Biology subjects

Xu, J.

Publications and source records attributed to Xu, J..

At least 127 records · Page 7Linked to original sources

bioRxiv2026

Gravid Anopheles stephensi Detects Indole for Oviposition Despite Ablation of Antennae and Maxillary Palps

Oviposition site selection is critical for mosquito population dynamics. Gravid mosquitoes rely on chemical cues to identify suitable breeding habitats. However, the sensory mechanisms governing this behavior in Anopheles stephensi remain poorly understood. Here, we examined the role of indole, a microbial volatile associated with aquatic environments, in oviposition site choice and assessed the involvement of sensory organs in its detection. In two-choice oviposition assays, water conditioned with first-instar larvae attracted gravid females (OAI = 0.56), whereas water from fourth-instar larvae was repellent (OAI = -0.20), consistent with avoidance of suboptimal, resource-depleted habitats. Indole elicited strong oviposition attraction across a broad concentration range (0.1-50 {micro}M), with no clear dose-response relationship. Surgical ablation of antennae and maxillary palps did not abolish indole-mediated preference but significantly reduced behavioral variability, suggesting that these structures modulate, rather than solely mediate, indole detection. Reanalysis of transcriptomes of antennae, maxillary palps, and legs in An. gambiae and An. coluzzii, along with quantitative RT-PCR in An. stephensi, revealed the expression of chemosensory genes (including Obp1, Obp13, Obp25, Obp71, Or2, and Or10) in the legs, indicating a potential role for leg chemosensation in oviposition decisions. These findings underscore the complexity of chemoreception and chemoperception in mosquito habitat assessment.

animal behavior and cognition↗

bioRxiv2026

A dendrite-resolved, in vivo transfer function from spike patterns to dendritic Ca2+

Dendrites transform local electrical activity into intracellular Ca2+ signals that drive plasticity1,2, yet the voltage[->]Ca2+ mapping during natural behavior remains poorly defined. Here, we measure this transfer function via simultaneous voltage and Ca2+ imaging throughout the dendritic arbors of hippocampal CA2 pyramidal neurons in behaving mice. Dendritic Ca2+ exhibited a hierarchical activation pattern dominated by back-propagating action potentials: simple spikes primarily drove somatic and proximal Ca2+, whereas complex spikes produced larger somatic Ca2+ signals and propagated farther into distal dendrites, sometimes in a branch-selective manner. Dendrite-restricted co-activation of voltage and Ca2+ without concurrent somatic events was rare. A biophysics-inspired model accurately predicted local Ca2+ transients from local voltage waveforms. Our data and model provide a quantitative understanding of when - and why - dendritic Ca2+ signals in CA2 pyramidal cells arise during behavior.

neuroscience↗

bioRxiv2026

Autism associated mutation in Cacna1d causes perseverative behavioral phenotype in mice

Behavioral inflexibility and perseveration are core features of autism spectrum disorder and are frequently modeled in mice using reversal learning and repetitive behavior assays. Mutations in CACNA1D, which encodes the L-type calcium channel Cav1.3, have been linked to autism, yet their behavioral consequences remain incompletely characterized. We examined mice carrying the autism-associated Cacna1dG407R gain-of-function mutation across a battery of assays assessing learning, flexibility, and repetitive behavior. Mutant mice learned spatial discriminations and instrumental contingencies at rates comparable to wild-type controls but exhibited deficits during reversal learning following intermediate and extended overtraining, as well as under probabilistic reinforcement. Across ethological assays, mutant mice showed increased grooming, marble burying, and nestlet shredding, consistent with enhanced perseverative behavior. Anxiety-related measures and general locomotion were largely unaffected. These results identify Cav1.3 gain-of-function as a selective regulator of behavioral flexibility and support a role for calcium-dependent corticostriatal plasticity in autism-associated perseveration.

neuroscience↗

bioRxiv2026

Reactive Astrocytes Drive Extracellular Acidification to Mediate α-Synuclein Neurodegeneration

Astrocytes are increasingly recognized as key players in neurodegeneration1-3, yet the molecular mechanisms by which they drive disease remain elusive. Here, we uncover a fundamental pathway in which reactive astrocytes fuel neurodegeneration in -synucleinopathies--including Dementia with Lewy bodies and Parkinsons disease dementia--by acidifying the brains extracellular environment. We demonstrate that both human patient tissue and a gut-to-brain -synuclein mouse model exhibit accumulation of reactive astrocytes and extracellular acidosis. Mechanistically, we show that astrocytic lysosomal exocytosis releases acidic contents, driving a drop in pH that activates neuronal acid-sensing ion channel 1a (ASIC1a), resulting in neuronal loss and behavioral decline. Blocking this pathway--either by inhibiting astrocytic lysosomal exocytosis or genetically or pharmacologically targeting neuronal ASIC1a--mitigates pathology and rescues neurodegenerative phenotypes in vivo. These findings provide a conceptual advance by establishing a mechanistic link between glial inflammation, acid-base homeostasis, and neuronal vulnerability, and suggest that targeting astrocyte-driven acidification or ASIC1a signaling could offer new avenues for disease modification in -synucleinopathies.

neuroscience↗

bioRxiv2026

Intermittent AP-1 activation in muscles contributes to exercise-induced health benefits

Regular physical exercise extends healthspan, yet the molecular mechanisms that translate intermittent contractile stress into lasting benefit remain incompletely understood. Using global nuclear run-on (GRO-seq) in mouse skeletal muscle after treadmill running, we profiled enhancer RNA (eRNA), a sensitive marker of enhancer activity. Activation protein-1 (AP-1), a family of pioneering factors for senescence, emerged as the top transcription factor with motif enrichment in exercise-activated enhancers. Our screen in the contracting C2C12 myotubes pinpointed cFos/JunD as the primary AP-1 factor responsible for contraction-induced transcriptional changes. Muscle-specific overexpression of A-Fos, a dominant-negative mutant of cFos, disrupted transcriptomic responses to exercise and attenuated exercise-mediated improvement in muscle functions. Interestingly, intermittent but not continuous overexpression of cFos/JunD in mouse muscles mimicked exercise-induced transcriptomic changes, increased mitochondrial volume density, enhanced muscle strength and fatigue resistance, and improved glucose tolerance. These results define a transcriptional regulatory signaling pathway linking exercise intermittency to beneficial adaptations and highlight the necessary recovery cycles in training. The paradoxical anti- and pro-aging roles of AP-1 offer insights into the timing and dynamics of stressors and stress responses in shaping senescence and healthspan.

molecular biology↗

bioRxiv2026

MR-μScope: a multi-scale and simultaneous MRI-miniaturized microscopy system for elucidating neurovascular coupling

Blood Oxygen Level Dependent functional MRI (BOLD-fMRI) revolutionized non-invasive brain mapping, yet the physiological origins of its signal, linking microscopic neurovascular activity to macroscopic hemodynamics, remain elusive. To bridge this gap, we developed MR-Scope: a simultaneous and multimodal platform that integrates preclinic high-field MRI (9.4T) and miniaturized fluorescence microscopy (Miniscope). Our system contains an MR-compatible Miniscope with electromagnetic shielding, a customized radiofrequency coil with a central optical window, and an adjustable animal cradle, enabling artifact-free acquisition of whole-brain fMRI alongside microscopic vascular dynamics. Phantom validation confirmed negligible cross-modal interference (fMRI SNR [≥] 15 dB; optical SNR [≥] 26 dB). MR-Scope captured stimulus-evoked microvascular dilation and blood flow velocity changes in the somatosensory cortex concurrent with BOLD signals, revealing vessel-size-dependent neurovascular coupling. MR-Scope provides an effective solution for deciphering multi-scale neurovascular interactions and offers unique potential for advancing research into brain function and disease mechanisms involving vascular pathology.

bioengineering↗

bioRxiv2026

Coronavirus Nucleocapsid Proteins Hijack Host Protein Kinase A Catalytic Subunit α into Nucleus to Evade from STAT1 Signaling

The role of the cAMP/PKA pathway in antiviral innate immunity, including during coronavirus infections, remains unclear. We discovered coronavirus N proteins initiate cAMP-ADCY10-PKA cascade. Cytoplasmic PKA activates STAT1 independently of canonical JAK/TYR2 signaling. Coronavirus N proteins, via a conserved arginine (e.g., PEDV R58, SARS-CoV-2 R92), directly bind and sequester PKA C into the nucleus to evade STAT1 activation. Using PEDV as a model, mutant viruses with NmutNLS and NR58A were generated. Wildtype PEDV infection suppressed STAT1 activation in cells expressing PKA C/PKA CS339A deficient in STAT1 phosphorylation. However, in rXS0101mutNLS- or rXS0101R58A-infected cells, only PKA CS339A expression inhibited STAT1 activation. Downregulation of STAT1 activation is accompanied with increased viral replication. This study first elaborates that PKA C activates STAT1 in the cytoplasm of infected cells distinctly from canonical JAK/STAT1 signaling, while coronaviruses evade this antiviral response by sequestering PKA C into the nucleus via direct N protein interaction.

microbiology↗

bioRxiv2026

Dendritic excitations primarily mediate back-propagation in CA1 pyramidal neurons during behavior

Dendrites integrate synaptic inputs to trigger action potentials, and dendrites carry back-propagating action potentials (bAPs) to synapses where these signals contribute to plasticity. Despite strong evidence for a rich repertoire of nonlinear dendritic excitations, the in vivo roles of these excitations in dendritic integration and back-propagation remain uncertain. Here, we used high-speed voltage imaging through a chronically implanted microprism to map membrane potential dynamics from basal to apical dendrites of CA1 neurons in mice navigating in a virtual reality environment. Despite complex dendritic branch morphology, the dynamics were largely captured by 2 or 3 electrical compartments: basal, soma, and apical. Fast dendritic spikes almost always started from bAPs, indicating that dendritic spikes are primarily a consequence rather than a cause of somatic spiking. These fast spikes sometimes triggered slower apical dendritic plateau depolarizations, which drove complex spikes at the soma. We found that the biophysics of dendritic excitability determined the distribution of simple and complex spikes across a place field. Our results show how CA1 pyramidal neurons convert synaptic inputs to spiking outputs and suggest a primary role of dendritic nonlinearities in mediating activity-dependent plasticity.

neuroscience↗

bioRxiv2026

Phenotype-Guided In Silico Molecular Generation Using Large Language Models

Complex diseases often emerge from coordinated, system-level cellular state changes that are difficult to address with target centric drug discovery. Phenotypic drug discovery offers a principled alternative but remains constrained by the cost and scalability of pathologically relevant assays. Here we present GEMGen, a large language model-based framework that performs in silico phenotypic drug discovery by generating small molecules directly from transcriptomic representations of cellular states. GEMGen encodes desired phenotypic transitions as text-based representations of up- and down-regulated gene sets, enabling transferable modeling across experimental platforms and data modalities. Trained on large scale chemical perturbation data, GEMGen robustly identifies phenotype-oriented compounds and mechanistically related but structurally distinct candidates across multiple benchmarks. Applied to signatures induced by genetic perturbations, GEMGen produces small molecules that phenocopy gene knockdown effects and identifies chemically novel inhibitors, including previously unreported KEAP1 inhibitors that activate NRF2 signaling. Extending this approach to a disease relevant model of fibrosis, GEMGen generates compounds that reverse profibrotic transcriptional programs and cellular phenotypes. These results establish a scalable framework for translating transcriptomic phenotypes into candidate therapeutic molecules, enabling systems-level exploration of vast chemical space and offering a complementary in silico counterpart to physical phenotypic drug screens.

cell biology↗

bioRxiv2025

Fully computational design of PAM-relaxed Staphylococcus aureus Cas9 with expanded targeting capability

CRISPR-Cas9 nucleases have transformed genome engineering, yet their application is often constrained by protospacer-adjacent motif (PAM) requirements. Staphylococcus aureus Cas9 (SaCas9) is particularly attractive for in vivo applications due to its compact size; however, its NNGRRT PAM limits targetable genomic sites. Here, we report KRH, a SaCas9 variant designed entirely from the wild-type enzyme through a fully computational point-mutation design workflow, UniDesign, without additional experimental optimization. As expected, KRH efficiently recognizes an expanded NNNRRT PAM and exhibits substantially enhanced editing efficiency at non-canonical PAM sites, with improvements of up to 116-fold over the wild type. KRH achieves genome- and base-editing efficiencies comparable to, or exceeding, those of the well-known evolution-derived KKH variant. Computational modeling by UniDesign provides a mechanistic explanation for the PAM relaxation observed in both KRH and KKH, with structural and energetic analyses revealing that KRH relaxes PAM specificity by fine-tuning the balance between sequence-specific interactions with PAM bases and nonspecific contacts with the DNA backbone. Beyond its practical utility, KRH demonstrates that computational design can identify a minimal set of mutations sufficient to remodel the PAM interface while preserving high nuclease activity. This approach recapitulates--and in some cases surpasses--the performance of evolution-derived variants, offering a scalable strategy for high-throughput Cas9 engineering. Overall, these results establish KRH as a blueprint for rationally engineered, PAM-relaxed nucleases and underscores the power of computational design to accelerate next-generation genome editing.

bioengineering↗

bioRxiv2025

A Foundational Generative Model for Cross-platform Unified Enhancement of Spatial Transcriptomics

Spatial transcriptomics (ST) platforms are limited by spatial resolution, sensitivity to low expression levels, alignment with tissue structures, and the balance across tissue complexity. Computational enhancement typically targets a single challenge, e.g., super-resolution using hematoxylin and eosin (H&E) images or sensitivity enhancement with single-cell RNA sequencing (scRNA-seq). However, most ignore the interdependence across challenges, yielding biologically inconsistent enhancement. Here we introduce FOCUS, a foundational generative model for unified ST enhancement, conditioned on H&E images, scRNA-seq references, and spatial co-expression priors. With large-scale pretrained encoders, FOCUS uses a modular design for multimodal integration and a cross-challenge coordination strategy to target co-occurring challenges, enabling joint optimization. FOCUS was trained and comprehensively benchmarked on >1.7 million H&E-ST pairs and >5.8 million single-cell profiles, demonstrating state-of-the-art performance across ten ST platforms, on both individual and coupled challenges. The real-world utility and generalizability were validated on a rare suprasellar tumor, papillary craniopharyngioma, and an unseen ST platform (Open-ST) for primary and metastatic head and neck squamous cell carcinoma.

bioengineering↗

bioRxiv2025

Residual blinking-driven channel alignment for multicolor single-molecule localization microscopy

Given the nanometer-scale resolution of single-molecule localization microscopy (SMLM), sequential multicolor SMLM is inherently challenged by inter-channel misalignment arising from unpredictable sample drift during channel switching. Traditional fiducial-based strategies are limited by added complexity in sample preparation. Here, we report a residual blinking-driven method for channel alignment in multicolor SMLM, termed ReBling alignment. By exploiting residual blinking events under dual-wavelength excitation, our method extracts shared localizations as intrinsic registration anchors and performs accurate cross-correlation-based alignment. We validated ReBling alignment across biological systems featuring distinct spatial patterns, including continuous patterned structures (mitochondria-microtubule co-imaging, dual-labeled microtubules), and discrete point-cluster assemblies (dual-color nuclear pore complex components), demonstrating its broad applicability and reliability. These results establish ReBling alignment as a practical, versatile, fiducial-free solution for accurate channel registration in sequential multicolor SMLM, enabling more precise and reliable characterization of complex cellular architecture and molecular interactions.

cell biology↗

bioRxiv2025

Demonstrating and engineering the de novo synthesis of two aromatic chemicals estragole and anethole in Escherichia coli

Estragole and anethole are the major flavoring and aroma components of the essential oils extracted from basil (Ocimum basilicum L.), anise (Pimpinella anisum), star anise (Illicium verum), and fennel (Foeniculum vulgare). Besides, they also exhibit bioactivities, such as antioxidation, antimicrobial, immunomodulation, inti-inflammation, and anti-diabetes. These properties make them being faced with substantial applications in the industries of food, cosmetics, pharmaceutics, and agriculture. Commercial estragole and anethole are currently obtained from extraction from their original plants, which suffers from unstable quality and resources. Microbial synthesis is a promising alternative approach to sustainably obtain estragole and anethole, but has not been achieved. In this study, we modularly redesigned the synthetic pathways based on the Escherichia coli chassis. Firstly, a p-coumaryl alcohol over-accumulator (436.28 mg/L) was engineered to facilitate the validation of the undemonstrated downstream module. De novo biosynthesis of estragole and anethole was achieved by stepwise analysis and BioBricks assembly. The intracellular availability of S-adenosyl-L-methionine (SAM) was revealed to be the key limiting factor, and was enhanced by deregulating the synthesis. Finally, the productions of estragole and anethole were improved by 246.88% and 202.44% compared with the initial strains. This study represents the first synthesis of estragole and anethole in microbial chassis, and the demonstration of microbial synthesis of propenyl phenols. Besides, it provided an alternative sustainable approach to obtain flavoring and aroma chemicals.

synthetic biology↗

bioRxiv2025

Structural guidance in 3D microgel-in-hydrogel systems to improve chondrogenesis

Anisotropic biomaterials are broadly studied in regenerative medicine as they aim to mimic the hierarchical structures of native tissue. The Anisogel, an anisotropic microgel-in-hydrogel system, involves two key factors for tissue engineering: guidance cues - magnetically aligned rod-shape structures - and a surrounding matrix - polyethylene glycol-vinylsulfone (PEG-VS) with a degradable peptide crosslinker. This research shows the potential of using a PEG-VS-based Anisogel to allow for guided ingrowth and chondrogenic differentiation of human mesenchymal stromal cells (hMSCs) modulated by the alignment and size of anisometric microgels. The properties of the surrounding matrix are optimized for the availability of anchoring peptides (RGD concentration) and matrix density (hydrogel precursor concentration). The microgels of highest tested dimensions (10x10x100 {micro}m3) lead to a donor-independent significant upregulation of chondrogenic markers (SOX 9, ACAN and COL2AI) and a decrease of hypertrophic chondrogenic markers (RUNX 2), compared to unaligned and smaller microgel sizes. As a proof of concept, the Anisogel is tested in a semi-orthotopic mouse model where the effect of microgel alignment on cell infiltration and osteochondral tissue formation is evaluated.

bioengineering↗

bioRxiv2025

Immunotherapy with Pro-regenerative Macrophages from Embryonic Stem Cells Ameliorate Osteoarthritis via TNFAIP3-Mediated Chondroprotection

Immune cell-based therapies for osteoarthritis (OA) remains underexplored. Macrophages coordinate tissue repair, yet their functional heterogeneity and therapeutic applicability, particularly for designed stem cell-derived populations with tailored reparative properties are not fully delineated. Inspired by embryonic skeletal development as a paradigm of scarless regeneration, we identified a pro-regenerative macrophage population through a single-cell RNA atlas of developing skeletal tissues. We subsequently established a mechanically dynamic induction approach to efficiently generate pro-regenerative macrophages from human embryonic stem cells (hESCs), mimicking this developmental phenotype. In vitro, these macrophages mitigate cartilage degradation in OA explants and suppress pro-inflammatory, catabolic signaling in chondrocytes. Injection into murine OA joints robustly attenuates disease progression, reduces extracellular matrix breakdown, and resolves synovial inflammation, representing the first demonstration of immune cell-based therapy for OA. Mechanistically, these macrophages orchestrate chondroprotection not through broad immunosuppression, but by activating a TNFAIP3-dependent signaling hub that restrains inflammatory and catabolic responses in chondrocytes. This TNFAIP3 activation precisely reversed the OA-associated gene signature, suppressing catabolic mediators while enhancing reparative factors, thereby restoring the anabolic-catabolic balance. Our findings uncover a developmental blueprint for engineering pro-regenerative macrophages from stem cells and establish a pioneering targeted immune cell therapy that engages an intrinsic chondroprotective program, offering a transformative and translationally relevant strategy for OA treatment.

immunology↗

bioRxiv2025

Single-cell atlas reveals alveolar macrophage-specific Oncostatin-M drives pulmonary fibrosis via fibroblast activation in PCV2d infection

A hallmark of pulmonary fibrosis is the aberrant activation of lung fibroblasts into pathological fibroblasts that produce excessive extracellular matrix(1). Clarifying the cell-specific mechanisms by which viruses induce this process is crucial for developing effective strategies to intervene in disease progression. Here, we demonstrate that alveolar macrophage subsets specifically express tumor suppressor M (Osm) after infection by PCV2d infection and related intervention experiments in mice, combined with single-cell transcriptome sequencing (scRNA-seq). Through validation using histopathological analyses and an in vitro macrophage-fibroblast co-culture model, these alveolar macrophage-derived oncostatin M (Osm) were confirmed to specifically drive fibroblast activation. Vaccine intervention experiments further confirmed that targeted inhibition of oncostatin M (Osm) expression in alveolar macrophages significantly attenuated fibroblast activation and extracellular matrix deposition, thereby mitigating pulmonary fibrosis progression. Therefore, subgroup-specific secretion of oncostatin M (Osm) by alveolar macrophages represents a key driver mediating PCV2d infection-induced pulmonary fibrosis, and targeting this pathway offers a potential therapeutic strategy for viral-induced pulmonary fibrosis.

genomics↗

bioRxiv2025

Mitochondrial redox homeostasis links organellar stress surveillance to germline and somatic integrity in Caenorhabditis elegans

Mitochondrial redox homeostasis is essential for cellular metabolism and organismal development. To investigate the consequences of disrupting redox homeostasis in this organelle in a metazoan organism, we generated a double mutant lacking mitochondrial glutathione reductase (gsr-1a) and thioredoxin reductase (trxr-2) genes in Caenorhabditis elegans. While gsr-1a or trxr-2 single mutants are phenotypically normal, double gsr-1a trxr-2 mutants displayed small body size, gonadal migration defects, reduced brood size, and prolonged egg-laying period, without developmental delay or lethality. Transcriptomic analysis revealed strong induction of ATFS-1-dependent stress and detoxification genes. Consistent with this, gsr-1a trxr-2 worms exhibited constitutive ATFS-1 nuclear localization and robust Phsp-6::gfp expression. Triple gsr-1a trxr-2; atfs-1 mutants were nonviable, demonstrating that unfolded protein response (UPRmt) activation is essential under mitochondrial redox stress. Despite the induction of a stress response at the transcriptional level, gsr-1a trxr-2 double mutants were not more resistant to oxidative or pathogen stressors. Moreover, these mutants maintained normal respiration, ATP and ROS production while displaying altered mitochondrial morphology in a tissue-specific manner, independent of mitophagy genes but dependent on mitochondrial fission or fusion machinery. Functionally, gsr-1a trxr-2 mutants showed impaired motility, reduced calcium uptake upon carbachol stimulation, enhanced hypodermal wound repair, and decreased fertilization efficiency associated with lower muscle exopher production. Overall, our data show that simultaneous loss of mitochondrial GSR-1a and TRXR-2 compromises growth, fertility and muscle performance and triggers a constitutive ATFS-1-dependent UPRmt that sustains viability revealing mitochondrial redox control as a core determinant of organismal proteostasis. HighlightsO_LIgsr-1a or trxr-2 single mutants have no overt phenotypes. C_LIO_LIgsr-1a trxr-2 double mutants are viable but show small size, gonad migration defects and reduced progeny. C_LIO_LILoss of both reductases in mitochondria triggers a constitutive ATFS-1-dependent UPRmt. C_LIO_LIATFS-1 is essential for gsr-1a trxr-2 worms survival. C_LIO_LIgsr-1a trxr-2 animals remodel mitochondrial morphology in a tissue-specific manner. C_LIO_LIgsr-1a trxr-2 double mutants exhibit impaired muscle and sperm function but enhanced wound healing. C_LI Graphical abstract (to be incorporated)

genetics↗

bioRxiv2025

Mineralized Tissue-Targeting Expression System for Local Control of Gene Expression

Targeted control of gene expression in mineralized tissue would enable the use of nucleic acids to modulate the local microenvironment at diseased sites, ultimately promoting bone regeneration. Piperazine-linked bisphosphonate ionizable lipids provide a facile approach to targeting the transfection of mineralized tissue with lipid nanoparticles (LNPs). Here, we develop a Mineralized Tissue-Targeting Expression System (MiTEX) using bisphosphonate LNPs to locally target mineralized tissues by adsorption to mineral surfaces and bone graft materials. MiTEX demonstrated a significant increase in the adsorption of RNA onto hydroxyapatite substrates, which retained the ability to transfect bone mesenchymal cells via the adsorbed layer of mRNA LNPs. Bone graft scaffolds functionalized by adsorbed Cre mRNA-LNP were implanted to genetically label newly formed bone tissues in vivo. The surface affinity and adsorption of bisphosphonate lipids provided a local reservoir in mineralized tissues, sustaining the in vivo delivery of MiTEX. Furthermore, the targeted delivery of RNA therapeutics was demonstrated using STAT3 siRNA to modulate gene expression and proinflammatory cytokine release in ex vivo periodontal tissues. The design of this new RNA-functionalized delivery platform will promote the development of precision nucleic acid therapeutics for local anti-inflammatory treatments and bone regeneration at mineralized tissue interfaces.

bioengineering↗