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Biology subjects

Yan, J.

Publications and source records attributed to Yan, J..

At least 37 records · Page 2Linked to original sources

Programmable Self-Assembly of RNA Nanostructures with >100 Unique Components

Sophisticated biomolecular functions often arise from large, precisely organized architectures, motivating efforts to construct increasingly complex structures through programmed nucleic acid self-assembly. Although RNA offers a richer repertoire of structural motifs and biological functions than DNA, RNA nanostructures constructed to date have remained substantially less complex and less scalable than their DNA counterparts, most notably DNA origami and DNA bricks, which rely on large libraries of synthetic single-stranded (ss) DNA strands. Directly adapting these strategies to RNA, however, faces two major barriers: (i) the high cost of producing large libraries of distinct synthetic ssRNA strands, and (ii) the limited stability of ssRNA under conditions commonly used for assembling multicomponent nucleic acid nanostructures. Here we present the double-stranded RNA (dsRNA) bricks approach, which addresses both barriers by adopting principles inspired by natural RNA systems: (i) many distinct RNA components ("bricks") are encoded within a single precursor transcript and released by enzymatic processing, (ii) each brick's predominantly double-stranded nature enhances stability. The resulting dsRNA bricks self-assemble through programmable branched kissing-loop interactions. Using this approach, we constructed complex two- and three-dimensional RNA nanostructures with more than 100 distinct components, representing, to our knowledge, the largest and most compositionally complex RNA nanoarchitectures reported to date. Overall, the dsRNA bricks approach establishes a scalable and robust framework for constructing complex RNA nanostructures with compositional and architectural sophistication approaching that of DNA-based systems, thereby opening new opportunities for programmable RNA materials and RNA-based devices.

synthetic biology↗

Quantifying sprint force-velocity elasticity: implications for individualized training decisions

This study aimed to (1) develop an elasticity framework for the sprint force-velocity (F-V) relationship and (2) examine how maximal force (F_{0}), maximal velocity (v_{0}), and sprint distance modulate the four derived elasticity metrics, and (3) explore these elasticity metrics' interrelation. After modelling the F-V relationship differential equation, four elasticity metrics were defined as force elasticity (F_{e}), the elasticity of sprint time to F_{0}; velocity elasticity (v_{e}), the elasticity of sprint time to v_{0}; the force-velocity elasticity norm {(\mathrm{F}-\mathrm{V}}_{\mathrm{EN}}=\sqrt{F_{e}^{2}+v_{e}^{2}}), capturing the combined sprint time sensitivity to proportional changes in F_{0} and v_{0}; and the force-velocity elasticity ratio {(\mathrm{F}-\mathrm{V}}_{\mathrm{ER}}=F_{e}{\div v}_{e}), indicating which variable dominates the sprint time response. Model simulations showed that F_{e} decreased with rising F_{0} and increased with rising v_{0}, while v_{e} showed the opposite pattern. With increasing sprint distance, F_{e} decreased and v_{e} increased. Given its negligible effect on sprint time, ignoring air resistance yields a conservation law (2F_{e}+v_{e}\equiv 1), indicating that a gain in one elasticity metric necessarily diminishes the other in a fixed proportion. This framework also identifies a valley distance (d_{valley}) at {\mathrm{F}-\mathrm{V}}_{\mathrm{ER}}=2, where {\mathrm{F}-\mathrm{V}}_{\mathrm{EN}} is minimized (\sqrt{0.2}) and sprint time is least responsive to changes in F-V relationship variables. Empirical data confirmed that the two theoretical laws still hold approximately when air resistance is considered. By linking changes in F_{0} and v_{0} to sprint time across different distances, the elasticity framework provides a quantitative basis for estimating the theoretical sprint time response to documented changes in F-V relationship variables.

biophysics↗

Differential expression of NEAT1 in the corneal endothelium increases susceptibility to oxidative stress in Fuchs Endothelial Corneal Dystrophy

Fuchs endothelial corneal dystrophy (FECD) is a disease of the corneal endothelium (CE) characterized by the loss of corneal endothelial cells (CECs) and guttae formation, ultimately resulting in corneal edema and vision loss. FECD primarily affects the central CE while sparing the peripheral CE, however the underlying mechanism contributing to the spatial differences remain unknown. Oxidative stress has been increasingly recognized as a key contributor to the pathogenesis of FECD, with CECs being particularly susceptible to damage from reactive oxygen species (ROS), high metabolic activity and ultraviolet induced DNA damage. The non-proliferative nature of CECs, along with the accumulation of oxidative damage can ultimately lead to CEC loss, a key feature of FECD. In this study, we induced oxidative stress with hydrogen peroxide (H2O2) on ex-vivo corneal specimens and observe increased cell death in the central region compared to the peripheral CE. To investigate these underlying differences, we performed bulk RNA sequencing (RNA-seq) on the central and peripheral regions of CE from FECD and normal cadaveric donors. Pathway analysis identified an enrichment of genes involved in collagen and extracellular matrix between the central and peripheral regions of CE in both normal and FECD, as well as between normal and FECD CE. Intriguingly, we identified the long non-coding RNA (lncRNA), NEAT1 as a top differentially expressed gene, with reduced expression in the central CE compared to the peripheral CE and lower expression in FECD compared with normal CE. Using corneal endothelial cell lines and ex-vivo specimens from FECD patients and normal cadavers, we found decreased NEAT1 expression levels in FECD and increased susceptibility to H2O2-induced oxidative stress. We observed that NEAT1 knockdown in normal and FECD cells exacerbated H2O2-mediated oxidative stress, and that NEAT1 overexpression protected FECD cells. We report in this study, a novel insight in the spatial differences in gene expression in the CE and identify reduced expression of NEAT1 in the central CE as a potential contributor to oxidative stress-related cell death in FECD. These findings provide novel insight into FECD pathogenesis and why FECD pathology preferentially affects the central CE. Antioxidants targeting NEAT1 signaling could be developed into novel therapeutics aimed at preventing FECD pathogenesis.

cell biology↗

Cross-Regional Trajectory Analysis Reveals Distinct Temporal Progression of Shared Proteomic Programs in Alzheimer's Disease

Alzheimer's pathology progresses through anatomically distinct brain regions, yet how molecular programs are temporally organized across vulnerable regions remains poorly understood. Here, we reconstructed continuous proteomic trajectories from matched dorsolateral prefrontal cortex (DLPFC) and superior temporal gyrus (STG) proteomes to investigate cross-regional molecular progression in AD. The inferred trajectories closely recapitulated established neuropathological staging while remaining independent of age, sex, and race. Across regions, a mitochondrial bioenergetic protein subset declined substantially earlier in the STG than in the DLPFC, revealing a previously unrecognized regional temporal offset in metabolic dysfunction. In parallel, a broadly shared proteomic program progressed in both regions but more rapidly in the STG, indicating that shared molecular responses differ in their temporal progression despite overall coordination. Together, these findings demonstrate that regional vulnerability in AD is reflected not only by the molecular programs involved but also by their temporal organization during disease progression.

neuroscience↗

C. elegans Nuclear Hormone Receptor NHR-49 promotes attractive chemotaxis independently of its role in fatty acid metabolism

All organisms must sense and adapt to environmental cues to survive and thrive. In the nematode worm Caenorhabditis elegans, the nuclear hormone receptor nhr-49 is required for lipid homeostasis, stress resilience, pathogen defense, and longevity. In addition, recent studies suggest that NHR-49 controls avoidance behaviors and aversive memory to pathogenic bacteria and mitochondrial disruption, acting via its established role in fatty acid desaturation and fatty acid oxidation, respectively. However, the role of NHR-49 in neuronal signaling and behavior remains poorly understood. Here, we uncover a new role for NHR-49 in AWA neuron-mediated attractive chemotaxis. We show that nhr-49 is required for chemotaxis towards diacetyl and pyrazine, two AWA neuron-sensed compounds, but not for AWC- or ASH-mediated chemotaxis. Supplementation with unsaturated fatty acids and mutational analysis of additional genes involved in fatty acid desaturation or {beta}-oxidation reveal that these processes do not affect attractive chemotaxis; this suggests that NHR-49 mediates attractive chemotaxis independently of its role in fatty acid desaturation and oxidation. Tissue-specific expression of NHR-49 in neurons or body wall muscle is sufficient to rescue chemotaxis defects, while nhr-49 depletion in neurons alone causes chemotaxis defects. Finally, nhr-49 mutants also show defects in another behavior, the response and habituation to mechanosensory stimuli. Together, our data reveal new functions for NHR-49 in sensory responses and non-associative learning, which are distinct from its roles in aversive behaviors and memory and, notably, independent of its well-established role in lipid metabolism.

neuroscience↗

The cellular and genetic basis of inflorescence divergence between maize and teosinte

The domestication of maize from teosinte involved dramatic remodeling of the ear, yet the cellular and genetic bases of this transformation remain unclear. Here, we generate a single-nucleus and spatial transcriptome atlas of developing maize and teosinte ears. Comparative analysis reveals divergence in cob-associated cell types, with enhanced cytokinin signaling and reduced growth-inhibitory signals collectively driving cob thickening and enlargement in maize. We further demonstrate that domestication expanded the spatial expression domain of key transcription factors in maize meristem cells, enhancing the potential for increasing kernel number. Additionally, we verified a major domestication gene, ZmSPD1, in which two nonsynonymous SNPs differentiate maize from teosinte and alter jasmonic acid (JA) levels in the ear, thereby suppressing spikelet abortion to effectively double kernel production. These findings provide a cell-resolved mechanistic framework for how cob architecture and kernel number were shaped during maize domestication, offering new insights into the formation of key agronomic traits.

plant biology↗

A biofilm-derived peptide as an underwater adhesive

Wet adhesives that perform under water have broad applications in industrial and biomedical settings. To date, molecular designs for underwater adhesives have largely been inspired by marine animals including mussels and barnacles. Here, we propose bacterial biofilms as an alternative source of inspiration for underwater adhesives. Specifically, we demonstrate the application potential of a peptide derived from biofilms formed by the notorious pathogen Vibrio cholerae. We characterize the ability of this biofilm-derived peptide to adsorb onto various surfaces and to glue wet surfaces, by using a combination of confocal microscopy, molecular dynamics simulations, atomic force microscopy, lap shear tests, and spectroscopic tools. We further show that the peptide can co-aggregate with microspheres acting as an effective flocculant. Finally, we succeeded in purifying this peptide from E. coli in a functional form, setting the stage for large-scale production. Our results open new design possibilities for underwater adhesives inspired by natural biofilms. TeaserA peptide derived from biofilms adheres to diverse surfaces and shows promising potential as a wet adhesive and flocculant.

bioengineering↗

Structure of a key adhesin-exopolysaccharide interaction provides insights into matrix assembly in Vibrio cholerae biofilms

Biofilms serve as a protective mechanism for bacteria, including many pathogens. To form such communities, bacteria secrete macromolecules that form an extracellular matrix serving as a barrier against environmental threats, such as predation, antibiotics, and the host immune system. To be effective, a biofilm must anchor to foreign surfaces and retain sufficient stiffness, in the environment or in a host. However, how this matrix self-organizes to support biofilm formation remains a mystery at the molecular level. The human pathogen Vibrio cholerae produces biofilms primarily composed of an exopolysaccharide called VPS (Vibrio polysaccharide), consisting of an unusually-modified repeating tetrasaccharide core unit. VPS engages with two secreted adhesion proteins, Bap1 and RbmC, which adhere the biofilm to abiotic and biotic surfaces, and serve to strengthen the biofilm by interacting with VPS using a conserved {beta}-propeller. To pinpoint the interaction between the adhesins and purified segments of VPS, we determined the [~]1.6 [A] X-ray crystal structure of Bap1 bound to fragmented VPS and used the structure to carry out molecular dynamics simulations. The structure revealed a single binding site consisting of one tetrasaccharide unit involving an induced magnesium binding site. Unexpectedly, the tetrasaccharide adopted a bent state caused by a rotation of the glycosidic bond between the central two monosaccharide units. Using a combination of mutagenesis, light scattering, and in situ fluorescent microscopy, we demonstrate that Bap1 not only facilitates biofilm adhesion, but is also required for proper VPS organization, through the identified binding pocket. Our structure reveals for the first time the interaction between a biofilm exopolysaccharide and matrix protein, as well as insights into conformational changes of exopolysaccharide induced by this binding. Our findings provide a generalizable approach for studying the biophysical and biochemical properties of carbohydrate-dependent biofilm assembly, which may lead to new ways to treat disease caused by biofilm-forming bacterial pathogens by disrupting the exopolysaccharide-protein interactions.

microbiology↗

Sequential intra-articular HCAd-NFκB-IL-1Ra delivery improves therapeutic efficacy in post-traumatic osteoarthritis

Osteoarthritis is the most common joint disease for which disease-modifying therapies remain unavailable. Intra-articular gene delivery of interleukin-1 receptor antagonist (IL-1Ra) using high-capacity adenovirus (HCAd) has shown therapeutic promise; however, the duration of therapeutic benefit and the feasibility of repeat dosing under anti-adenoviral immunity remain unresolved. Using the murine anterior cruciate ligament transection model of osteoarthritis, we show that a single intraarticular injection of HCAd5-NF{kappa}B-IL-1Ra provides structural preservation and functional improvement in early-stage osteoarthritis but fails to sustain cartilage protection as disease progresses. However, HCAd5 transduction following repeated treatment is limited due to pre-existing immunity against this serotype. Notably, exchanging serotypes for repeated treatments effectively restores vector transduction and transgene expression in both healthy and osteoarthritic joints. Leveraging this strategy, we demonstrate that sequential intra-articular HCAd-NF{kappa}B-IL-1Ra administration does not further improve pain or motor function compared to the initial treatment, but preserves cartilage as assessed by histopathology and phase-contrast CT, irrespective of serotype. These findings establish HCAd serotype switching as a feasible approach to overcome immune barriers to repeat intra-articular gene therapy. Importantly, sequential HCAd-NF{kappa}B-IL-1Ra administration enhances therapeutic durability in post-traumatic osteoarthritis, providing a translational framework for repeat intra-articular gene delivery strategies aimed at long-term disease modification in osteoarthritis.

molecular biology↗

Cross-Species Efficacy of Combinatorial Gene Therapy for Osteoarthritis and Correction of Neuro-Inflammatory Pain Mechanisms

Osteoarthritis is a leading cause of chronic pain and disability, which lacks disease-modifying treatment. Given the complex multi-tissue and multifactorial drivers behind disease progression, effective treatments will require simultaneously targeting several mechanisms underlying joint degeneration and pain. Here, we developed and evaluated a combinatorial gene therapy, consisting of a high-capacity adenoviral vector carrying two therapeutic genes to target distinct pathological mechanisms: inflammation (IL-1Ra) and chondrocyte health (PRG4). Intra-articular delivery of this treatment improved functional, structural, and pain outcomes in murine and equine osteoarthritis models. In addition, treatment normalized inflammatory environments in joint tissues, as well as in the dorsal root ganglia (DRG) known to harbor joint-innervating sensory neurons. Moreover, gene therapy reversed OA-induced molecular signatures of neural hyperexcitability, suggesting amelioration of peripheral sensitization. Collectively, these findings support combinatorial gene therapy as a promising treatment for osteoarthritis, while identifying neuroinflammatory signatures for correction of disease progression and pain. One Sentence SummaryA single intra-articular injection of a combinatorial gene therapy slows OA progression and reduces pain in small and large animal models.

systems biology↗

Conformational dynamics of exopolysaccharides underlie biofilm matrix mechanics in Vibrio cholerae

Polysaccharides remain the least understood biomacromolecules, particularly in terms of the relationship between their chemical structure and physical properties. On the other hand, polysaccharides often serve as the main structural components in biofilms: surface-attached aggregates of bacterial cells encased within a mechanically resilient extracellular matrix. The large chemical space explored by bacteria within biofilms provides excellent opportunities to establish the structure-function relationship for polysaccharides. In this paper, we systematically characterize various polymer properties of Vibrio polysaccharide (VPS), the major exopolysaccharide in biofilms formed by Vibrio cholerae, the causative agent of pandemic cholera. Using a combination of shear rheology, dynamic and static light scattering, and small-angle X-ray scattering, we measure the viscosity, molecular weight, persistence length, radius of gyration, and hydrodynamic radius of this chemically unique biopolymer. Combining all-atom and coarse-grained simulations, we show how the conformational flexibility of a single glycosidic linkage within each VPS monomer can lead to dramatic compaction of the entire polymer chain and nonclassical entanglement behavior. Our comprehensive quantification represents a rare endeavor for bacterial biofilms, whose matrix composition and physical properties remain largely nebulous; it also represents a significant step towards a detailed understanding of the molecular origins of biofilm mechanics.

biophysics↗

Tumor-derived stearic acid induces macrophage Egr2 signaling to suppress anti-tumor immunity in breast cancer

BackgroundMacrophages in breast cancer are highly heterogeneous and targeting both tissue-resident and bone marrow-derived macrophages represents a high-potential strategy in breast cancer immunotherapy. MethodsMyeloid-specific Egr2 knockout (KO) mice were used to determine roles of macrophage Egr2 signaling in tumor progression and anti-tumor immune responses. RNA-seq analysis and Flow cytometry were used to examine regulation of Egr2 in tumor-associated macrophages (TAMs) and fatty acid-stimulated macrophages. Tumor cell and macrophage admixture study was used to evaluate effects of fatty acid educated macrophages on anti-tumor responses. ResultsHere we showed that early growth response 2 (Egr2) was highly expressed in mammary tissue macrophages and recruited macrophages upon tumor progression. Depletion of Egr2 in myeloid cells significantly decreased the immunosuppressive function of polarized M2-like macrophages and TAMs. Tumor progression was delayed in myeloid cell Egr2 knockout mice, which was associated with enhanced function of effector CD8+ T cells and NK cells. Mechanistically, we showed that retinol and nicotinamide metabolism in TAMs were impaired after Egr2 depletion. Further, tumor cell-derived stearic acid (SA) was identified as an important fatty acid inducing Egr2 expression. SA stimulation induced macrophage-mediated immunosuppression in an Egr2 dependent manner. Addition of oleic acid (OA) uniquely repressed SA-induced Egr2 expression and immunosuppressive activity in macrophages. ConclusionsOur study thus uncovers a novel SA-Egr2 pathway driving macrophage immunosuppression and novel molecular mechanism of OA mediated anti-tumor effect. WHAT IS ALREADY KNOWN ON THIS TOPICLipid-associated macrophages (LAMs) accumulate lipids and promote immune suppression, tumor growth and metastasis in breast cancers. Fatty acids play a dual, complex role in tumor immunity, acting as both pro-tumorigenic and anti-tumorigenic effects. However, molecular mechanisms underlying fatty acid modulated macrophages and their roles in tumor remain not fully elucidated. WHAT THIS STUDY ADDSWe demonstrate that Egr2 is essential for the immunosuppressive function of IL-4 polarized M2-like macrophages and TAMs. Tumor cell-derived stearic acid (SA) was identified as an important fatty acid inducing Egr2 expression and immunosuppression in macrophages. Adding oleic acid (OA) uniquely repressed SA-induced Egr2 expression and immunosuppression. HOW THIS STUDY MIGHT AFFECT RESEARCH, PRACTICE OR POLICYSA-Egr2 axis is a novel pathway driving macrophage immunosuppression. OA treatment enhances macrophage anti-tumor immunity via inhibiting Egr2 signaling and immunosuppression. The data supports the notion that diets enriched in OA may have potential for prevention and suppression of breast cancer.

immunology↗

Sustained Delivery of a SARS-CoV-2 Subunit Vaccine in An Adjuvanted Hydrogel Depot Enhances Vaccine Responses in Nonhuman Primates

While natural infections expose the immune system for days to weeks of inflammation and antigen presentation, immunizations with conventional bolus vaccines often lead to rapid clearance of antigens and adjuvants. Prolonged exposure to vaccines using controlled delivery devices or repeated dosing regimens has been shown to enhance germinal center reactions, leading to improved humoral responses, including increased magnitude of antibody titers and enhanced neutralizing activity. Herein, we report the use of injectable polymer-nanoparticle (PNP) hydrogels as a vaccine depot technology for sustained delivery of the clinically relevant SARS-CoV-2 Hexapro subunit antigen and a toll-like receptor agonist adjuvant. In mice, we demonstrated that PNP hydrogel vaccines enhanced germinal center responses and antibody responses relative to bolus vaccination. In nonhuman primates, hydrogel vaccines induced enhanced and durable antibody responses against wildtype and variants of concern such as Omicron BA.5 compared to bolus vaccination. We report the first use of a biomaterials-based approach for sustained delivery of vaccines in nonhuman primates, further advancing toward clinical translation.

bioengineering↗

IgGM2: An All-Atom Foundation Model for Adaptive Immune Receptor Design

Accurate immune receptor design requires modeling the coupled variation of aminoacid sequence, full-atom conformation, and target-binding geometry across antibodies, nanobodies, and T-cell receptors (TCRs). Existing methods often address only part of this problem, either by separating structure generation from sequence design, relying on fixed-backbone inverse folding, or focusing on a single receptor class. We introduce IgGM2, a unified all-atom generative framework for immune receptor structure prediction and CDR sequence-structure co-design. IgGM2 follows a structure-to-design strategy: it first learns how immune receptors are positioned around fixed target structures, and then transfers this target-conditioned structural prior to CDR design. Unlike modular design pipelines, IgGM2 jointly generates CDR residue identities and full-atom receptor structures, allowing frame-work geometry to adapt to designed CDRs without separate inverse folding or external sidechain packing. Unlike continuous residue encodings based on virtualatom geometry, IgGM2 keeps sequence prediction explicit while using atom14 placeholders only for full-atom representation. On structure prediction benchmarks, IgGM2 better captures receptor-target spatial relationships than AlphaFold3 on FoldBench and achieves strong performance on TCR-pMHC modeling. On sequence design benchmarks, IgGM2 achieves competitive amino-acid recovery and improves Rosetta-based interface preference metrics, suggesting more favorable generated binding interfaces. These results support IgGM2 as a unified all-atom framework for adaptive immune receptor structure prediction and design.

bioinformatics↗

Surface-specific film assembly of a Vibrio cholerae adhesin peptide modulated by environmental salts

Underwater adhesion research increasingly draws on bioinspired systems to uncover the molecular mechanisms that enable strong interfacial binding in aqueous environments. The biofilm adhesin Bap1 from Vibrio cholerae contains a short peptide motif, SYWFFGWHTK (CP), which exhibits exceptional adhesive performance, surpassing mussel foot protein mfp5 under comparable conditions. Despite its promise, the roles of ionic environments and aggregation behavior in governing CP adhesion remain unclear. In this study, we investigate how ion identity influences CP aggregation, film formation, and interfacial properties. Using dynamic light scattering, we identify the formation of micron-scale assemblies of aggregated molecular clusters (AAMCs), with size distributions modulated by salt type. Quartz crystal microbalance with dissipation and liquid atomic force microscopy reveal that CP film formation is both surface- and ion-dependent. On gold substrates, AAMCs preferentially adsorb and collapse into rigid, smooth nanofilms, consistent with hydrophobic-driven compaction. In contrast, silicate surfaces inhibit such collapse, yielding distinct morphologies and interfacial energetics. These findings demonstrate that surface chemistry and ionic conditions jointly regulate peptide aggregation and adhesion. This work provides mechanistic insight into hydrophobic-rich peptide systems and informs the rational design of next-generation wet adhesives, with broader implications for biomaterials and peptide-based formulations. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=129 SRC="FIGDIR/small/733527v2_ufig1.gif" ALT="Figure 1"> View larger version (39K): org.highwire.dtl.DTLVardef@1f3f3cborg.highwire.dtl.DTLVardef@10aae0corg.highwire.dtl.DTLVardef@289970org.highwire.dtl.DTLVardef@171b026_HPS_FORMAT_FIGEXP M_FIG C_FIG

biophysics↗

Tumor-Derived SPP1 Drives Immunosuppressive Macrophage Reprogramming in Gastric Peritoneal Carcinomatosis

Peritoneal carcinomatosis is a major cause of death in gastric cancer, yet effective therapies remain limited. Tumor-derived soluble factors are increasingly recognized as key regulators of the peritumoral microenvironment. Here, we nominate osteopontin (SPP1) as a tumor-derived mediator that orchestrates macrophage-driven immunoregulation in gastric peritoneal carcinomatosis. Using integrated analyses of human clinical datasets and murine models, we demonstrate that tumor-secreted SPP1 promotes macrophage recruitment and induces tolerogenic IL-10 production. Clinically, SPP1 correlated with inferior overall survival and progression-free survival in gastric cancer. In syngeneic murine models of gastric peritoneal carcinomatosis, intracavitary pharmacologic inhibition of SPP1 restricted peritoneal dissemination, impaired macrophage infiltration and suppressed IL-10 production. Consistent with these findings, macrophage depletion phenocopied antitumor effects of SPP1 inhibition, resulting in decreased metastatic burden. Collectively, these findings define a mechanism of tumor-macrophage crosstalk that promotes peritoneal dissemination and provide a rationale for therapeutic targeting of SPP1 in gastric peritoneal carcinomatosis.

Cancer Biology↗

Targeted Photodegradation of Misfolded Proteins via Self-photosensitizing with Molecularly Produced Light

Misfolded proteins are tightly associated with various neurodegenerative diseases, and removing these misfolded proteins is one of the actively pursued approaches for seeking therapeutics for these diseases. In this study, we demonstrated that molecularly produced light (molecular light) from ADLumin-5, a self-photosensitizing chemiluminescence compound, could induce photo-oxidation and photodegradation of misfolded proteins, including beta-amyloid, tau, alpha-synucleins, and TDP-43 proteins in vitro. We validated the oxidation and degradation via LC-MS, MADLI-MS, and western blotting. Using beta-amyloid as a showcase, we demonstrated that, upon photo-oxidation and photodegradation, the toxicities of this misfolded protein were significantly reduced. To investigate the therapeutic effects of ADLumin-5 in vivo, we used the 5xFAD mouse model for longitudinal treatment for 4 months. In vivo molecular imaging results indicated that ADLumin-5 could reduce the accumulation of beta-amyloid proteins. Our study presents a novel approach to seek therapeutics for neurodegenerative disease via molecular light-induced degradation of misfolded proteins. In addition, because ADLumin-5 is dual-functional--enabling both photodegradation and in vivo imaging of misfolded protein changes--it can be considered a photo-theranostic agent for neurodegenerative diseases, representing a novel approach to drug discovery for neurodegenerative diseases.

neuroscience↗

Predicting Human mRNA Isoform Levels from Site-Specific Splicing Kinetics in silico

Splicing of pre-mRNA can result in multiple possible mRNA isoforms per gene due to alternative splicing. The frequency at which individual isoforms occur depends on the intrinsic splicing kinetics of the pre-mRNA as well as intracellular chemical conditions. Computational modeling can potentially provide a platform to rapidly assess how variations in intracellular and environmental conditions, for example differential levels of regulatory splicing proteins, affect kinetics and resulting mRNA isoforms. Overcoming the vast combinatoric possibilities of splicing, however, has remained a significant challenge in modeling its kinetics. Here we report the development of a stochastic kinetic model of splicing that is extensible to most protein-coding genes in the human genome. Our model allows for variations in site-specific reaction rates as well as the ability to introduce additional splicing factors. We experimentally validate the predictive capability of our computational model by exploring the spliced isoform ratio of a target gene (SRSF6) under normoxia and hypoxia. This work provides a resource for quantitative, computational analysis of pre-mRNA splicing, allowing for a rapid computational-experimental approach to assess biological hypotheses. Author summarymRNA splicing is a key step in human gene expression with deep impact on the molecular processes determining cell physiology and affecting development and disease. Computational models of splicing are highly attractive to understand life processes but so far have been limited in directly accounting for the chemistry of splicing and are not extensible to most of the human genome. We report here a model that overcomes both of these challenges, providing a computational benchtop to probe splicing kinetics for most genes in the human genome. This model has the capability to rapidly pose biological hypotheses for experimental validation. As a targeted demonstration, we explore the effects of the pathologically-relevant chemical condition hypoxia on the pre-mRNA of a single gene.

biophysics↗