improves hit rates. More broadly, this work establishes a framework for evaluating next-generation deep-learning co-folding models and quantifying their impact on small-molecule discovery.

pharmacology and toxicology↗

Ventral Hippocampal Temporoammonic and Schaffer Collateral Pathways Differentially Control Fear- and Anxiety-Related Behaviors

The ventral hippocampus plays a crucial role in regulating anxiety- and fear-related behaviors. Previously, we demonstrated that diazepam reduces anxiety-like behavior by inhibiting the dentate gyrus and CA3 principal neurons via 2-GABAARs, while inhibition of CA1 pyramidal neurons is necessary to suppress fear-related responses. This study investigated the role of inputs from ventral CA3 (vCA3) and entorhinal cortex to ventral CA1 (vCA1) in anxiety- and fear-like behavior using bidirectional optogenetic modulations. Adult C57BL/6J male and female mice were subjected to bilateral stereotaxic injection of a viral vector expressing channelrhodopsin or halorhodopsin into vCA3 or into layers II-III of lateral entorhinal cortex, followed by bilateral implantation of fiberoptic ferrules into vCA1. After four weeks of recovery, mice were assessed for anxiety-like behavior in the novel open field, elevated plus maze, and Vogel conflict tests, and by contextual and trace fear conditioning for fear. The behavior of the mice was recorded under laser ON and OFF conditions in all experiments. The activation of vCA3 to vCA1 projections (i.e., Schaffer collateral pathway) increased anxiety- and fear-related behaviors, whereas inhibition reduced such behaviors. In contrast, optogenetic activation or inhibition of EC to vCA1 projections (i.e., temporoammonic pathway) had no effect on anxiety-related behavior but positively or negatively modulated fear-related behavior, respectively. These results suggest that while fear-related behavior is modulated by both inputs to vCA1, modulation of anxiety-related behavior is input-specific for the vCA3 to vCA1 projection. In summary, this study offers mechanistic insights into the complex organization of hippocampal circuitry underlying fear and anxiety. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=183 SRC="FIGDIR/small/690696v1_ufig1.gif" ALT="Figure 1"> View larger version (42K): org.highwire.dtl.DTLVardef@1a3a0d7org.highwire.dtl.DTLVardef@194b96forg.highwire.dtl.DTLVardef@11a62b7org.highwire.dtl.DTLVardef@1471977_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

Butyrate blocks specific histone acetylation by preventing recruitment of p300 to acetylated histones

Butyrate, a short-chain fatty acid (SCFA) produced by microbial fermentation of dietary fiber, exerts beneficial metabolic and immunomodulatory functions through hyperactivation of the histone acetylase (HAT) p300 and inhibition of histone deacetylases (HDAC). These effects are widely believed to result in the acetylation of distinct histones that regulate specific genes, including at transcription starting sites (TSS) and enhancers. However, we show that this is not the case, as butyrate dose-dependently increases the acetylation of histones throughout the entire genome. Molecular dynamics simulations suggest that the RING-loop prevents the recruitment of p300 to acetylated histones through its bromodomain, and thereby cannot maintain the acetylation of specific histones through positive feedback. This was confirmed by showing that only catalytically inactive p300 stably binds to acetylated histones. Thus, the epigenetic regulation of specific genes by butyrate is limited, but butyrate instead increases histone acetylation globally resulting in opening of the entire chromatin structure.

molecular biology↗

Combining Selenocystine Based Fluorescence Assay with Structural Prediction for Enhanced Detection and Analysis of Cystine Stone Pathology

BackgroundCystine stones, a rare but recurrent type of kidney stones, primarily result from cystinuria, an inherited disorder caused by mutations in the genes SLC3A1 and SLC7A9, which encode renal cystine transporters. These mutations impair cystine reabsorption, resulting in elevated urinary cystine concentrations and stone formation. Current diagnostic methods are limited, particularly for detecting molecular-level dysfunctions. We aimed to develop a nonradioactive method for functional assessment of cystine transporters and mutation-specific pathologies. MethodsWe designed an innovative diagnostic approach combining a selenocystine-based fluorescence assay with structural predictions using AlphaFold to rapidly and accurately assess cystine transporter function and the molecular impacts of genetic mutations. ResultsOur assay demonstrated comparable transport efficiencies of cystine and selenocystine by the SLC3A1/SLC7A9 complex, and effectively differentiated mild, moderate, and severe functional impairments associated with known clinical mutations, including A354T and P482L. Structural modeling further provided mechanistic insights into mutation-induced dysfunctions. ConclusionThis integrated approach--combining a sensitive selenocystine fluorescence assay with AI-powered structural analysis--enables rapid, precise diagnosis of cystinuria variants and delivers mechanistic insights for personalized therapeutic strategies.

genetics↗