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Biology subjects

Choi, J. H.

Publications and source records attributed to Choi, J. H..

At least 19 recordsLinked to original sources

Predicting conformational changes induced by biomolecular interactions

Biomolecular interactions trigger structural changes of protein complexes essential for cellular signaling, regulation, and drug action. Modern co-folding models can now generate detailed structures of multi-component complexes directly from sequence. However, recent evaluations reveal that they frequently fail to capture specific conformational states induced by a ligand or partner. Here, we show that explicitly modeling the structural transition from an unbound to a bound state, rather than generating the bound complex alone, better resolves these interaction-induced states. Our generative learning framework, K-Fold, transforms independently predicted unbound component priors into an assembled complex through an ultrafast diffusion bridge, operating entirely without multiple sequence alignments. By eliminating co-evolutionary dependencies, K-Fold accurately recovers non-coevolved interfaces in antibody-antigen and targeted-degrader complexes, as well as ligand-directed regulatory states in GPCRs and kinases. Furthermore, by coupling this diffusion bridge with diverse monomeric equilibrium ensembles, K-Fold provides a computationally tractable foundation for sampling complex multi-state landscapes without retraining. These results demonstrate that formulating molecular assembly as an explicit structural transition moves structure prediction beyond static geometries toward capturing biomolecular dynamics.

molecular biology↗

Designing a reoriented H5 hemagglutinin to generate stem-directed, heterosubtypic immunity to influenza A viruses

Human infections with the highly pathogenic avian influenza viruses highlight the risk of novel pandemics, against which seasonal vaccines provide limited cross-protection. Whereas antibody responses to current vaccine candidates are typically biased toward the immunodominant and variable head region of hemagglutinin (HA), the stem region of HA is highly conserved and targeted by broadly neutralizing antibodies. Here we describe a reoriented H5 HA (reoH5HAPhe, based on A/Vietnam/1203/2004) displayed on alum as a vaccine candidate to elicit stem-directed antibody responses and confer cross-protective immunity. We show that a single immunization with reoH5HAPhe protected naive mice against heterologous H5N1 lethal challenge (A/Texas/37/2024), and boosting with reoH5HAPhe conferred complete heterologous protection in mice pre-immunized with seasonal vaccines. The stem-directed response elicited by reoH5HAPhe also protected against heterosubtypic H1N1 challenge in both naive and pre-immune mice. Electron microscopy polyclonal epitope mapping revealed that reoH5HAPhe elicited antibodies targeting the central stem and anchor epitopes on heterologous H5 and H1 HAs, alongside antibodies against the (H5) vestigial esterase or (H1) lateral patch epitopes. Despite limited cross-neutralizing activity, increased stem-directed responses with balanced IgG1 and IgG2 subclasses reduced viral replication and improved survival. Our results highlight antigen reorientation as an effective approach for designing variant-resilient vaccines and demonstrate the potential of reoH5HAPhe as an H5 pandemic influenza vaccine candidate that confers protective immunity against both emerging and seasonal influenza viruses.

immunology↗

Muscarinic signaling sustains delay-period selectivity in prefrontal cortex by preserving thalamic drive

Short-term memory (STM) requires the temporary maintenance of task-relevant information in prefrontal cortex (PFC). Reciprocal interactions between the mediodorsal thalamus (MD) and PFC have been implicated in sustaining this activity, but how thalamofrontal communication is maintained despite the biophysical constraints of repetitive synaptic transmission remains unclear. Here, we show that MD--PFC synapses exhibit profound frequency-dependent short-term depression, causing repetitive thalamic input to progressively lose its ability to drive PFC neurons. During STM performance, acetylcholine (ACh) levels in PFC rose rapidly following cue presentation and remained elevated throughout the delay period. Muscarinic ACh receptor (mAChR) activation did not alleviate synaptic depression, but instead increased the intrinsic excitability of PFC neurons, thereby preserving their responsiveness to weakened thalamic input. Conversely, mAChR blockade impaired STM performance and progressively disrupted delay-period directional representations at both the single-neuron and population levels, while largely sparing initial encoding. These findings identify muscarinic signaling as a postsynaptic gain mechanism that compensates for declining thalamofrontal efficacy and sustains task-relevant prefrontal representations during STM.

neuroscience↗

Helicase-deficient TFIIH causes severe disease features via persistent DNA excision without damage removal

Nucleotide excision repair (NER) removes helix-distorting DNA lesions through the ten subunit TFIIH complex, whose XPB and XPD translocase/helicase activities unwind DNA to enable damage verification and subsequent endonucleolytic DNA incisions. While most XPD mutations cause xeroderma pigmentosum, specific helicase-deficient mutations cause severe Cockayne syndrome (CS) features, including progressive neurodegeneration, for which the basis remains unclear. Here we show that loss of XPD helicase activity traps TFIIH in a futile repair cycle in which DNA is incised at the wrong position, leading to repeated DNA excision and resynthesis without removal of the lesion. Using C. elegans, we find that this futile DNA excision cycle produces severe neuronal dysfunction in vivo that depends on transcription-coupled NER activity and is rescued by preventing recruitment of helicase deficient TFIIH. These findings demonstrate that NER incisions can occur without XPD mediated damage verification and that persistent futile DNA excision cycles cause severe disease features, indicating that persistent NER intermediates are more pathogenic than unrepaired DNA lesions.

genetics↗

Computational Design Strategies for Nanoscale 3D Auxetic Metastructures from DNA

Auxetic metamaterials exhibit negative Poissons ratio behaviors due to their architecture of periodically arranged unit cells. Although mechanical metamaterials are well established at the macroscale, programmable auxetic units remain scarce at the nanoscale. DNA origami offers a promising platform to bridge this gap, but design principles for dynamically deformable 3D auxetic nanostructures remain largely unexplored. Here, we develop design strategies for such 3D auxetic metastructures built from wireframe DNA origami. As a model system, we use a 3D re-entrant triangular unit composed of double-stranded DNA (dsDNA) bundle edges connected by single-stranded DNA (ssDNA) joints. Using coarse-grained molecular dynamics (MD) and umbrella-sampling free-energy simulations, we examine how edge design and joint-connection scheme govern auxetic responses and the energetics of the structural transformation. Our results show that auxetic performance and deformation energetics emerge from the coupled effects of DNA bundle rigidity and connector mechanics at the joints. This study provides mechanistic insights and design guidelines for programmable auxetic motion and energetics in 3D DNA origami metamaterials, advancing the development of stimuli-responsive nanomechanical devices.

biophysics↗

Programmable assembly of higher-order DNA nanostructures from microbial ssDNA staple libraries

Bottom-up manufacturing of structural DNA nanotechnology requires a long single-stranded DNA (ssDNA) scaffold and hundreds of short ([~]30 nt) ssDNA staples. However, scaling production remains bottlenecked by the high economic cost and environmental footprint of solid-phase chemical staple synthesis. To address these limitations, a phage-free, biological nanomanufacturing platform engineered in Escherichia coli is developed here. Two intracellular strategies for producing programmable ssDNA were systematically evaluated: retron-based multicopy ssDNA (msDNA) synthesis via the Ec67 system and plasmid-encoded rolling circle replication (RCR). While native structural topology constraints within the retron (msd) cassette limit its sequence-design flexibility, the alternative RCR-driven engine successfully decouples ssDNA replication from sequence secondary structures, enabling the synthesis of arbitrary staples. This RCR platform reliably generates long circular ssDNA (cssDNA) precursors of at least 1.8 kb with exceptional sequence fidelity (>99%). Integrating programmable BseGI cleavage sites allows targeted strand-selective enzymatic processing to cleanly release stoichiometric, origami-grade pools of 32-nt staple strands. Atomic force microscopy (AFM) confirms that these biologically produced staples successfully drive the high-fidelity self-assembly of complex DNA tiles and hollow tubules. Crucially, robust structural folding is demonstrated directly within crude, unpurified cellular lysates, establishing a green, cost-effective framework for the one-pot fabrication of advanced DNA-based nanomaterials.

synthetic biology↗

Time-structured communication through cross-frequency bursts

Adaptive brain function requires communication that is selective in both space and time, yet the circuit mechanisms that transiently favor specific routes of information transfer remain unclear. Here we show that, when coupled, spiking populations with distinct inhibitory timescales can reprogram one anothers intrinsic burst preferences, generating irregular multi-frequency bursts that self-organize into Multi-Frequency Oscillatory Patterns (MFOPs). State-resolved transfer entropy revealed that different MFOPs were associated with distinct Information Routing Patterns (IRPs), defining transient windows of enhanced directed transfer with specific delays and directions. At the microscopic level, the same oscillatory states selectively increased or decreased delayed spike transmission across monosynaptic pathways, yielding transmission barcodes that significantly resembled the corresponding IRPs. This repertoire was markedly reduced when inhibitory diversity was removed. These results identify coordinated multi-frequency bursting as a mechanism by which recurrent circuits can dynamically filter inputs according to source and latency.

neuroscience↗

Hydration-Controlled Proton Transport in Respiratory Complex I

Proton pumping by respiratory Complex I is one essential element for generating the proton motive force that drives ATP synthesis in mitochondria. Although it is understood that electrons from NADH reduce ubiquinone at the peripheral arm and that four protons are transferred in the membrane domain, the mechanism by which this redox reaction initiates proton translocation remains unclear. A lateral pathway linking the quinone binding site to the membrane domain via ND1, ND3, and ND4L subunits has been proposed as the initial path of an excess proton. However, in experimental structures this region lacks a continuous water network between D66ND3 and E34ND4L, resulting in a hydration bottleneck that may regulate proton transfer. Using multiscale reactive molecular dynamics (MS-RMD) and a water wire connectivity metric, we directly simulate proton transport through this region as coupled the the hydration by water molecules. Our results reveal that proton transfer is thermodynamically feasible when transient hydration aligns with the presence of an excess proton, revealing the strong coupling between hydration and proton (PT) in this region of Complex I. These findings support a model where proton injection enhances local hydration, dynamically opening the pathway for proton transfer and regulating the onset of proton pumping in Complex I.

biophysics↗

Thalamofrontal synaptic weakening underlies short-term memory deficits from adolescent NMDAR hypofunction

N-methyl-D-aspartate receptor (NMDAR) hypofunction is linked to schizophrenia, but prevailing models centered on reduced number and activity of inhibitory interneurons, and the resulting excitation-inhibition (E-I) imbalance, do not explain selective cognitive impairments. Here, we show that repeated adolescent NMDAR antagonism produces short-term memory (STM) deficits by weakening thalamofrontal (TF) synaptic transmission. In mice repeatedly exposed to ketamine, STM impairment coincided with reduced release probability and vesicle refilling at mediodorsal thalamus (MD) [->] dorsomedial prefrontal cortex (dmPFC) synapses, without detectable changes in layer 2/3 [->] layer 2/3 synaptic release probability, intrinsic excitability, or synaptic ultrastructure. These presynaptic deficits were accompanied by diminished direction-selective population coding in the dmPFC, as revealed by decoding analysis, and impaired delayed alternation performance in the Y-maze. Chemogenetic strengthening of MD [->] dmPFC projections restored both neural selectivity and behavior. Our findings identify a circuit-specific presynaptic mechanism linking adolescent NMDAR hypofunction to cognitive dysfunction, challenging interneuron-centric models and establishing TF synapses as a potential therapeutic target in NMDAR-related disorders.

neuroscience↗

A Nanoscale Jitterbug Transformer from DNA

Many viruses have intricate polyhedral shells capable of symmetric transformations in response to external stimuli to initiate payload release. Such deployable auxetic nanostructures are not available in the synthetic realm. Here we present a nanoscale Jitterbug transformer using DNA origami that can reconfigure its structure upon chemical and optical signals while maintaining a Poissons ratio of -1. By leveraging molecular dynamics simulations, we design the Jitterbug DNA to form a compact octahedron by storing elastic energy and spontaneously transition into an expanded cuboctahedron by releasing it. DNA transformers are explored like viruses that can create nanopores on lipid membranes and regulate payload release into vesicles. This work integrates programmable DNA self-assembly with free-energy-guided mechanical design, providing a pathway toward adaptive nanomaterials with potential in synthetic organelles and stimuli-responsive nanodevices.

biophysics↗

Microstructural Spine Alterations Increase Neuronal Excitability in Focal Cortical Dysplasia

Focal cortical dysplasia(FCD) is a leading cause of drug-resistant epilepsy, traditionally attributed to impaired inhibition. However, recent ultrastructural evidence suggests excitatory synaptic alterations may also contribute. To investigate this, we performed computational modeling of human pyramidal neurons in NEURON, incorporating electron microscopy-derived dendritic spine morphologies. Baseline and FCD-like models were constructed with differences in spine density and morphology while maintaining comparable net synaptic input. Simulations revealed that reduced spine density increased input resistance and amplified excitatory postsynaptic potentials, enhancing dendritic-to-somatic transmission. Spine neck geometry, but not head size, critically shaped voltage compartmentalization. The altered model required markedly fewer synchronous inputs to reach spiking threshold and exhibited higher firing rates under Poisson-distributed synaptic activity, particularly under sparse input conditions. These results demonstrate that excitatory microstructural changes - reduced spine density and weakened neck compartmentalization - can elevate neuronal excitability, in addition to the inhibitory deficit which is the biggest known effect. These findings highlight excitatory spine remodeling as another key driver of epileptogenesis. We speculate that extending this analysis will be essential to fully understand circuit-level hyperexcitability and to identify new therapeutic targets.

neuroscience↗

Understanding Structural Mechanics of Ligated DNA Crystals via Molecular Dynamics Simulation

DNA self-assembly is a highly programmable method that can construct arbitrary architectures based on sequence complementarity. Among various constructs, DNA crystals are macroscopic crystalline materials formed by assembling motifs via sticky end association. Due to their high structural integrity and size ranging from tens to hundreds of micrometers, DNA crystals offer unique opportunities to study structural properties and deformation behaviors of DNA assemblies. For example, enzymatic ligation of sticky ends can selectively seal nicks resulting in more robust structures with enhanced mechanical properties. However, the research efforts have been mostly on experiments such as different motif designs, structural optimization, or new synthesis methods, while their mechanics are not fully understood. The complex properties of DNA crystals are difficult to study via experiment alone, and numerical simulation can complement and inform the experiment. Coarse-grained molecular dynamics (MD) simulation is a powerful tool that can probe the mechanics of DNA assemblies. Here, we investigate DNA crystals made of four different motif lengths with various ligation patterns (full ligation, major directions, connectors, and in-plane) using oxDNA, an open-source, coarse-grained MD platform. We find that several distinct deformation stages emerge in response to mechanical loading and that the number and the location of the ligated nucleotides can significantly modulate structural behaviors. These findings should be useful for predicting crystal properties and thus improving the design.

biophysics↗

Optimal inhibitory-to-excitatory ratio governs slow and fast oscillations for enhanced neural communication

Neural oscillations at distinct frequency bands facilitate communication within and between neural populations. While single-frequency oscillations are well-characterized, the simultaneous emergence of slow (beta) and fast (gamma) oscillations within the same network remains unclear. Here, we demon-strate that multi-frequency oscillations naturally arise when the ratio of inhibitory-to-excitatory synaptic strength falls within a specific regime using a biologically plausible Izhikevich model. We show that this regime maximizes both information capacity and transmission efficiency, suggesting an optimal balance for neural communication. Deviations from this range lead to single-frequency oscillations and reduced communication efficiency, mirroring disruptions observed in neurological disorders. These findings provide mechanistic insight into how the brain leverages multiple oscillatory frequencies for efficient information processing and suggest a potential biomarker for impaired neural communication. 1. SIGNIFICANCE STATEMENTBeta (slow) and gamma (fast) oscillations often coexist in the brain, yet their origin and functional role remain unclear. Our study reveals that the inhibitory-to-excitatory synaptic strength ratio governs the emergence of this multifrequency state. Furthermore, we demonstrate that information capacity and transmission efficiency are maximized in this regime, leading to significantly enhanced neural communication. These findings provide mechanistic insight into how multiple oscillatory frequencies support efficient brain function and offer a potential framework for understanding disruptions in neural communication associated with neurological disorders.

neuroscience↗

High-throughput microbiome profiling and co-occurrence with antibiotic resistance genes in Lucilia sericata

Blow flies such as Lucilia sericata (Diptera: Calliphoridae) serve important ecological functions as decomposers. However, due to their close association with decaying organic matter they also play potential roles as reservoirs for pathogenic bacteria and antimicrobial resistance genes (ARGs). In this study, we characterized the bacterial communities and resistome profiles of L. sericata specimens collected from six provinces across South Korea using 16S rRNA gene metabarcoding and targeted PCR screening. The microbiome was dominated by Dysgonomonas, Vagococcus, Pseudomonas, Ignatzschineria, and Providencia with geographic variation in community structure. Flies from Chungnam exhibited the lowest microbial diversity, while samples from Jeonnam and Gyeonggi showed greater richness and evenness. Beta diversity analyses confirmed geographic structuring of bacterial communities, with semi-urban, rural locations harboring more diverse taxa. Notably, opportunistic pathogens such as Proteus mirabilis and Providencia were detected, alongside a range of ARGs (blaTEM, ermB, sul1, aac(6')-Ib-cr, cat and mecA) and integron elements (intI and intII), suggesting that L. sericata may act as a reservoir of clinically important microbes and resistance genes. ImportanceThe environment plays a significant role in shaping the microbiome of flies. Due to their motile nature and close association with decomposing matter blow flies of the species Lucilia sericata can harbor diverse bacterial communities, including potential pathogens that threaten human and animal health. Furthermore, due to their synanthropic lifestyle, this species is also exposed to bacteria that host antibiotic resistance genes (ARGs). Here we investigate the role of blowflies as reservoirs of potential pathogens and ARGs using metabarcoding. Our study revealed a diverse microbiome and resistome shaped by location and possible biotic or abiotic factors. These findings provide baseline information for wildlife surveillance and emphasize the importance of including synanthropic flies in strategies aimed at controlling the dissemination of antibiotic resistance.

ecology↗

Neural dynamics of emergent social roles in collective foraging by mice

We investigated how neural dynamics support role differentiation in group foraging by mice cohabiting with a predator-like spider robot serving as a mobile food platform. While solitary foraging behaviors were consistent among mice, group foraging revealed distinct roles-working, participating, and freeriding-that solidified over time, leading to an imbalance (Gini = 0.5) across five groups. Recordings from the medial prefrontal cortex (mPFC), nucleus accumbens (NAc), and basolateral amygdala (BLA) revealed enhanced beta power in active foragers. Workers exhibited a stronger fast beta drive from mPFC to BLA compared to participants, and role prediction accuracy based on spectral features improved over trials. Our findings highlight how neural dynamics underlie the emergence of distinct roles in collective action by mice. One-Sentence SummaryDistinct foraging roles emerge in group-housed mice, driven by fast beta (24-32 Hz) activity in the mPFC-NAc-BLA circuit.

animal behavior and cognition↗

A ketogenic diet mitigates hippocampal astrogliosis in epileptic brain

The ketogenic diet (KD) is an established treatment for patients with medically intractable epilepsy and is chiefly characterized by high fat/low-carbohydrate intake and the production of ketone bodies (KB) such as {beta}-hydroxybutyrate (BHB). However, after more than a century of clinical use, the mechanisms underlying its efficacy remain unclear. While prior investigations have examined the effects of the KD and its metabolic substrates on synaptic transmission, few studies have explored a potential connection between astrocytic ion channels and seizure genesis. One essential function of astrocytes is spatial potassium buffering which influences passive potassium conductance (PPC), and when impaired, can result in neuronal hyperexcitability. In the present study, we demonstrate that the KD can mitigate hippocampal astrogliosis in the Kcna1-null (KO) mouse model of developmental epilepsy. Specifically, we observed a significant increase in GFAP expression in KO mice fed a control diet compared to wild-type (WT) mice, and that the KD prevented this change. Furthermore, we noted a reduction in hippocampal astrocytic PPC in epileptic mice, whereas KD-treated KO animals exhibited nearly normal passive conductance levels. In this regard, we found that while Kir4.1, TREK-1 and TWIK-1 RNA expression levels were not significantly altered by KD treatment in either WT or KO mice, BHB appeared to only minimally affect Kir4.1-mediated currents in transfected HEK cells. Furthermore, bulk RNA-seq analysis of the various treatment groups revealed KD-induced down-regulation of factors linked to hippocampal astrogliosis. Our findings indicate that the KD protects against epilepsy-associated astrogliosis and astrocytic PPC changes, underscoring a novel mechanism of action, and implicate extracellular potassium in its anti-seizure effects.

neuroscience↗

Structural insights into the ubiquitin independent MIDN-proteasome pathway

The protein midnolin (MIDN) augments proteasome activity in lymphocytes, where it is predominantly expressed in adult mice. MIDN binds both to proteasomes and to substrates, but the mechanism by which MIDN facilitates substrate degradation in a ubiquitin-independent manner is unknown. Here, we present cryo-electron microscopy structures of the substrate-engaged, MIDN-bound human proteasome in two conformational states. MIDN induces proteasome conformations similarly to ubiquitinated substrates by using its ubiquitin-like domain to bind to the deubiquitinase RPN11. By simultaneously binding to RPN1 with its C-terminal -helix, MIDN positions its substrate-carrying Catch domain above the proteasome channel through which substrates are translocated before degradation. Our findings suggest that both ubiquitin-like domain and C-terminal -helix must bind to the proteasome for MIDN to stimulate proteasome activity.

biophysics↗

Short-term memory errors are strongly associated with a drift in neural activity in the posterior parietal cortex

Understanding the neural mechanisms behind short-term memory (STM) errors is crucial for unraveling cognitive processes and addressing deficits associated with neuropsychiatric disorders. This study examines whether STM errors arise from misrepresentation of sensory information or decay in these representations over time. Using 2-photon calcium imaging in the posterior parietal cortex (PPC) of mice performing a delayed match-to-sample task, we identified a subset of PPC neurons exhibiting both directional and temporal selectivity. Contrary to the hypothesis that STM errors primarily stem from mis-encoding during the sample phase, our findings reveal that these errors are more strongly associated with a drift in neural activity during the delay period. This drift leads to a gradual divergence away from the correct representation, ultimately leading to incorrect behavioral responses. These results emphasize the importance of maintaining stable neural representations in the PPC for accurate STM. Furthermore, they highlight the potential for therapeutic interventions aimed at stabilizing PPC activity during delay periods as a strategy for mitigating cognitive impairments in conditions like schizophrenia.

animal behavior and cognition↗