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Liang, Q.

Publications and source records attributed to Liang, Q..

At least 37 records · Page 2Linked to original sources

Adenosine-specific transcriptional programs in murine connective tissue type mast cells

Mast cells are tissue-resident immune cells that are critical for the pathogenesis of allergic and inflammatory disorders. In addition to classic host defense against parasites, food quality control through antigen avoidance has been recently elucidated as additional physiological mast cell function. The purine nucleoside adenosine (ADO), like other mast cell activators, such as antigens or Mrgprb2 agonists, increases intracellular Ca2+ concentration; however, it fails to induce degranulation of preformed mediators when applied to isolated mast cells alone, and there is limited knowledge of whether ADO evokes the de novo synthesis and release of inflammatory mediators such as cytokines in tissue mast cells. An unbiased genome-wide analysis of gene expression triggered by various mast cell activators should enable identification of the gene program specifically activated by adenosine in mast cells and thereby reveal new components of the associated inflammatory responses. To this end, we performed bulk RNA sequencing (RNA-Seq) in primary murine peritoneal mast cells (PMCs) as connective tissue mast cells. By comparing responses evoked by ADO stimulation with those of the Mrgprb2 compound 48/80 and antigens that activate Fc{varepsilon}RI receptors, we identified 393 genes whose expression was uniquely regulated by ADO, including upregulation of genes encoding de novo synthesized mediators such as Tgfa and Il7. Transcription factor activity inference, protein classification, functional enrichment analysis, protein-protein interaction network, and topology analysis revealed that these genes play roles in phosphoinositide signaling, vesicle trafficking, glycolysis, mitochondrial activity, and cell cycle arrest. In summary, our work elucidates a distinct ADO-triggered response and identifies a set of proteins including de novo synthesized mediators whose functional relevance in adenosine-evoked mast cell activation and inflammatory reactions can be evaluated in future studies.

pharmacology and toxicology↗

Hypobaric hypoxia drives citrate cycle reprogramming to suppress tumor progression

High altitude residents present lower tumor incidence and mortality than plain residents, suggesting that hypobaric hypoxia displays protective effect against tumor development. The results of our studies showed that hypobaric hypoxia exposure significantly suppressed tumor progression in subcutaneous bearing and lung metastasis tumor models. With single-cell transcriptome analysis, we identified HIF-1 pathway was significantly downregulated in tumor tissues with high altitude hypoxia, leading to decreased glycolysis and angiogenesis and improved antitumor immune response. Mechanistically, systemic hypoxia rewired citric acid cycle, with enhanced CS and IDH2 expression and reduced OGDH and SUCLG2 expression, to induce -ketoglutarate accumulation and succinate decline in tumor microenvironment, further mediating HIF-1 pathway inhibition. Moreover, hypobaric hypoxia treatment significantly improved the antitumor effects of adjuvant therapies (including chemotherapy, anti-angiogenic therapy and immunotherapy). Our findings reveal the role and mechanism of hypobaric hypoxia for tumor regression and yield new insights into tumor therapy.

cancer biology↗

The growth and pathogenesis of Citrobacter rodentium is compromised by disrupted mucin sugar pathways that accumulate N-acetylglucosamine 6-phosphate

Many enteric bacterial pathogens, including the attaching/effacing (A/E) Escherichia coli strains, cause acute gastroenteritis in humans. Considering the highly competitive nature of the mammalian gastrointestinal (GI) tract, these pathogens must rely on specific metabolic adaptations to establish successful infections. We hypothesized that A/E pathogens exploit host-derived nutrients within GI mucus, including the monosaccharides N-acetylglucosamine (GlcNAc) and N-acetylneuraminic acid (NeuNAc) to fuel their pathogenesis. Using Citrobacter rodentium, a murine-specific A/E pathogen, we disrupted both GlcNAc and NeuNAc catabolism by deleting nagA, which encodes the GlcNAc-6-phosphate (GlcNAc-6P) deacetylase that converts GlcNAc-6P into glucosamine-6-phosphate (GlcN-6P). The {Delta}nagA mutant displayed dramatically impaired colonization in C57BL/6J mice and accumulated significant levels of GlcNAc-6P, unlike the {Delta}mana strain, a mutant lacking all GlcNAc and NeuNAc transporters, suggesting that the attenuation was due to sugar-phosphate stress rather than nutrient deprivation alone. Supplementation with glucosamine (GlcN) restored growth, indicating that dysregulated GlcN-6P synthesis, rather than GlcNAc-6P toxicity, underlies the defect. Furthermore, {Delta}nagA exhibited increased susceptibility to several cell wall-dependent stress conditions, in concert with compromised peptidoglycan biosynthesis due to reduced UDP-GlcNAc synthesis. These findings reveal a previously unrecognized metabolic vulnerability in C. rodentium and suggest that targeting sugar-phosphate stress responses may provide a new therapeutic strategy against GI bacterial pathogens. ImportanceEnteric pathogens like Citrobacter rodentium can exploit sugars, including N-acetylglucosamine and N-acetylneuraminic acid, derived from intestinal mucus to grow and infect their hosts. This study shows that disruption of mucin-derived sugar catabolism impairs the fitness of C. rodentium in infecting the murine intestine by causing the accumulation of a toxic intermediate of mucin sugar metabolism. Rather than impaired nutrient acquisition, the bacteria are impaired due to the buildup of N-acetylglucosamine-6-phosphate, which depletes substrates for peptidoglycan synthesis. This metabolic bottleneck weakens the bacterial cell wall, making the pathogen more sensitive to environmental stress. These findings identify a conserved metabolic stress response that could be targeted to combat enteric pathogen infections.

microbiology↗

Precision culturomics enabled by unlabeled single-cell morphology and Raman spectra

Selective enrichment of target bacteria from complex communities such as the human microbiome has remained a challenge. Here we report a solution based on morphology, Raman spectrometry and the Laser-Induced Forward Transfer technology, which works at microbial single cells, many generations before they appear as colonies. We develop a machine learning-based framework that enables species-level targeted sorting of single microbial cells from complex microbiome. We illustrate the utility of this approach in selecting for or against specific bacteria in fecal microbiome samples and the potential for quantifying the molecules expressed based on Raman spectra. Analysis of single-cell cultured genomes reveals that brief antibiotic use drives both pre-existing resistance and de novo mutations in the transpeptidase or efflux pumps of gut commensals, along with convergent evolution between different species. Our precision culturomics method should enable detailed morphological, metabolic, and genomic insights into variations in microbial phenotypes at the single-cell level for microbiome studies.

microbiology↗

From Pan-Life Phase Insights to PhaseHub: Analyzing Condensate Complexity

Macromolecular condensation is crucial in biological signaling pathways that regulate development and adaptation processes. However, lacking conserved residues in disordered region of condensate proteins hampers alignment-based analyses of their evolutionary trajectory. To gain a comprehensive overview of phase-separating protein evolution across the Tree of Life, we analyzed phase-separating proteins of proteomes from 1,106 species. Eukaryotes and prokaryotes showed high contrast in need for phase-separating proteins and with a clear genome size-dependent correlation. Evolutionary success appears to hinge on the balance between functional condensation and avoiding harmful aggregation-prone biophysical signatures, such as certain amino acid homorepeats embedded in molecular grammar. We also identified potential phase separation-regulated signaling hubs across kingdoms by integrating phase-separation-positive proteins with protein abundance and interactome data across four model eukaryotic species. Consequently, we created PhaseHub (https://phasehub.sbs.ntu.edu.sg/), a user-friendly interface that explores key scaffold proteins and binders to pinpoint associated partners and potential multicomponent phase separation hubs. TeaserAnalyse phase separation behavior of 1,106 species across kingdoms on proteome level reconstruct the evolutional history of protein condensation.

systems biology↗

Prg4+ fibro-adipogenic progenitors in muscle are crucial for bone fracture repair

Clinically, compromised fracture healing often occurs at sites with less muscle coverage and muscle flaps can provide the necessary healing environment for appropriate healing in severe bone loss. However, the underlying mechanisms are largely unknown. Here, we established a mouse reporter model for studying muscle cell contribution to bone fracture repair. Analyzing skeletal muscle scRNA-seq datasets revealed that Prg4 marks a fibro-adipogenic progenitor (FAP) subpopulation. In mice, Prg4+ cells were specifically located in the skeletal muscle, but not at the periosteum or inside cortical bone. These cells expressed FAP markers, responded to muscle injury, and became periosteal cells under normal and muscle injury conditions. Fracture fragmented muscle fibers, rapidly expanded Prg4+ FAPs at the injury site and promoted their migration into the fracture site. Later, they gave rise to many chondrocytes, osteoblasts, and osteocytes in the outer periphery of callus next to muscle. In repaired bones, the descendants of Prg4+ FAPs were detected as mesenchymal progenitors in the periosteum and osteocytes at the prior fracture site. A second fracture activated those cells and stimulated them to become osteoblasts in the inner part of callus. Importantly, ablation of Prg4+ FAPs impaired fracture healing and functional repair. In an intramembranous bone injury model (drill-hole), Prg4+ FAPs became periosteal cells, but their contribution to bone defect repair was significantly less than in fractures. Taken together, we demonstrate the critical role of FAPs in endochondral bone repair and uncover a novel mechanism by which mesenchymal progenitors transform from muscle to cortical bone. Significance statementFracture healing is often impaired in areas with less muscle coverage, but the mechanisms behind this are poorly understood. In this work, we uncovered a critical role of specific muscle cells, known as Prg4+ fibro-adipogenic progenitors (FAPs), in bone regeneration. Using mouse models, we show that these muscle-resident mesenchymal progenitors expand after bone injury, migrate to the fracture site, transform into various bone cells in the fracture callus, and eventually become bone surface progenitors after the bone is healed. This finding highlights the importance of muscle cells in endochondral fracture repair and reveals a novel crosstalk mechanism between muscle and bone tissues. Future studies targeting these muscle progenitor cells could develop new treatments for delayed and nonunion fractures.

cell biology↗

Restoration of tumor suppressor protein with enhanced activity using engineered tRNAs to induce tumor regression

Cancer develops through a gradual accumulation of mutations including nonsense mutations in tumor suppressor genes (TSGs), which drive tumor proliferation and progression due to the impairment or complete loss of tumor suppressor protein function. The ability to restore functional tumor suppressor protein from mutant driver TSGs is a longstanding aspiration in cancer therapy, however, current strategies face formidable challenges in recovering proteins harboring heterogeneous mutations and circumventing dominant-negative effects exerted by endogenous mutant proteins. Therefore, the development of therapeutic interventions that are effective and generalizable across diverse nonsense mutations in cancer, to rescue endogenous mutant tumor suppressor proteins remains an urgent yet unmet need. Here we find that engineered suppressor transfer RNA (sup-tRNA) could overcome nonsense mutations in key driver tumor suppressor genes, such as TP53, thereby avoiding the dominant-negative effects through the restoration of endogenous mutant p53 with its original functions. Optimized sup-tRNA that we named super tRNA, enabling high-fidelity incorporation of desired amino acids, can further enhanced the transcriptional activity of p53 to suppress tumor cell proliferation. Moreover, we also establish a computational model to guide super tRNAs design, and demonstrate that super tRNA could effectively inhibit tumor growth by targeted readthrough of nonsense mutations in different tumor suppressor genes. In two xenograft models harboring nonsense mutant TP53, we observed up to a 70% reduction in tumor volume after lipid nanoparticle (LNP)-based sup-tRNA treatment, along with robust recovery of p53 expression and function, and no hematological or histological abnormalities detected. Our findings demonstrate the potential of sup-tRNA as a feasible and effective strategy to rescue and enhance tumor suppressor protein function, thereby preventing cancer development. As a novel therapeutic RNA, sup-tRNA provides a flexible strategy for targeting driver mutations in cancer, thereby expanding the potential of tRNA-based therapy in precision oncology.

bioengineering↗

Short 5' UTRs serve as a marker for viral mRNA translation inhibition by the IFIT2-IFIT3 antiviral complex

Recognition of "non-self" nucleic acids, including cytoplasmic dsDNA, dsRNA, or mRNAs lacking proper 5 cap structures, is critical for the innate immune response to viruses. Here, we demonstrate that short 5 untranslated regions (UTRs), a characteristic of many viral mRNAs, can also serve as a molecular pattern for innate immune recognition via the interferon-induced proteins IFIT2 and IFIT3. The IFIT2-IFIT3 heterodimer, formed through an intricate domain swap structure resolved by cryo-EM, mediates viral mRNA 5 end recognition, translation inhibition, and ultimately antiviral activity. Critically, 5 UTR lengths <50 nucleotides are necessary and sufficient to sensitize an mRNA to translation inhibition by the IFIT2-IFIT3 complex. Accordingly, diverse viruses whose mRNAs contain short 5 UTRs, such as vesicular stomatitis virus and parainfluenza virus 3, are sensitive to IFIT2-IFIT3-mediated antiviral activity. Our work thus reveals a pattern of antiviral nucleic acid immune recognition that takes advantage of the inherent constraints on viral genome size.

microbiology↗

Shared and individual tuning curves for social vision

Stimuli with light are clearly visual; stimuli with sound are clearly auditory. But what makes a stimulus "social", and how do socialness judgments differ across people? Here, we characterize group-level and individual thresholds for perceiving the presence and nature of a social interaction. We leverage the fact that humans see social interactions--e.g., chasing, playing, fighting--even in very un-lifelike stimuli like animations of geometric shapes. Unlike most prior work that used hand-crafted stimuli, we exploit these animations most advantageous property: their visual features are fully parameterizable. Using this property, we construct psychophysics-inspired "social tuning curves" for individuals. We find not only that simple visual features influence social perception, but also that the exact shape of the tuning curve is unique to and stable within each person. Further, individual differences in tuning curves are related to socio-affective traits. Our approach lays the foundation to study how social percepts emerge from interactions between features of a stimulus and features of an individual observer.

neuroscience↗

Comparison of imaging-based single-cell resolution spatial transcriptomics profiling platforms using formalin-fixed, paraffin-embedded tumor samples

Imaging-based spatial transcriptomics (ST) is evolving rapidly as a pivotal technology in studying the biology of tumors and their associated microenvironments. However, the strengths of the commercially available ST platforms in studying spatial biology have not been systematically evaluated using rigorously controlled experiments. In this study, we used serial 5-m sections of formalin-fixed, paraffin-embedded surgically resected lung adenocarcinoma and pleural mesothelioma tumor samples in tissue microarrays to compare the performance of the single cell ST platforms CosMx, MERFISH, and Xenium (uni/multi-modal) platforms in reference to bulk RNA sequencing, multiplex immunofluorescence, GeoMx Digital Spatial Profiler, and hematoxylin and eosin staining data for the same samples. In addition to objective assessment of automatic cell segmentation and phenotyping, we performed pixel-resolution manual evaluation of phenotyping to carry out pathologically meaningful comparison between ST platforms. Our study detailed the intricate differences between the ST platforms, revealed the importance of parameters such as tissue age and probe design in determining the data quality, and suggested reliable workflows for accurate spatial profiling and molecular discovery.

bioinformatics↗

Synthetic ratio computation for programming population composition and multicellular morphology

Recent advancements in genetic engineering have provided diverse tools for artificially synthesizing population diversity in both prokaryotic and eukaryotic systems. However, achieving precise control over the ratios of multiple cell types within a population derived from a single founder remains a significant challenge. In this study, we introduce a suite of recombinase-mediated genetic devices designed to achieve accurate population ratio control, enabling the distribution of distinct functionalities across multiple cell types. We systematically evaluated key parameters influencing recombination efficiency and developed data-driven models to reliably predict binary differentiation outcomes. Using these devices, we implemented parallel and series circuit topologies to create user-defined, complex cell fate branching programs. These branching devices facilitated the autonomous differentiation of precision fermentation consortia from a single founder strain, optimizing cell-type ratios for applications such as pigmentation and cellulose degradation. Beyond biomanufacturing, we engineered multicellular aggregates with genetically encoded morphologies by coordinating self-organization through cell adhesion molecules (CAMs). Our work provides a comprehensive characterization of recombinase-based cell fate branching mechanisms and introduces a novel approach for the bottom-up, high-resolution construction of synthetic consortia and multicellular assemblies.

synthetic biology↗

Microbial succession, community assembly and adaptation over five years in a newly discovered deep-sea cold seep

Deep-sea cold seeps, characterized by the release of hydrocarbon-rich fluids such as methane from the seafloor, create unique ecosystems with evolving biological communities. Microorganisms serve as pioneers, initially colonizing early-stage cold seeps and providing essential matter and energy for subsequent colonizers. However, microbial succession, community assembly, and adaptation in these environments remain largely unexplored due to challenges associated with locating early-stage cold seeps. Here, we collected sediment samples from a newly discovered early-stage cold seep site, QDN-W07, in the South China Sea at varying depths over five years. We also sampled two previously reported cold seep sites, QDN-S18 and HM-ROV01, for comparative analysis. Amplicon sequencing revealed a high relative abundance of ANME-3 (up to 99%) and Methylomonadaceae (up to 83%) in surface sediments, and indicated changes in microbial community structures over time. Dispersal limitation dominated community assembly, while the contribution of homogeneous selection decreased over time, accompanied by a declined in the intensity of microbial association. Metagenomic analysis of core microbiome, comprising 172 metagenomic-assembled genomes at QDN-W07, revealed tolerance to low temperatures and oxygen. Core microbiome genomes were enriched with genes related to aerobic methane oxidation, urea metabolism, and the oxidation of sulfur, ammonia and carbon monoxide. These results indicate that core microorganisms obtain energy from the oxidation of inorganic compounds, allowing them to thrive in cold, methane-rich and unstable conditions. Overall, this study enhances our understanding of deep biosphere life, biogeochemical cycling, and the ecological management of cold seep environments.

microbiology↗

Identification and characterization of ugpE required for the full virulence of Streptococcus suis

Streptococcus suis (S. suis) is an emerging zoonotic pathogen that threatens both animal and human health worldwide. UgpE is a protein subunit of the Ugp (uptake of glycerol phosphate) transporter system that is involved in glycerophospholipid synthesis in bacterial membranes. In this study, an ugpE deletion mutant was constructed and the effects of ugpE deletion on cell morphology, biofilm formation, and virulence were investigated. Deletion of ugpE did not affect bacterial growth but impaired cell chain formation and capsular synthesis by downregulating the mRNA levels of the capsular regulon genes cps-2B, cps-2C, and cps-2S. Deletion of ugpE also led to decreased tolerance to heat, oxidative, and acid-base stress. Crystal violet staining and scanning electron microscopy demonstrated ugpE negatively regulated biofilm formation in liquid culture and the rdar biofilm morphotype on agar plates. Moreover, ugpE deletion not only reduced hemolysin activity, survival in whole human blood, and anti-phagocytosis ability against porcine alveolar macrophages (PAM) but also enhanced bacterial adhesion and invasion of human cerebral microvascular endothelial cells (hCMEC/D3) by upregulating the expression of multiple genes associated with cell adhesion. In a mouse infection model, ugpE deletion significantly attenuated virulence and lowered the number of viable bacteria in the blood and major organs, as well as distribution of macrophages. In conclusion, this study identified UgpE as a novel virulence factor that plays a pivotal role in the regulation of virulence and biofilm formation of S. suis.

microbiology↗

VHL synthetic lethality screens uncover CBF-beta as a negative regulator of STING

Clear cell renal cell carcinoma (ccRCC) represents the most common form of kidney cancer and is typified by biallelic inactivation of the von Hippel-Lindau (VHL) tumour suppressor gene. Here, we undertake genome-wide CRISPR/Cas9 screening to reveal synthetic lethal interactors of VHL, and uncover that loss of Core Binding Factor {beta} (CBF-{beta}) causes cell death in VHL-null ccRCC cell lines and impairs tumour establishment and growth in vivo. This synthetic relationship is independent of the elevated activity of hypoxia inducible factors (HIFs) in VHL-null cells, but does involve the RUNX transcription factors that are known binding partners of CBF-{beta}. Mechanistically, CBF-{beta} loss leads to upregulation of type I interferon signalling, and we uncover a direct inhibitory role for CBF-{beta} at the STING locus controlling Interferon Stimulated Gene expression. Targeting CBF-{beta} in kidney cancer both selectively induces tumour cell lethality and promotes activation of type I interferon signalling.

cancer biology↗

Single-cell omics for complex microbial communities

Metagenomics has enabled understanding of the microbial composition and functional potential in various environments. Using Laser-Induced Forward Transfer (LIFT) technology, we report high-quality microbial single-cell genome or transcriptome in complex samples such as saliva, mouse gut and human tumor sections. Neighboring cells could be separately retrieved and bacteria could be fluorescently labelled. We illustrate cell-fate commitment with sporulation. The method is scalable and precise, and would empower fundamental insight for microbial populations and single-cell interactions with the host.

microbiology↗

Elucidating immune-related gene transcriptional programs via factorization of large-scale RNA-profiles

Recent developments in immunotherapy, including immune checkpoint blockade (ICB) and adoptive cell therapy, have encountered challenges such as immune-related adverse events and resistance, especially in solid tumors. To advance the field, a deeper understanding of the molecular mechanisms behind treatment responses and resistance is essential. However, the lack of functionally characterized immune-related gene sets has limited data-driven immunological research. To address this gap, we adopted non-negative matrix factorization on 83 human bulk RNA-seq datasets and constructed 28 immune-specific gene sets. After rigorous immunologist-led manual annotations and orthogonal validations across immunological contexts and functional omics data, we demonstrated that these gene sets can be applied to refine pan-cancer immune subtypes, improve ICB response prediction and functionally annotate spatial transcriptomic data. These functional gene sets, informing diverse immune states, will advance our understanding of immunology and cancer research.

bioinformatics↗

MePHD1.2 affects the synthesis of cyanogenic glycosides by regulating the transcription of MeCYP79D2 in cassava

The high content of cyanogenic glycosides (CG) in cassava storage tubers seriously affects human food safety. CG play crucial roles in plant growth and development and can protect cassava leaves from being masticated by herbivorous predators. Nevertheless, the regulatory mechanism of CG biosynthesis, which results in a low CG content in storage tubers and high CG content in leaves, remains poorly understood. Here, yeast one-hybrid assay was performed using a mixed cDNA library of cassava storage roots and leaves as prey and the promoter of MeCYP79D2 as bait. MeCYP79D2, a cytochrome P450 protein, is the rate-limiting enzyme for CG synthesis in cassava. From this information, a candidate regulator of MeCYP79D2, that is, transcription factor MePHD1.2, was selected. MePHD1.2, which is located in the nucleus and exhibits a transcription inhibitory activity, can directly bind to PD2 segment in the promoter of MeCYP79D2, which results in its repressed expression. In cassava, the transcriptional activity of MeCYP79D2 was considerably enhanced in mephd1.2 lines, which caused an increase in the contents of linamarin and lotaustralin. Our findings unveil a novel regulatory module governing CG biosynthesis, wherein mutation of MePHD1.2 attenuates its transcription inhibition on MeCYP79D2 and boosts CGs biosynthesis in cassava.

molecular biology↗

Interpretable Spatial Gradient Analysis for Spatial Transcriptomics Data

Cellular anatomy and signaling vary across niches, which can induce gradated gene expressions in subpopulations of cells. Such spatial transcriptomic gradient (STG) makes a significant source of intra-tumor heterogeneity and can influence tumor invasion, progression, and response to treatment. Here we report Local Spatial Gradient Inference (LSGI), a computational framework that systematically identifies spatial locations with prominent, interpretable STGs from spatial transcriptomic (ST) data. To achieve so, LSGI scrutinizes each sliding window employing non-negative matrix factorization (NMF) combined with linear regression. With LSGI, we demonstrated the identification of spatially proximal yet opposite directed pathway gradients in a glioblastoma dataset. We further applied LSGI to 87 tumor ST datasets reported from nine published studies and identified both pan-cancer and tumor-type specific pathways with gradated expression patterns, such as epithelial mesenchymal transition, MHC complex, and hypoxia. The local gradients were further categorized according to their association to tumor-TME (tumor microenvironment) interface, highlighting the pathways related to spatial transcriptional intratumoral heterogeneity. We conclude that LSGI enables highly interpretable STG analysis which can reveal novel insights in tumor biology from the increasingly reported tumor ST datasets.

bioinformatics↗