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Li, C.

Publications and source records attributed to Li, C..

At least 379 records · Page 21Linked to original sources

Coordinated alternative splicing decisions via stepwise exon definition

Alternative splicing of pre-mRNA is a fundamental step in human gene regulation and aberrant slic-ing is tightly linked to diseases including cancer. Various splicing events, such as alternative exon (AE) choice and intron retention (IR), are controlled by a common molecular machinery, the spliceo-some. However, it remains elusive how the regulation of spliceosome activity coordinately affects these splicing decisions. Here, we analyze a large-scale mutagenesis screen and genome-wide RNA sequencing data to show that IR and AE choice are tightly coupled, as IR products primarily accu-mulate in alternative exons showing intermediate inclusion levels. Using data-driven mathematical modeling, we reveal that multistep exon recognition by the spliceosome explains the observed AE-IR dependency for cis-acting sequence mutations and upon knockdown of trans-acting RNA-binding proteins. Furthermore, we show that multistep exon definition is frequently perturbed in cancer cells, which leads to the coordinated deregulation of intron retention and AE choice. In conclusion, we showed that the spliceosome coordinates complex splicing decisions via stepwise exon definition, which potentially facilitates the search for common molecular mechanisms for mis-splicing in cancer.

systems biology↗

Lipids modulate open probability of RyR1 under cryo-EM conditions

Ryanodine receptors (RyRs) are intracellular tetrameric ion channels responsible for Ca2+ release from the sarcoplasmic and endoplasmic reticulum. Among the three known mammalian RyR isoforms, RyR1 is critical for muscle contraction and has been studied most extensively. The cytoplasm-exposed multidomain fragment of RyRs integrates multiple cellular signals that regulate channel gating and small deviations from the physiological open probability of RyRs leads to life-threatening diseases. While cryo-EM has been instrumental in revealing near-atomic details of RyR gating mechanisms, the open probability of RyR1 under cryo-EM conditions is notably lower than that observed in electrophysiological studies, complicating structural investigations of RyR1 gating modulation. Here, we present a cryo-EM study examining the open probability of RyR1 solubilized in CHAPS with varying lipid concentrations. We found that increasing lipid concentration from 0.001% to 0.05% raised the RyR1 open probability from 16 to 84%; however, RyR1 reconstituted into lipid nanodiscs remained closed. We modelled 72 lipid molecules in the map reconstructed at the highest lipid concentration. These findings demonstrate critical role of lipids in modulating RyR1 gating under cryo-EM conditions and suggest optimal lipid-mimetics for structural studies of RyR1 gating modulation.

biochemistry↗

White Spot Syndrome Virus Immediate-Early Protein (wsv100) Antagonizes the NF-kappaB Pathway to Inhibit Innate Immune Response in shrimp

Viruses have evolved sophisticated strategies to evade host immune defenses, often targeting conserved signaling pathways. In shrimp, the NF-{kappa}B signaling pathway is crucial for antiviral immunity, yet its regulation during White Spot Syndrome Virus (WSSV) infection remains poorly understood. Here, we identify and characterize wsv100, an immediate-early (IE) protein of WSSV, as a key antagonist of the NF-{kappa}B pathway. wsv100 interacts directly with the transcription factor Dorsal and the adaptor protein IMD, preventing Dorsal phosphorylation by Pelle kinase. This inhibition suppresses Dorsals nuclear translocation and downstream expression of antimicrobial peptides (AMPs), essential for antiviral defense. Knockdown of wsv100 reduced WSSV replication, increased Dorsal phosphorylation, and enhanced AMP expression, leading to higher survival rates in infected shrimp. Conversely, wsv100 overexpression promoted WSSV replication and AMPs suppression. These findings reveal a novel immune evasion mechanism by which WSSV subverts the NF-{kappa}B pathway and highlight the evolutionary arms race between hosts and viruses. This study enhances our understanding of host-virus interactions and offers potential targets for antiviral strategies in shrimp aquaculture. Author SummaryThe innate immune system is the first line of defense against viral infections in invertebrates, with the NF-{kappa}B signaling pathway playing a central role in orchestrating antiviral responses. In this study, we uncover a novel immune evasion mechanism employed by White Spot Syndrome Virus (WSSV), a devastating pathogen in shrimp aquaculture. The WSSV immediate-early protein wsv100 directly targets the transcription factor Dorsal and prevents its phosphorylation by Pelle kinase, a critical step in NF-{kappa}B activation. This interaction suppresses Dorsals nuclear translocation and downstream expression of antimicrobial peptides (AMPs), thereby impairing the shrimps ability to mount an effective immune response. Knockdown of wsv100 significantly reduced WSSV replication and enhanced shrimp survival, while wsv100 overexpression had the opposite effect. These findings not only elucidate how WSSV exploits the NF-{kappa}B pathway but also underscore its central role in shrimp antiviral immunity. This work advances our understanding of host-virus co-evolution and provides a foundation for developing novel antiviral strategies to mitigate the economic losses caused by WSSV in shrimp aquaculture.

microbiology↗

Epigenetic reprogramming induced by Acetyl-CoA and SAM depletion is an evolutionarily-ancient path to malignant growth

Despite the vast diversity of life forms and living histories, it appears that all branches of Metazoa face the challenge of tumor growth. Contrary to human tumors, which take years to form, tumors in short-living species can arise within days without accumulating multiple mutations, raising the question whether the paths to tumorigenesis in diverse species have any commonalities. In a fly tumor model caused by loss of cell polarity genes, we first identified the rise of a glycolytic cell population over time, resembling the Wartburg effect observed in human tumors. We further identified two key metabolic changes in these fly tumors. First, a systemic depletion of acetyl-CoA leads to a reduction in histone acetylation levels and stochastic silencing of actively-transcribed genes. Second, defects in the methionine cycle cause a systemic depletion of S-Adenosyl methionine, which further reduces histone methylation levels and causes stochastic activation of transposons. Perturbation of the methionine metabolic process strongly inhibits tumor growth. Finally, to understand the evolutionary origin of tumorigenesis, we performed comparative studies of fly and human tumors, and identified human tumors that exhibit metabolic signatures similar to those of fly tumors. We found that human tumors with high metabolic similarity to fly tumors have a lower mutational load, younger patient age, and lower DNA methylation levels. This study suggests that tumorigenesis processes have a deep evolutionary origin and highlights that depletion of key metabolites is an evolutionarily-ancient driving force for tumorigenesis.

developmental biology↗

Relaxation selective Intravoxel Incoherent Motion Imaging of Microvascular Perfusion and Fluid Compartments in the Human Choroid Plexus

The choroid plexus (ChP) plays an important role in the glymphatic system of the human brain as the primary source of the cerebrospinal fluid (CSF) production. Development of a non-invasive imaging technique is crucial for studying its function and age-related neurofluid dynamics. This study developed a relaxation-selective intravoxel incoherent motion (IVIM) technique to assess tissue and fluid compartments in the ChP in a prospective cross-sectional study involving 83 middle-aged to elderly participants (age: 61.5 {+/-} 17.1 years old) and 15 young controls (age: 30.7 {+/-} 2.9 years old). Using a 3T MRI scanner, IVIM, FLAIR-IVIM, LongTE-IVIM, and VASO-LongTE-IVIM were employed to measure diffusivity and volume fractions of fluid compartments and evaluate aging effects on microvascular perfusion and interstitial fluid (ISF). FLAIR-IVIM identified an additional ISF compartment with free-water-like diffusivity (2.4 {+/-} 0.9 x10-3 mm2/s). Older adults exhibited increased ChP volume (2320 {+/-} 812 mm3 vs 1470 {+/-} 403 mm3, p=0.0017), reduced perfusion (6.5 {+/-} 4.7 vs 3.6 {+/-} 2.9 x10-3 mm{superscript 2}/s, p=0.0088), decreased ISF volume fraction (0.58 {+/-} 0.09 vs 0.67 {+/-} 0.06, p=0.0042), and lower tissue diffusivity (1.16 {+/-} 0.14 vs 1.29 {+/-} 0.17 x10-3 mm{superscript 2}/s, p=0.031) compared to younger adults. Relaxation-selective IVIM may offers enhanced specificity for characterizing age-related changes in ChP structure and fluid dynamics.

neuroscience↗

NCPepFold: Accurate Prediction of Non-canonical Cyclic Peptide Structures via Cyclization Optimization with Multigranular Representation

Artificial intelligence-based peptide structure prediction methods have revolutionized biomolecular science. However, restricting predictions to peptides composed solely of 20 natural amino acids significantly limits their practical application, as such peptides often demonstrate poor stability under physiological conditions. Here, we present NCPepFold, a computational approach that can utilize a specific cyclic position matrix to directly predict the structure of cyclic peptides with non-canonical amino acids. By integrating multi-granularity information at the residue- and atomic-level, along with fine-tuning techniques, NCPepFold significantly improves prediction accuracy, with the average peptide RMSD for cyclic peptides being 1.640 [A]. In summary, this is a novel deep learning model designed specifically for cyclic peptides with non-canonical amino acids without length restrictions, offering great potential for peptide drug design and advancing biomedical research.

bioinformatics↗

Structure of the SMYD2-PARP1 Complex Reveals Both Productive and Allosteric Modes of Peptide Binding

Allosteric regulation allows proteins to dynamically respond to environmental cues by modulating activity at sites away from the catalytic center. Despite its importance, the SET-domain protein lysine methyltransferase superfamily has been understudied. Here, we present four crystal structures of SMYD2, a unique family member with a MYND domain. Our findings reveal a novel allosteric binding site with high conformational plasticity and promiscuity, capable of binding peptides, proteins, PEG, and small molecules. This site exhibits positive cooperativity with substrate binding, influencing catalytic activity. Mutations here significantly alter substrate affinity, changing the enzymes kinetic profile. Specificity studies show interaction with PARP1 but not histones, suggesting targeted regulation. Interestingly, this sites function remains unaffected by active site changes, indicating unidirectional mechanisms. Our discovery provides novel insights into SMYD2s biochemical regulation and lays the foundation for broader research on allosteric control in lysine methyltransferases. Given SMYD2s role in various cancers, this work opens exciting avenues for designing specific allosteric inhibitors with reduced off-target effects.

biochemistry↗

The evolution of irreversible cell differentiation under cell death effect

Cell differentiation is an important characteristic of multicellular organisms which produce new-typed cells to engage in diverse life functions. Irreversible differentiation, as an important differentiation, describes cells differentiated by determined trajectories to form specialized cell types. It has been found that differentiated cell types often show different death rates. Yet, it is still unclear what role cell death plays in shaping the formation of irreversible cell differentiation. Here, we establish a theoretical model to investigate the impact of cell death on the evolution of irreversible cell differentiation in multicellular organisms. Irreversible differentiation refers to the loss of a cell types differentiation potential, and it is constructed by the sequences of differentiation probabilities of a cell type across cell divisions. We show that irreversible differentiation is more likely to occur when cell death rates between cell types are linear. Meanwhile, differences in death rates between cell types affect the emergence conditions of irreversible differentiation, whereas no significant impacts on that from equal cell death rates. Additionally, we found that cell death impacts the cell number and cell composition of a mature organism. These findings provide insights into understanding the role of cell death in the formation of cells irreversible differentiation.

evolutionary biology↗

Gut microbiota-derived GlcNAc-MurNAc is a TLR4 agonist that protects the host gut

Gut microbiota-derived peptidoglycan fragments (PGNs) are key signaling molecules that regulate multiple aspects of the hosts health. Yet the exact structures of natural PGNs in hosts have not been fully elucidated. Herein, we developed an LC-HRMS/MS analytical platform for global quantification and profiling of natural PGN subtypes in host gut and sera, unexpectedly revealing the abundance of PGN-derived saccharide moieties that do not resemble canonical ligands of mammalian NOD1/2 receptors. Focusing on the disaccharide GlcNAc-MurNAc (GM), a natural gut PGN that does not activate NOD1/2 yet still exhibits robust immunostimulatory effects in host immune cells, we unambiguously established GM as a TLR4 agonist, adding to the growing knowledge of NOD-independent mechanisms of PGN sensing in hosts. Importantly, the administration of GM effectively mitigates colonic inflammation in the DSS-induced colitis model in mice via TLR4-dependent mechanisms, highlighting the in vivo significance of natural gut microbiota-derived PGNs in maintaining host intestinal homeostasis.

biochemistry↗

Molecular epidemiology of carbapenem-resistant hypervirulent Klebsiella pneumoniae: Risk factors and resistance mechanism of ceftazidime/avibactam in China

The high morbidity and mortality rates associated with carbapenem-resistant hypervirulent Klebsiella pneumoniae have become a global public health problem. We analyzed the whole genome sequence and epidemiological data of 81 carbapenem-resistant Klebsiella pneumoniae strains and conducted sensitivity experiments to explore the optimal concentration of carbapenem-resistant Klebsiella pneumoniae. We verified the resistance and virulence genes of carbapenem-resistant Klebsiella pneumoniae using polymerase chain reaction and compared virulence between carbapenem-resistant hypervirulent Klebsiella pneumoniae a ndcarbapenem-resistant-non-hypervirulent Klebsiella pneumoniae through Galleria mellonella assays.The prevalent types of multilocus sequence typing in our carbapenem-resistant Klebsiella pneumoniae strains were ST11 (69.14%, 56/81). ST11-K64-O1/O2v1 has become an epidemic type in our hospital, with drug-resistance genes dominated by blaKPC-2 (90.12%, 73/81). Ceftazidime/avibactam has better antibacterial effects on carbapenem-resistant Klebsiella pneumoniae, and its resistance is mainly mediated by a resistance plasmid containing the blaKPC-2 gene. 52 carbapenem-resistant hypervirulent Klebsiella pneumoniae strains carry the blaKPC-2, with a high detection rate of siderophore. Further research has shown that the genetic environment of the blaKPC-2 contains TnpR_Tn3 and ISKpn27 upstream and ISKpn6 insertion sequences downstream. Galleria mellonella revealed that the survival rate of carbapenem-resistant hypervirulent Klebsiella pneumoniae was lower than that of carbapenem-resistant-non-hypervirulent Klebsiella pneumoniae, and the survival rate of carbapenem-resistant hypervirulent Klebsiella pneumoniae-K64 was lower than that of carbapenem-resistant hypervirulent Klebsiella pneumoniae-K47.The spread of carbapenem-resistant hypervirulent Klebsiella pneumoniae strains is alarming, necessitating molecular monitoring of hypervirulent strains and strengthening the nosocomial infection prevention and control measures. Antibiotics should be used reasonably based on patients infection status and local epidemiological data. ImportanceCarbapenem-resistant Klebsiella pneumonia is a global public health concern. We conducted a molecular epidemiological analysis of 81 carbapenem-resistant hypervirulent Klebsiella pneumoniae strains from our hospital and explored the resistance mechanism of ceftazidime/avibactam. We identified the blaKPC-2 gene to be primarily responsible for carbapenem resistance in our hospital, and ST11-K64 was the dominant clone. A high-risk clone, ST307-K102, was detected, necessitating strengthened surveillance to prevent its spread. This studys findings contribute to the optimization of antimicrobial management and indicate that genomic research can assist with the tracking of hospital infection outbreaks and the improvement of infection-control measures.

microbiology↗

Whole-Genome Sequencing of the Wild Barley Diversity Collection: A Resource for Identifying and Exploiting Genetic Variation for Cultivated Barley Improvement

To exploit allelic variation in Hordeum vulgare subsp. spontaneum, the Wild Barley Diversity Collection was evaluated for several agronomic traits and subjected to paired-end Illumina sequencing at [~]9X depth, generating 109.5 million single nucleotide polymorphisms after alignment to the Morex V3 assembly. A genome-wide association study of lemma color identified one marker-trait association (MTA) on chromosome 1HL close to HvBlp, the cloned gene controlling black lemma. Four MTAs were identified for stem rust resistance: one co-locating to the complex RMRL1-RMRL2 locus on 5HL, and three novel loci on 1HS, 1HL, and 5HL. Six MTAs for days to heading (DTH) on vernalized plants were identified on all chromosomes except 1H and 6H. Two MTAs for DTH on non-vernalized plants were identified on chromosomes 1HL and 2HS. All MTAs for DTH were novel. The whole genome sequence data described herein will facilitate the identification and utilization of new alleles for barley improvement.

genomics↗

Limited involvement of Ca2+/calmodulin-dependent kinase II alpha and beta in mammalian sleep

While sleep is important, our understanding of its molecular mechanisms is limited. Over the last two decades, protein kinases have been implicated in sleep regulation, with a prominent role for Ca++/calmodulin-dependent kinase II (CaMKII) {beta}. Of all the known mouse genetic mutants, the biggest changes in sleep was reported to be observed in Camk2b gene knockout mice: sleep was reduced by approximately 120 minutes (mins) over 24 hours (hrs). We have reexamined the sleep phenotype in Camk2a and Camk2b knockout mice, and while we have observed sleep reduction in Camk2a knockout mice, we did not find sleep reduction in Camk2b mutants.We did find both Camk2a and Camk2b participated in homeostatic sleep rebound, though. Because CamKII and {beta} are widely known to be crucial kinases with interesting properties, it is worthwhile to keep our results in record for a general service to the field.

animal behavior and cognition↗

Diverse quorum sensing systems regulate microbial communication and biogeochemical processes in deep-sea cold seeps

Quorum sensing is a fundamental chemical communication mechanism that enables microorganisms to coordinate behavior and adapt to environmental conditions. In deep-sea cold seep ecosystems, where diverse microbial communities thrive, quorum sensing is likely a key mechanism driving microbial interactions. However, the distribution, mechanisms, and ecological roles of quorum sensing in cold seeps remain poorly understood. To address this, we analyzed 173 metagenomes, 33 metatranscriptomes, and 18 metabolomes from 17 global cold seep sites. We identified 299,355 quorum sensing genes from the seep non-redundant gene catalog, representing 34 gene types across six quorum sensing systems, with distribution patterns influenced by sediment depth and seep type. These quorum sensing genes were present in 3,576 metagenome-assembled genomes from 12 archaeal and 108 bacterial phyla, revealing a complex network of intraspecies and interspecies communication. Microbial groups involved in key metabolic processes, such as sulfate-reducing bacteria, anaerobic methanotrophic archaea, diazotrophs and organohalide reducers, were extensively regulated by quorum sensing, influencing biogeochemical cycles of carbon, nitrogen, and sulfur. Phylogenetic analysis and protein domain identification highlighted the functional roles of key quorum sensing-related proteins (e.g., PDEs, CahR, RpfC/G and LuxR) in modulating microbial behaviors, such as motility and chemotaxis. Heterologous expression and metabolomic profiling further confirmed the activity of representative LuxI-R pairs and identified inhibitors of quorum sensing in cold seep sediments. Overall, these findings highlight complexity and significance of quorum sensing in microbial interactions, ecological adaptation, and biogeochemical cycling within cold seep ecosystems, advancing our understanding of microbial communication in the deep biosphere.

microbiology↗

Alveolar macrophages initiate the spatially targeted neutrophil recruitment during nanoparticle inhalation

Exposure to air pollution, including nanoparticles (NPs), is a major health concern associated with various diseases, triggered by subtle inflammatory responses in the lung. To investigate the dynamic immune response in vivo, lung intravital microscopy (L-IVM), was used to analyze the behavior of alveolar macrophages (AMs) and neutrophils, combined with ventilator-assisted inhalation of nebulized NPs in mice. Inhalation of fluorescent quantum dot NPs (cQDs) and soot-like carbon black NPs (CNPs, ambient pollutants), led to rapid spatially focused recruitment of neutrophils near alveolar deposited NPs. Neutrophil recruitment was initiated by NPs uptake by AMs, dependent on AM motility and AM NP surface recognition. Prior airway application of neutralizing antibodies against alveolar ICAM-1 and LFA-1, leading to reduced AM motility, inhibition of C5aR1 and Fc{gamma}RI receptor mediated NPs uptake by AMs, as well as neutralizing of TNF and application of a cellular degranulation inhibitor, abolished the early immune response induced by NPs. Overall, our data demonstrates the crucial role of AM activity (migration, phagocytosis, cytokine release) in the rapid and site-specific recruitment of neutrophils during the early phase of particle inhalation, suggesting these processes to be key events in mounting the immune response upon NP inhalation in the lung. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=175 HEIGHT=200 SRC="FIGDIR/small/623349v1_ufig1.gif" ALT="Figure 1"> View larger version (52K): org.highwire.dtl.DTLVardef@d67e38org.highwire.dtl.DTLVardef@1f8c139org.highwire.dtl.DTLVardef@55be9dorg.highwire.dtl.DTLVardef@1555042_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

ABA increases fatty acids levels in apple roots to boost colonization by arbuscular mycorrhizal fungi

The roots of most land plants are in symbiosis with arbuscular mycorrhizal (AM) fungi. The fungus promotes nutrient uptake from the soil while receiving plant photosynthate as lipids and sugars. Nutrient exchange must be regulated by both partners, but the mechanisms underlying the regulation of lipid supplement from the plant to the AM fungus remain elusive. Here, we conducted a molecular study on the role of increased abscisic acid (ABA) levels during AM fungus infection in the roots of apple (Malus spp.). AM fungus induced the expression of two ABA synthesis genes, MdNCED3.1 and 3.2, in apple roots and increased the ABA content, which promoted the growth of the AM fungus. The effect of ABA on symbiosis was confirmed in transgenic apple roots either overexpressing or silencing MdNCED3.1 or MdNCED3.2. Transcriptome analysis and transgenic manipulation revealed that the transcription factor MdABF2 played a key role in the ABA-mediated formation of symbiosis during AM infection and that MdABF2 could regulate the expression levels of genes related to fatty acid (FA) synthesis (e.g., MdKASIII) and translocation (such as MdSTR2) in apple roots. Activation of these genes boosted the levels of available fatty acids in the roots and increased the AM fungal colonization and arbuscule development in the roots. These results revealed a molecular pathway in which positive regulation of FA synthesis and transport by the ABA signaling pathway increases supplementation to AM fungi and promotes AM symbiosis.

molecular biology↗

KLF7-Regulated ITGA2 as a Therapeutic Target for Inhibiting Oral Cancer Stem Cells

Cancer stem cells (CSCs) play crucial roles in tumor metastasis, therapy resistance, and immune evasion. Identifying and understanding the factors that regulate the stemness of tumor cells presents promising opportunities for developing effective therapeutic strategies. In this study on oral squamous cell carcinoma (OSCC), we confirmed the key role of KLF7 in maintaining the stemness of OSCC. Using chromatin immunoprecipitation sequencing and dual-luciferase assays, we identified ITGA2, a membrane receptor, as a key downstream gene regulated by KLF7 in the maintenance of stemness. Tumor sphere formation assays, flow cytometry analyses, and in vivo limiting dilution tumorigenicity evaluations demonstrated that knocking down ITGA2 significantly impaired stemness. When bound to its ECM ligand, type I collagen, ITGA2 activates several stemness-related pathways, including PI3K-AKT, MAPK, and Hippo. TC-I 15, which inhibits the ITGA2-collagen interaction, showed a synergistic anti-tumor effect when combined with cisplatin in both in vitro and xenograft models. In summary, we reveal that the KLF7/ITGA2 axis is a crucial modulator of stemness in OSCC. Our findings suggest that ITGA2 is a promising therapeutic target, offering a novel anti-CSC strategy. Highlights1) KLF7 as a key molecule in maintaining oral cancer stemness. 2) ITGA2as a key downstream gene regulated by KLF7 in the maintenance of stemness. 3) ITGA2 interacts with extracellular matrix type I collagen, activating stemness-related pathways and promoting YAP1 nuclear translocation to sustain OCSCs. 4) ITGA2 as a novel anti-CSC target, providing a new strategy to overcome OSCC drug resistance.

cancer biology↗

Machine learning engineered PoLixNano nanoparticles overcome delivery barriers for nebulized mRNA therapeutics

There continues to be a dearth of competent inhalable mRNA delivery although it holds great potential for addressing a wide variety of refractory diseases. The huge advances seen with parenteral-administered lipid nanoparticle (LNP) have not been translated into nebulized mRNA delivery due to the aggressive nebulization process and insurmountable barriers inherent to respiratory mucosa. Here, we show amphiphilic block copolymers revealed by machine learning (ML) can spontaneously form stabilized nanoparticles (PoLixNano) with the lipids components of LNP and simultaneously impart the PoLixNano with "shield" (shear force-resistant) and "spear" (pulmonary barriers-penetrating abilities) capabilities. We present a ML approach that leverages physicochemical properties and inhaled mRNA transfection profiles of a chemically diverse library of polymeric components to validate the integration of "shield" and "spear" properties as highly predictive indicators of transfection efficiency. This quantitative structure-mRNA transfection prediction (QSMTP) model identifies top-performing amphiphilic-copolymers from more than 10000 candidates and suggests their mucus-penetrating ability outweights the shear force-resistant property in contributing to efficient mRNA transfection. The optimized PoLixNano substantially outperforms the LNP counterpart and mediates up to 1114-times higher levels of mRNA transfection in animal models with negligible toxicities. The PoLixNano promotes overwhelming SARS-CoV-2 antigen-specific sIgA antibody secretion and expansion of TRM cells which collectively confers 100% protection in mice against lethal SARS-CoV-2 challenges and blocks the transmission of Omicron variant between hamsters. PoLixNano also displays versatile therapeutic potential in lung carcinoma and cystic fibrosis models. Our study provides new insights for designing delivery platforms of aerosol-inhaled mRNA therapeutics with clinical translation potential.

synthetic biology↗

A polyketide-based biosynthetic platform for diols, amino alcohols and hydroxyacids

Medium- and branched-chain diols and amino alcohols are important industrial solvents, polymer building blocks, cosmetics and pharmaceutical ingredients, yet biosynthetically challenging to produce. Here, we present a novel approach utilising a modular polyketide synthase (PKS) platform for the efficient production of these compounds. This platform takes advantage of a versatile loading module from the rimocidin PKS and NADPH-dependent terminal thioreductases (TRs), previously untapped in engineered PKSs. Reduction of the terminal aldehyde with specific alcohol dehydrogenases enables production of diols, oxidation enables production of hydroxy acids, and transamination with specific transaminases enables production of various amino alcohols. Furthermore, replacement of the malonyl-coenzyme A (CoA)-specific acyltransferase (AT) in the extension module with methyl- or ethylmalonyl- CoA-specific ATs enables production of branched-chain diols and amino alcohols. In total, we demonstrated production of nine 1,3-diols (including the difficult-to-produce insect repellent and cosmetic ingredient 2-ethyl-1,3-hexanediol), six amino alcohols, and two carboxylic acids using our PKS platform in Streptomyces albus. Finally, tuning production of the PKS acyl-CoA substrates enabled production of high titers of specific diols and amino alcohols (1 g/L diol titer in shake flasks), demonstrating high tunability and efficiency of the platform.

bioengineering↗