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Walker, J.

Publications and source records attributed to Walker, J..

At least 19 recordsLinked to original sources

Genetically-encoded discovery and development of peptide-macrocycle imaging agents for PD-L1

The unique cell surface composition of tumor cells forms the molecular basis for many targeting and cell-based therapies. Here, we describe the development of novel peptide-based targeting agents for programmed death ligand 1 (PD-L1). Molecular imaging by peptide agents, coupled with therapeutic intervention using the same modality, represents a critical advancement in cancer management. Whole-body PET imaging of PD-L1 expression offers a superior alternative to traditional immuno-histochemistry, making PD-L1 radiodiagnostic imaging a highly sought-after modality. PD-L1 targeting modalities developed for clinical imaging to date can be divided into antibodies, protein domains, and small macrocyclic peptides with fewer than 20 amino acids. The latter modalities can address many challenges seen in antibody-based targeting vectors. All potent PD-L1 targeting peptide modalities reported to date rely extensively on non-canonical amino acids (ncAAs). Here, we report a comprehensive structure-activity relationship (SAR) analysis of a family of macrocycles discovered from an Sx2Cx8Cx2 phage-display library composed entirely of natural amino acids (x represents 19 natural amino acids excluding Cys). Using >10,000 variants in ''focused'' phage-display libraries, we optimized these macrocycles to achieve single-digit-nanomolar potency in protein- and cell-based assays. En route to this optimization, the activity of 216 synthetic macrocycles towards PD-L1 was measured in five distinct assays; two leads have been evaluated by imaging in tumor xenografts in mice, and the X-ray structure of one advanced lead in complex with PD-L1 has been determined at 2.78 [A] resolution. This publication demonstrates the development potential of PD-L1-targeting macrocycles that do not require extensive incorporation of ncAAs and the democratization of discovery by mapping the optimization path to single-digit-nanomolar assets for targeted radiopharmaceuticals via canonical phage-display technology.

pharmacology and toxicology↗

Distinct extracellular matrix states uncouple collagen accumulation from pathological fibrosis in Duchenne muscular dystrophy

Fibrosis severity is routinely inferred from collagen abundance, although whether collagen quantity determines pathological fibrosis remains unclear. In Duchenne muscular dystrophy (DMD), chronic muscle injury and inflammation drive extracellular matrix accumulation, making these processes difficult to disentangle. We exploit sarcospan overexpression in mdx mice, a model of DMD (mdxTG), which improves membrane integrity and muscle function despite persistent matrix remodeling. mdxTG muscle accumulates more collagen than mdx yet lacks its dense macrophage-rich scars. Matrisome proteomics and spatial transcriptomics reveal compositionally and spatially distinct matrix states, while decellularized mdxTG matrix protects myotubes from membrane damage relative to mdx matrix. Despite these differences, both dystrophic matrices remain stiff and induce nuclear YAP in fibro-adipogenic progenitors. Verteporfin suppresses collagen production and reduces fibrosis in vivo, while nuclear YAP is increased in FAPs from patients with DMD. Thus, collagen abundance alone does not define pathological fibrosis; matrix organization, biological activity, and mechanosignaling distinguish functionally distinct fibrotic states.

physiology↗

Single-Nuclear RNA Sequencing Reveals Regional Specialization and Cellular Interactions in Epicardial and Perivascular Adipose Tissue

Background: Adipose tissue surrounding the heart and vasculature plays critical roles in cardiovascular homeostasis and disease, yet the cellular and molecular milieu of these depots at single-cell resolution remains incompletely characterized. Understanding how regional adipocytes differ transcriptionally and communicate with neighboring cardiovascular cells is essential for developing targeted therapeutic strategies. Methods: We performed single-nucleus RNA sequencing (snRNA-seq) on human adipose tissue from four anatomically distinct depots: ascending aorta, left atrium, right coronary artery, and subcutaneous fat. We characterized cellular composition, adipocyte and progenitor heterogeneity, depot-specific transcriptional programs, and intercellular communication networks. We further examined signaling remodeling in disease contexts, including atrial fibrillation and aortic aneurysm. Results: We identified six transcriptionally distinct adipocyte subpopulations and six adipocyte stromal and progenitor cell (ASPC) subpopulations were shared across depots but showed marked differences in abundance and gene expression reflecting developmental imprinting, including HOX family genes and anterior-posterior patterning programs. Intercellular communication analysis revealed depot-specific ligand-receptor interactions, with EPHA signaling identified as selectively enriched in the left atrial adipose depot. Disease-state analyses demonstrated extensive change in cell-cell communication in atrial fibrillation and aortic aneurysm, with differential regulation of FN1, EGF, SLIT, NOTCH, and CD46 signaling pathways. Conclusions: Our study reveals that cardiac and vascular adipose depots harbor transcriptionally specialized adipocytes and progenitors with distinct intercellular communication programs that are remodeled in atrial fibrillation and aortic aneurysm.

physiology↗

Recreating the Native Airway Microenvironment Using Tissue-Specific Extracellular Matrix Bioinks for Proximal Airway Engineering

Ex vivo airway engineering approaches such as 3D bioprinting offer a promising strategy for generating functional airway replacements, but the fabrication of hollow, patient-specific proximal airway constructs using translationally relevant bioinks remains challenging. This study describes the development of biocompatible, polymer-blended human airway-derived decellularized extracellular matrix (AW-dECM) bioinks for engineering structurally and mechanically relevant airway tissues. An optimal formulation consisting of 30 mg/mL AW-dECM and nanofibrillar cellulose alginate conjugated to RGD supported the bioprinting of simple and complex hollow airway structures with mechanical properties comparable to native airways ([~]8-10 kPa). The bioinks also promoted primary human airway epithelial cell viability, adhesion, and differentiation into mucociliary and secretory phenotypes during 28 days of air-liquid interface culture. Furthermore, subcutaneous implantation in immunocompetent rats demonstrated excellent biodegradative stability and overall biocompatibility over 30 days. Collectively, these findings establish a foundation for improved physiological airway models and future tissue-engineered airway replacements.

bioengineering↗

Chromosome-scale genome assembly of diploid halophyte Thinopyrum bessarabicum excludes J genome from polyploid Thinopyrum ancestry

Wild relatives of wheat harbour genetic diversity essential for improving resilience to climate-driven stresses, yet their deployment is hampered by unresolved evolutionary relationships and the absence of reference genomes. Here we present a chromosome-scale reference genome for Thinopyrum bessarabicum, a diploid halophyte and high-priority donor for wheat salt tolerance breeding. A key unresolved question is whether the diploid J genome contributed directly to the subgenome composition of extant polyploid Thinopyrum species, and which genomic features underpin its exceptional salt tolerance. Using this resource, we show that the diploid J genome of Th. bessarabicum is not represented among the subgenomes of polyploid Thinopyrum species, resolving a long-standing ambiguity in Triticeae genomics. Gene-level resolution of the reciprocal 4/5 chromosomal translocation across six related Triticeae species identifies conserved breakpoint gene pairs, supporting a single ancestral rearrangement. Genome-wide gene content analysis shows that halophytic capacity is underpinned by quantitative expansion of conserved stress-response gene families. Salt tolerance phenotyping validates chromosome 5J as a tolerance locus in both Th. bessarabicum and wheat introgression lines. A physically anchored marker framework and dual-reference skim-sequencing pipeline enable precise megabase-resolution characterisation of Th. bessarabicum introgressions in wheat, providing a genomic foundation for deploying J-genome diversity in crop improvement.

plant biology↗

Novel integrated risk index reveals uneven impact of climate change on fascioliasis risk across Africa and Europe

Fascioliasis, a zoonotic parasitic disease caused by the liver flukes Fasciola hepatica and Fasciola gigantica, poses a significant threat to livestock and human health globally. Climate change is altering the transmission dynamics of this disease; however, the direction and magnitude of this change remain uncertain due to a lack of mechanistically grounded predictions at continental scale. In this study, we developed a novel risk index to assess how climate change may affect the potential for fascioliasis transmission across Africa and Europe. The index integrates the following three components that together capture the environmental requirements for Fasciola transmission: the temperature dependence of the parasite transmission; climatic suitability for the snail intermediate host; and availability of freshwater habitats. To estimate these components, we used data from published experimental studies, thousands of snail occurrence records, and both mechanistic and correlative modelling approaches. We predict that climate change will generally reduce fascioliasis risk across most of the ranges of the two investigated liver fluke species, albeit with marked geographical differences. The transmission risk of F. gigantica is predicted to decrease in the Sahel and West Africa, due to above-optimal temperatures for parasite transmission and climatic suitability for the intermediate hosts. However, risk for F. hepatica transmission is projected to increase in parts of Northern Europe, Scandinavia, and Iceland, where livestock densities are high. We also find that the potential for hybridization between F. hepatica and F. gigantica may decline due to reduced geographic overlap in areas that are highly suitable for transmission. By providing a scalable, ecologically informed framework for predicting fascioliasis risk under climate change, this study lays the groundwork for improved local risk assessment. Our results provide a more nuanced perspective on the potential impact of climate change on fascioliasis transmission, showing that this will be highly uneven across Africa and Europe. Author summaryFascioliasis is a snail-borne, zoonotic disease that affects both humans and livestock, causing major health burden and economic losses worldwide. The liver flukes that cause the disease use freshwater snails as their intermediate hosts. They therefore require aquatic habitats and suitable temperatures to complete their life cycle. Climate change altering these conditions; however, it is unclear how this will affect transmission of liver flukes in the future. Here we develop a new risk index that combines three key environmental factors of importance for liver fluke transmission: how suitable temperatures are for parasite transmission, the climatic suitability for snail hosts, and the availability of water. We mapped current and projected future transmission risk for two main species, Fasciola hepatica and Fasciola gigantica, across Africa and Europe. Different from what has been predicted by earlier studies, our results suggest that transmission risk will decline in across most of the range of both species. This will have particularly big impacts in areas where livestock densities are high, including the Sahel region. In northern Europe, transmission risk increases slightly. This study also provides a modelling framework and novel ecological knowledge that can be used to assess risk of transmission at local and continental scale.

ecology↗

Staphylococcus aureus urease is controlled by a complex regulatory network and promotes dissemination during catheter-associated urinary tract infections (CAUTI)

Catheter-associated urinary tract infections (CAUTIs) are one of the most common hospital-associated infections in the United States, accounting for >1 million cases annually. One CAUTI-associated pathogen, Staphylococcus aureus, is commonly found persisting asymptomatically in the bladder of catheterized individuals, increasing these individuals risk of developing CAUTI. Importantly, S. aureus is not only associated with severe symptoms, including bacteremia and septic shock, but it also produces a common uropathogen associated virulence factor, urease. Despite its importance, urease has only been well-studied in the uropathogen Proteus mirabilis. While previous studies identified three S. aureus urease regulators, CodY, CcpA, and Agr, the environmental signals required for expression and activity, and the contribution of urease to CAUTI have not been explored. In this study, we investigate how the urease regulatory pathways coordinate expression and activity in response to environmental signals present within the catheterized urinary tract. Our findings demonstrate that stationary phase significantly induces S. aureus urease expression and activity. Additionally, we identified predicted binding sites in the urease promoter for three regulators previously implicated in urease expression - CodY, CcpA, and SigB - as well as SrrA - a previously unrecognized regulator of urease. A binding site for Agr was not present in the urease promoter. Expression and activity assays confirm the role of CodY, CcpA, SigB, SrrA, and Agr in regulating urease. Importantly, single nucleotide polymorphisms identified in the urease promoter of clinical isolates enhance urease expression. Additionally, urease promotes biofilm formation under catheterized urinary tract-like conditions in vitro and dissemination from the bladder to the kidneys at 1 day post infection in a mouse CAUTI model. Together, our data not only provide insight into the regulatory pathway controlling S. aureus urease but also emphasize the importance of studying these mechanisms in a model that mimics the host environment. AUTHOR SUMMARYCatheter-associated urinary tract infections (CAUTIs) are common hospital-associated infections and are caused by many different pathogens. Of these pathogens, Staphylococcus aureus is particularly problematic, as it often spreads to the bloodstream and results in septic shock. One of the primary virulence factors that is important for uropathogens is urease. Urease breaks down urea in urine, which results in crystalline structures that encrust urinary catheters and promote reflux to the kidney. Despite producing urease, little is known about how S. aureus regulates the enzyme. In this study, we investigate how regulatory pathways coordinate the expression and activity of urease in response to environmental signals. We show that growth during stationary phase and in conditions that mimic the urinary tract urease expression and activity are increased. We also show that five different regulators - CodY, CcpA, SigB, SrrA, and Agr control urease expression and activity. Additionally, genomic changes identified in the urease regulatory pathway of clinical urinary catheter-associated isolates enhance urease expression. Importantly, urease promotes biofilm formation and dissemination during CAUTI. Our study provides insight into the complex regulatory mechanisms controlling urease and highlights the role urease plays in the development and virulence of S. aureus CAUTI.

microbiology↗

Exercise intensity modulates the human plasma secretome and interorgan communication

Exercise is recognized as first-line therapy for many cardiometabolic diseases, including obesity, type 2 diabetes, and hypertension. Despite the abundant health-promoting effects of exercise, in-depth characterization of circulatory factors that mediate these benefits in humans remains incomplete. Moreover, how different modes and intensities of exercise uniquely regulate these processes is unclear. Here, we address these questions by conducting a multi-cohort human exercise intervention, incorporating sprint-interval exercise (SIE) and moderate-intensity exercise (MIE) to analyze intensity-dependent regulation of interorgan crosstalk. We find that exercise intensity distinctly influences the plasma proteome and metabolome in both untrained and trained participants. SIE led to immediate and robust changes to the plasma proteome, whereas MIE resulted in delayed secretory kinetics. By leveraging large, multi-organ gene and protein expression datasets, in combination with in vitro and in vivo tissue sampling, we map the differentially regulated proteins to their predicted tissue of origin and destination. We find that adipocytes are particularly sensitive to exercise intensity, undergoing broad transcriptomic remodeling following in vitro incubation with SIE as compared to MIE plasma. These findings underscore the integrated whole-body response following acute exercise and highlight exercise intensity as a key factor influencing interorgan communication.

physiology↗

The impact of microplastic contamination in cow manure on reproductive behavior and larval survival in the dung beetle Onthophagus taurus

Microplastics are an emerging environmental hazard on a global scale. Their detection in agricultural environments is of particular concern not only for food contamination, but also because microplastics negatively impact detritivores and their ecosystem functioning. Dung beetles in particular provide vital ecosystem services in agricultural environments and are often vulnerable to anthropogenic hazards, but whether they are affected by microplastics remains unclear. Here, we test whether artificial contamination of cow dung with thermoplastic polyurethane (TPU) has the potential to affect the juvenile development and maternal behavior of the bull-headed dung beetle Onthophagus taurus. Dung beetles exhibited high mortality when exposed to elevated concentrations of TPU. In addition, females were equally likely to provision offspring with TPU-spiked (and lethal) cow dung as with control dung, suggesting that females cannot differentiate between highly toxic microplastic-contaminated and uncontaminated cow dung. Our findings highlight potentially severe consequences for dung beetles if microplastics persist and accumulate, although the levels of exposure in the field are unknown. Although the direct environmental hazards and the mechanisms mediating the negative impacts of TPU microplastics remain to be assessed, this study suggests that microplastics may negatively impact dung beetles and their ecosystem services. Future work assessing exposure levels in the field as well as dung beetles potential to evolve resistance against microplastic pollution will be necessary to assess the long-term impact of microplastic presence on dung beetle ecosystem functioning.

ecology↗

Acute cold exposure in humans shifts the circulating proteome to a cardioprotective and anti-aging profile

Cold exposure has been proposed to provide a constellation of salutary effects, yet its molecular correlates remain largely unknown. Brown adipose tissue (BAT) is the main site of adaptive thermogenesis, and its prevalence is linked with cardiometabolic health. Since the benefits of BAT activation and cold exposure more generally may be mediated through blood-borne factors, we conducted an extensive analysis of the circulating proteome linked with an acute cold challenge in healthy adults. Our goal was to uncover early molecular changes triggered by cooling and establish their specific relationships with the human brown adipocyte secretome as well as various phenotypic traits. Based on comprehensive inter-cohort validations, we provide the first reproducible proteomic signature of cold exposure in humans. Our data demonstrate that cooling favorably modulates circulating mediators linked with chronological aging, as well as metabolic and cardiovascular diseases, providing new potential biochemical transducers of the benefits associated with cold therapy. HighlightsO_LICooling alters the plasma proteome with striking concordance in independent human cohorts. C_LIO_LICooling represses circulating proteins linked with type 2 diabetes, hypercholesterolemia, hypertension, coronary heart disease and heart failure. C_LIO_LIThe circulating signature of cooling resembles a cardioprotective and anti-aging profile. C_LI

physiology↗

Discovery of non-opioid receptor protein targets of fentanyl across tissues from animal models and humans using photoaffinity probes

Synthetic opioids such as fentanyl and related analogs have been widely used for pain management. However, their negative side effects, including respiratory depression and high potential for addiction, underscore the need for a deeper understanding of fentanyls interactions with proteins throughout the human body. Fentanyl analogs bind and activate opioid receptors in the central and peripheral nervous systems, triggering numerous downstream signaling pathways. Increasingly, fentanyl has been shown to interact with non-opioid receptors, and elucidation of these non-canonical fentanyl-protein interactions may provide insights into the mechanisms contributing to fentanyls adverse effects and illuminate novel countermeasure strategies. To identify proteins in mammalian tissues that may interact with fentanyl, we designed and synthesized three affinity-based probes (AfBPs) that include the fentanyl core and feature a diazirine photoaffinity group and alkyne handle for click chemistry at different positions. Molecular docking simulations predicted that these AfBPs bind the mu opioid receptor similarly to fentanyl. Affinity-based protein profiling using the FA-T1 probe in vitro in tissues from six animal species identified histamine N-methyltransferase (HNMT), endophilin-B1 (SH3GLB1), fructosamine-3-kinase (FN3K), cutA divalent cation tolerance analog (CUTA), and monoamine oxidase B (MAOB) among the top proteins that bind fentanyl in multiple species and tissue types. Molecular docking of fentanyl and remifentanil with these protein structures identified putative binding sites. The interaction of fentanyl with specific proteins was empirically assessed through protein structural analyses. These findings highlight potential fentanyl-protein interactions that may contribute to the acute and long-term impacts of fentanyl exposures.

pharmacology and toxicology↗

Context-dependent effects of ivermectin residues on dung insects: Interactions with environmental stressors, size, and sex in a sepsid fly (Sepsis neocynipsea)

Insects associated with livestock dung frequently encounter veterinary medication residues. These residues often have negative effects on insect survival, reproduction, and ecosystem functioning and may contribute to the rapid decline in temperate insect populations. Ivermectin is an antiparasitic drug widely used to treat parasites in livestock. While it has long been recognized that ivermectin effects insect survival, the potential interactive effects between ivermectin exposure and other ecologically relevant abiotic stressors remain poorly understood. Here, we study these effects in the black scavenger fly Sepsis neocynipsea, which depends on cow dung for reproduction. Using a fully factorial design, we test whether the effects of ivermectin exposure on adult survival interact with heat and desiccation stress, and whether these effects depend on size and sex. Ivermectin exposure had strong negative impacts on adult survival, but its effects were stronger in females and large individuals. While heat stress also had a strong effect on adult survival, the combined effects of heat and ivermectin exposure were less severe than the expected additive effects of both stressors applied independently, suggesting some cross-resistance. We did not find an interaction between ivermectin and desiccation stress. Taken together, our findings highlight how the complex interactions between insecticides and abiotic stressors could drive changes in coprophagous insect populations and their ecological functions across different ecosystems and climates.

ecology↗

A Modular Bacteriophage T4 Nanoparticle Platform Enables Rapid Design of Completely Protective Multivalent Mucosal Dual Vaccine Against COVID-19 and Flu

A multivalent, rapidly deployable, mucosal vaccine platform is desperately needed to prevent the acquisition and transmission of respiratory infections during epidemics and pandemics. We present one such bacteriophage T4-based platform, and design of dual COVID-19-Flu mucosal vaccines by exploiting its unique architecture. These include: T4s natural affinity for nasal mucosa, flexible engineering to incorporate multiple antigens, and repeat and symmetric epitope presentation for enhanced B cell responses. Hundreds of SARS-CoV-2 spike trimers and nucleocapsid proteins, and influenza hemagglutinin trimers and M2e peptides, were incorporated into a single phage, creating the highest density nanoparticle presentation yet reported. Intranasal administration of adjuvant-free vaccine induced robust mucosal immunity in mice including, neutralizing antibody and secretory IgA, lung-resident CD4+/CD8+ T cells, diverse memory B cells, and complete protection against SARS-CoV-2 and influenza challenges. The noninfectious T4 phage offers an extraordinary platform to rapidly design potent mucosal vaccines against emerging bacterial and viral threats.

microbiology↗

STK19 facilitates the clearance of lesion-stalled RNAPII during transcription-coupled DNA repair

Transcription-coupled DNA repair (TCR) removes bulky DNA lesions impeding RNA polymerase II (RNAPII) transcription. Recent studies have outlined the stepwise assembly of TCR factors CSB, CSA, UVSSA, and TFIIH around lesion-stalled RNAPII. However, the mechanism and factors required for the transition to downstream repair steps, including RNAPII removal to provide repair proteins access to the DNA lesion, remain unclear. Here, we identify STK19 as a new TCR factor facilitating this transition. Loss of STK19 does not impact initial TCR complex assembly or RNAPII ubiquitylation but delays lesion-stalled RNAPII clearance, thereby interfering with the downstream repair reaction. Cryo-EM and mutational analysis reveal that STK19 associates with the TCR complex, positioning itself between RNAPII, UVSSA, and CSA. The structural insights and molecular modeling suggest that STK19 positions the ATPase subunits of TFIIH onto DNA in front of RNAPII. Together, these findings provide new insights into the factors and mechanisms required for TCR.

molecular biology↗

Between-day reliability of local and global muscle-tendon unit assessments in female athletes whilst controlling for menstrual cycle phase

Measurements of muscle-tendon unit (MTU) function can be categorised into local (e.g. tendon strain) or global (e.g. jump height) assessments. Although menstrual cycle phase may be a key consideration when implementing these assessments in female athletes, the reliability of many MTU assessments is not well defined within female populations. Therefore, the purpose of this study was to report the test-retest reliability of local and global MTU function assessments during the early follicular phase of the menstrual cycle. Seventeen naturally menstruating females (age 28.5 {+/-} 7.3 years) completed local and global assessments of MTU function during two testing sessions separated over 24-72 hours. Local tests included Achilles tendon mechanical testing and isometric strength of ankle plantar flexors and knee extensors, whereas global tests included countermovement, squat, and drop jumps, and the isometric midthigh pull. Based on intraclass correlation coefficient (ICC) statistics, poor to excellent reliability was found for local measures (ICC: 0.096-0.936). Good to excellent reliability was found for all global measures (ICC: 0.788-0.985), excluding the eccentric utilisation ratio (ICC 0.738) and most rate of force development metrics (ICC: 0.635-0.912). Isometric midthigh pull peak force displayed excellent reliability (ICC: 0.966), whereas force-time metrics ranged from moderate to excellent (ICC: 0.635-0.970). Excluding rate of force development (coefficient of variation [CV]: 10.6-35.9%), global measures (CV: 1.6-12.9%) were more reproducible than local measures (CV: 3.6-64.5%). However, local metrics directly measure specific aspects of MTU function, and therefore provide valuable information despite lower reproducibility. The novel data reported here provides insight into the natural variability of MTU function within female athletes, which can be used to enhance the interpretation of other female athlete data, especially that which aims to investigate other aspects of variability, such as the menstrual cycle.

physiology↗

Synthesis of ionizable lipopolymers using split-Ugi reaction for pulmonary delivery of various size RNAs and gene editing

We present an efficient approach for synthesizing cationic poly(ethylene imine) derivatives using the multicomponent split-Ugi reaction to rapidly create a library of complex functional ionizable lipopolymers. We synthesized a diverse library of 155 polymers, formulated them into polyplexes to establish structure-activity relationships crucial for endosomal escape and efficient transfection. After discovering a lead structure, lipopolymer-lipid hybrid nanoparticles are introduced to preferentially deliver to and elicit effective mRNA transfection in lung endothelium and immune cells, including T cells with low in vivo toxicity. The lipopolymer-lipid hybrid nanoparticles showed 300-fold improvement in systemic mRNA delivery to the lung compared to in vivo-JetPEI(R). Lipopolymer-lipid hybrid nanoparticles demonstrated efficient delivery of mRNA-based therapeutics for treatment of two different disease models. Lewis Lung cancer progression was significantly delayed after treatment with loaded IL-12 mRNA in U155@lipids after repeated i.v. administration. Systemic delivery of human CFTR (hCFTR) mRNA resulted in production of functional form of CFTR protein in the lungs. The functionality of hCFTR protein was confirmed by restoration of CFTR- mediated chloride secretion in conductive airway epithelia in CFTR knockout mice after nasal instillation of hCFTR mRNA loaded U155@lipids. We further showed that, U155@lipids nanoparticles can deliver complex CRISPR-Cas9 based RNA cargo to the lung, achieving 5.6 {+/-} 2.4 % gene editing in lung tissue. Moreover, we demonstrated successful PD-1 gene knockout of T cells in vivo. Our results highlight a versatile delivery platform for systemic delivering of mRNA of various sizes for gene therapy for a variety of therapeutics.

bioengineering↗

Development of a series of genetically engineered NTRK fusion-driven pediatric-type high-grade glioma mouse models

Pediatric-type high-grade gliomas frequently harbor gene fusions involving receptor tyrosine kinase genes, including neurotrophic tyrosine kinase receptor (NTRK) fusions. Clinically, these tumors show high initial response rates to tyrosine kinase inhibition but ultimately recur due to the accumulation of additional resistance-conferring mutations. Here, we developed a series of genetically engineered mouse models of treatment-naive and -experienced NTRK1/2/3 fusion-driven gliomas. Both the TRK kinase domain and the N-terminal fusion partners influenced tumor histology and aggressiveness. Treatment with TRK kinase inhibitors significantly extended survival of NTRK fusion-driven glioma mice in a fusion- and inhibitor-dependent manner, but tumors ultimately recurred due to the presence of treatment-resistant persister cells. Finally, we show that ERK activation promotes resistance to TRK kinase inhibition and identify MEK inhibition as a potential combination therapy. These models will be invaluable tools for preclinical testing of novel inhibitors and to study the cellular responses of NTRK fusion-driven gliomas to therapy.

cancer biology↗

Yellow Fever Emergence: Role of Heterologous Flavivirus Immunity in Preventing Urban Transmission

During major, recent yellow fever (YF) epidemics in Brazil, human cases were attributed only to spillover infections from sylvatic transmission with no evidence of human amplification. Furthermore, the historic absence of YF in Asia, despite abundant peridomestic Aedes aegypti and naive human populations, represents a longstanding enigma. We tested the hypothesis that immunity from dengue (DENV) and Zika (ZIKV) flaviviruses limits YF virus (YFV) viremia and transmission by Ae. aegypti. Prior DENV and ZIKV immunity consistently suppressed YFV viremia in experimentally infected macaques, leading to reductions in Ae. aegypti infection when mosquitoes were fed on infected animals. These results indicate that, in DENV- and ZIKV-endemic regions such as South America and Asia, flavivirus immunity suppresses YFV human amplification potential, reducing the risk of urban outbreaks. One-Sentence SummaryImmunity from dengue and Zika viruses suppresses yellow fever viremia, preventing infection of mosquitoes and reducing the risk of epidemics.

microbiology↗