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Tong, T.

Publications and source records attributed to Tong, T..

13 recordsLinked to original sources

Enhanced glymphatic CSF tracer influx during α2-adrenergic agonist anesthesia is independent of tracer injection duration

The glymphatic system mediates brain-wide cerebrospinal fluid (CSF) transport and is highly sensitive to brain state. Experimental studies show that 2-adrenergic agonist- based anesthesia enhances glymphatic CSF influx, whereas isoflurane markedly suppresses it. However, it has been suggested that the reduced tracer influx observed during isoflurane anesthesia may reflect rapid clearance of tracer from the basal cisterns rather than genuine inhibition of glymphatic transport. To address this question, we compared conventional short-duration cisterna magna tracer injections with prolonged low-rate infusion while maintaining identical total tracer dose and anesthesia duration. Across both paradigms, ketamine/dexmedetomidine anesthesia consistently produced substantially greater perivascular CSF influx than isoflurane. In contrast, tracer accumulation in blood and cervical lymph nodes remained largely unchanged between conditions. These findings demonstrate that suppression of glymphatic influx during isoflurane anesthesia is independent of tracer injection duration and support the conclusion that 2-adrenergic agonist-based anesthesia promotes glymphatic transport through mechanisms linked to sleep-like brain states.

neuroscience↗

Mechanical Ventilation Suppresses Glymphatic Function in Parallel with Delirium-Like Symptoms in Mice

Delirium is a common and serious complication in critically ill patients, arising from multiple overlapping risk factors. Its pathogenesis remains poorly understood because it reflects the combined effects of interacting clinical insults, and because appropriate experimental models for mechanistic studies have been lacking. Delirium most commonly develops in patients undergoing major surgery or requiring intensive care, where inhalational anesthesia, opioid sedation, and mechanical ventilation are common clinical exposures. Here, we tested the hypothesis that these clinically relevant interventions are sufficient to induce delirium-like behavior in healthy young wild-type mice by disrupting cerebrospinal fluid (CSF) glymphatic transport. The analysis showed that inhalational anesthesia combined with mechanical ventilation increased intracranial pressure (ICP) and induced a sustained suppression and rerouting of glymphatic waste clearance, resulting in impaired waste clearance, and acute cytokine accumulation. These findings identify disruption of brain fluid dynamics as a potential mechanism contributing to delirium in perioperative and intensive care settings. Equally important, this model represents a distinct experimental platform that combines clinically relevant mechanical ventilation, inhalational anesthesia, and opioid analgesia to produce delirium-like behavioral abnormalities in otherwise healthy mice. It therefore provides a powerful tool for future mechanistic studies of delirium pathogenesis.

neuroscience↗

National Scale Genomic Engine for Precision Medicine: Singapore PRECISE-SG100K Experience

The whole-of-nation National Precision Medicine (NPM) programme in Singapore aims to integrate a genomics backbone into standard healthcare. Phase II recently completed the sequencing of 102,202 genomes from the diverse Asian population of Singapore, generating the PRECISE-SG100K dataset. The scaling from the pilot SG10K_Health phase to national production scale demanded a central shift: from earlier generation workflows to an integrated, industrial grade "Genomic Engine". The initiative was co-developed under a public-private partnership model. Our Genomic Engine was designed with an automation-first approach, as a modular platform linking a purpose-built, centralized biospecimen processing and DNA extraction facility (EXTRACT Lab), a high-throughput sequencing operation (Illumina Data Generation Infrastructure, IDGI), with the cloud-native analytics (GRIDS) running on a fully integrated PRECISE Sample Tracking System (STS). Here we describe the key design features of our Genomic Engine. Highlighting the Stress Test phase where the automated DNA extraction yields failed to meet expectations. We share the operational adjustments which were implemented to stabilize production and resulted in a three-fold reduction in sample triage due to improved DNA recovery. Without establishing the operational guardrails during the Stress Test, the Engine would not have reached a steady-state production evidenced by >3,000 genomes per month, median turnaround time 11 days, 99.6% operational success, within in six months. This framework offers a practical blueprint for other population-scale initiatives seeking to bridge the gap between scientific piloting and industrial delivery.

genomics↗

Electromagnetic Stimulated Microfillamented Hydrogels for Guided Neuronal Morphogenesis

Biohybrid materials that integrate structural and bioelectronic cues across scales offer new routes to regulate neural development and repair. We present a hybrid, hydrogel-electromagnetic stimulation platform with a 3D hierarchically anisotropic structure, combining FLight bioprinted hydrogel microfilaments with a melt-electrowritten wireless electromagnetic stimulation system, to guide neural morphogenesis across central and peripheral systems at cellular and tissue scale. In the central nervous system, the soft microfilaments selectively promoted healthy, white-matter-like neurite extension rather than glioblastoma-derived outgrowth in human cortical brain tissues, while the electrically stimulation further enhanced the hippocampal neurosphere networking along the microfilaments. As a peripheral nerve conduit, the system directs dorsal root ganglion alignment in vitro and, in rat sciatic defects, drives a coordinated pro-regenerative response that improves axonal guidance, remyelination, and functional recovery. This multiscale biohybrid strategy demonstrates how synergistic integration of soft biomaterials and systematic, wireless bioelectric cues can non-invasively regulate neural morphogenesis, establishing new design principles for next-generation bioelectronic interfaces and regenerative medicine.

bioengineering↗

Transposable Element (TE) insertion predictions from RNAseq inputs and TE impact on RNA splicing and gene expression in Drosophila brain transcriptomes.

Recent studies have suggested that Transposable Elements (TEs) residing in introns frequently splice into and alter primary gene coding transcripts. To re-examine the exonization of TEs into protein-coding gene transcripts, we re-analyzed a Drosophila neuron circadian rhythm RNAseq dataset and a deep long RNA fly midbrain RNAseq dataset using our Transposon Insertion and Depletion Analyzer (TIDAL) program. Our TIDAL results were able to predict several TE insertions from RNAseq data that were consistent with previous published studies. However, we also uncovered many discrepancies in TE-exonization calls, such as reads that mainly support intron retention of the TE and little support for chimeric mRNA spliced to the TE. We then deployed rigorous gDNA-PCR and RT-PCR procedures on TE-mRNA fusion candidates to see how many of bioinformatics predictions could be validated. By testing a w1118 strain from which the deeper long RNAseq data was derived from and comparing to an OreR strain, only 9 of 23 TIDAL candidates (<40%) could be validated as a novel TE insertion by gDNA-PCR, indicating that deeper study is needed on using RNAseq as inputs into current TE-insertion prediction programs. Of these validated calls, the RT-PCR results only supported TE-intron retention. Lastly, in the Dscam2 and Bx genes of the w1118 strain that contained intronic TEs, gene expression was 2-3 times higher than the OreR genes lacking the TEs. This studys validation approach indicates that chimeric TE-mRNAs are infrequent and cautions that more optimization is required in bioinformatics programs to call TE insertions using RNAseq datasets.

genetics↗

Efficient Gene Editing and Overexpression of Gametophyte Transformation in a Model Fern

The clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-related nuclease (Cas) system allows precise and easy editing of genes in many plant species. However, this system has not yet been applied to any fern species due to the complex characteristics of fern genomes, genetics and physiology. Here, we established, for the first time, a protocol for gametophyte-based screening single-guide RNAs (sgRNAs) with high efficiency for CRISPR/Cas-mediated gene editing in a model fern species, Ceratopteris richardii. We utilized the C. richardii Actin promoter to drive sgRNA expression and enhanced CaMV 35S promoter to drive the expression of Streptococcus pyogenes Cas9 in this CRISPR-mediated editing system, which was employed to successfully edit a few genes (e.g., nucleotidase/phosphatase 1, CrSAL1; Cryptochrome 4, CRY4) and CrPDS, encoding a phytoene desaturase protein that resulted in an albino phenotype in C. richardii. Knockout of CrSAL1 resulted in significantly reduced stomatal conductance (gs), leaf transpiration rate (E), stomatal/pore length, and abscisic acid (ABA)-induced reactive oxygen species (ROS) accumulation in guard cells. Moreover, CrSAL1 overexpressing plants showed significantly increased net photosynthetic rate (A), gs, E and intrinsic water use efficiency (iWUE) as well as most of the stomatal traits and ROS production in guard cells compared to those in the wild-type (WT) plants. Taken together, the optimized CRISPR/Cas9 system provides a useful tool for functional genomics in a model fern species, allowing the exploration of fern gene functions for evolutionary biology, herbal medicine discovery and agricultural applications.

plant biology↗

Impact of Glycan Depletion, Glycan Debranching and Increased Glycan Charge on HIV-1 Neutralization Sensitivity and Immunogenicity

Modifying HIV-1s envelope glycoprotein glycans can impact its neutralization sensitivity. The use of the knock out cell line GnT1-prevents the elaboration of complex-type glycans, and opens up the glycan shield, increasing bNAb vulnerability. Some bNAb precursors can bind to GnT1-trimers, supporting their use in vaccine priming. However, GnT1-trimers express poorly and exhibit very low infectious counts. Here, we describe two other potentially vaccine-relevant glycoengineered trimers, 1) To truncate complex glycans, we used of a cocktail of glycosidases, termed "NGAF3" (Neuraminidase, {beta}-Galactosidase, N-Acetylglucosaminidase and endoglycosidase F3). Like GnT1-trimers, NGAF3 reduced glycan clashes and increased bNAb potency while retaining a closed trimer conformation; 2) Modified by {beta}-1,4-galactosyltransferase 1 (B4GalT1) and {beta}-galactoside -2,6 sialyltransferase 1 (ST6Gal1) during Env biosynthesis. Glycan mass spectrometry revealed that NGAF3 removed glycan heads of 3 of 7 positions on the trimer that are largely occupied by complex glycans. It also revealed a novel B4GalT1 activity to favor glycan precursor conversion to hybrid glycans rather than complex glycans. A comparison to monomeric gp120 revealed that B4GalT1s new activity depends on tight glycan spacing. B4GalT1 affected more glycans than NGAF3 (6 out of 7 glycans), perhaps due to greater accessibility during Env folding rather than after folding. Surprisingly, the N611 glycan was unaffected by either modification. B4GalT1 and ST6Gal1 cooperatively increased the abundance of hybrid glycans and -2,6 hypersialylated termini. This occurred largely by amplifying the abundance of a limited number of hybrid glycan structures that are also present on unmodified trimers. In rabbit vaccinations, B4GalT1+ST6GalT1-modified virus-like particles reduced the frequency and titers of serum NAbs that showed a modest preference for modified glycans. Conversely, chronically HIV-1-infected donor plasma neutralizing antibody titers were 1.7- to 10.8- fold higher against B4GalT1+ST6GalT1-modified pseudovirus. Overall, our data provide tools for heterologous prime, boost and polishing vaccine regimens using modified glycans. AUTHOR SUMMARYAn HIV-1 vaccine remains one of the most significant biomedical challenges today. Vaccines often work by triggering virus fighting antibodies to stave off infection. For HIV-1, this has been exceedingly difficult because the target, called the HIV-1 envelope glycoprotein (Env) is extremely variable and carries a thick sugar coat, protecting it from all but a few rare broadly reactive antibodies (termed bNAbs) that sometimes develop during natural HIV-1 infection. Given these challenges, it is reasonable to propose that any successful vaccine will need to be rationally designed to trigger the rare bNAbs. To meet this goal might require more 3 different vaccine components. First, a vaccine "prime" to trigger rare bNAb proliferation, followed by heterologous "boosts" and "polishing" immunogens to select for bNAbs. In this study, we evaluated two potential immunogens. In one approach, we used cocktails of enzymes to strip Envs sugar coat, in the hope of reducing the barrier to stimulate bNAb precursors. In another, we used excess enzymes to build particular structures on Envs coat. We checked how well these two Env variants were recognized by antibodies. We also checked in fine detail how the sugars were changed at the molecular level. Finally, we immunized rabbits. Our data enrich the number of strategies available to further explore the concept of priming, boosting and polishing vaccine shots.

immunology↗

Glioblastoma cells imitate neuronal excitability in humans

BackgroundGlioblastomas are renowned for their pronounced intratumoral heterogeneity, characterized by a diverse array of plastic cell types. However, the physiological and transcriptomic features of the cells residing in the invasive leading edge (LE), including both neurons and glioblastoma cells (GBCs), remain unclear, challenging our comprehension of the glioblastoma pathophysiology. MethodsTo elucidate molecular and morphophysiological features of LE cells, we established an experimental workflow enabling the investigation of GBCs and neurons within cancer-infiltrated organotypic tissue specimens from the same patients. With this approach, we characterized the electrophysiological properties of cells in the neocortical tumor LE (LE cells). We further performed single-cell Patch-seq experiments, enabling transcriptomic analysis of electrophysiologically recorded LE cells. ResultsUpon depolarization, 58% of LE cells exhibited aberrant action potentials (aAPs). Electrophysiological assessment showed that a subset of GBCs generated aAPs, with no significant differences in aAP properties compared to LE neurons. Transcriptomic analysis of 144 LE cells revealed four transcriptomic clusters, including two GBC populations and two neuronal populations. LE GBCs exhibited diverse cellular states, including mesenchymal-like, astrocyte-like, neural progenitor-like, and oligodendrocyte-precursor cell-like phenotypes. Notably, LE GBCs exhibiting aAPs displayed reduced mitotic pathway activity and developmental regulatory ion channel CaV1.2. Cell-cell interaction analysis illustrates a higher signaling interaction between aAP LE cells compared to no-aAP LE cells. ConclusionIn summary, we find comparable electrical properties between neurons and a subset of GBCs in the leading edge, suggesting an active electrophysiological role of GBCs in the tumors pathophysiology. Key PointsO_LIHuman organotypic slice cultures enable long-term functional investigation of glioblastoma cells. C_LIO_LIGBCs and neurons in the LE exhibit similar aAPs. C_LIO_LILE GBCs display heterogeneous cellular states, with reduced proliferation signaling in aAP GBCs. C_LI Importance of studyThis study sheds light on the diverse pathophysiological and molecular features of cells in the neocortical infiltration zone of glioblastoma. By utilizing in vitro organotypic human brain slice cultures, a reliable platform for longitudinal observation, we unveiled the dichotomy of the electrical properties of LE cells. More than half of LE cells display aAP, contradicting findings from cultured tumor cells and animal models. Patch-seq analysis confirmed that both GBCs and neurons in the LE generate aAPs with indistinguishable electrical properties. aAP GBCs showed higher cell-cell interactions. We find aAP GBCs to express reduced proliferation signaling compared to no-aAP GBCs, suggesting a non-dividing and potentially more plastic cell state. These findings point to the electrical-active GBCs as an important attribute of the LE, linking the electrophysiological properties with functional implications, and implicate an active role of electrophysiological changes of GBCs in tumor pathophysiology.

cancer biology↗

Impact of Common Modifications on the Antigenic Profile and Glycosylation of Membrane-Expressed HIV-1 Envelope Glycoprotein.

Recent HIV-1 vaccine development has centered on "near native" soluble envelope glycoprotein (Env) trimers. These trimers are artificially stabilized laterally (between protomers) and apically (between gp120 and gp41). These same stabilizing mutations have been leveraged for use in membrane-expressed Env mRNA vaccines, although their precise effects in this context are unclear. To address this question, we investigated the effects of Env mutations expressed on virus-like particle (VLP) in 293T cells. Uncleaved (UNC) trimers were laterally unstable upon gentle lysis from membranes. However, gp120/gp41 processing improved lateral stability. Due to inefficient gp120/gp41 processing, UNC is incorporated into VLPs. A linker between gp120 and gp41 (NFL) neither improved trimer stability nor its antigenic profile. An artificially introduced enterokinase cleavage site allowed processing post-expression, resulting in increased trimer stability. Gp41 N-helix mutations I559P and NT1-5 both imparted lateral trimer stability, but concomitantly reduced gp120/gp41 processing and/or impacted V2 apex and interface NAb binding. I559P consistently reduced recognition by HIV+ donor plasmas, further supporting antigenic differences. Mutations in the gp120 bridging sheet failed to stabilize membrane trimers in a pre-fusion conformation, reduced gp120/gp41 processing and exposed non-neutralizing epitopes. Reduced glycan maturation and increased sequon skipping were common effect of mutations. In some cases, this may be due to increased rigidity which limits access to glycan processing enzymes. In contrast, viral gp120 did not show glycan skipping. We observed a minor species of high mannose glycan only gp160 in particle preparations. This was unaffected by any mutations and instead bypasses normal folding and glycan maturation processes. Including the full gp41 cytoplasmic tail led to markedly reduced gp120/gp41 processing and increased the proportion of high mannose gp160. Remarkably, NAbs were unable to bind to full-length Env trimers. Overall, our findings suggest caution in leveraging mutations to ensure they impart valuable membrane trimer phenotypes for vaccine use. AUTHOR SUMMARYA vaccine that induces virus-fighting antibodies to block HIV-1 infection remains elusive. To ablate HIV-1 infection, antibodies must bind to authentic envelope (Env) glycoprotein on the virus surface. However, Env can exist in various forms, many of which are relatively easy targets for non-effective antibodies. Therefore, a key challenge of vaccine design is to create pure authentic Env that is unfettered by these other forms of Env. Vaccine research to date has focused largely on stabilizing soluble Env trimers, as this format simplifies purification and translational studies. However, incomplete Env authenticity may blunt the efficacy of this approach. By comparison, the manufacture of particle-based vaccines that express Env in situ on membranes is cumbersome. In an alternative approach, lipid particles can deliver mRNA vaccines encoding membrane trimers, bypassing the manufacturing challenges of previous methods. Stabilizing mutations derived from soluble trimers are now being leveraged for membrane trimers. Here, we evaluated the effects of these mutations. Our results show that some mutations alter Env conformation, and therefore might best be omitted from membrane Env vaccines.

immunology↗

Molecular Evolution and Interaction of 14-3-3 Proteins with H+-ATPases in Plant Abiotic Stresses

Environmental stresses severely affect plant growth and crop productivity. Regulated by 14-3-3 proteins (14-3-3s), H+-ATPases (AHA) are important proton pumps that can induce diverse secondary transport via channels and co-transporters for the abiotic stress response of plants. Many studies demonstrated the roles of 14-3-3s and AHAs in coordinating the processes of plant growth, phytohormone signaling, and stress responses. However, the molecular evolution of 14-3-3s and AHAs has not been summarized in parallel with insights across multiple plant species. Here, we review the roles of 14-3-3s and AHAs in cell signaling to enhance plant responses to diverse environmental stresses. We analyzed the molecular evolution of key proteins that are associated with 14-3-3s and AHAs in plant growth and hormone signaling. The results revealed evolution, duplication, contraction, and expansion of 14-3-3s and AHAs in green plants. We also discussed the stress-specific expression of those 14-3-3s and AHAs in a eudicot (Arabidopsis thaliana), a monocot (Hordeum vulgare) and a moss (Physcomitrium patens) under abiotic stresses. We propose that 14-3-3s and H+-ATPases respond to abiotic stresses through many important targets and signaling components of phytohormones, which could be promising to improve plant tolerance to single or multiple environmental stresses. HighlightWe review the response and adaptation of 14-3-3s and AHAs to diverse environmental stimuli and we analyze the evolutionary features and molecular functions of 14-3-3s and AHAs.

plant biology↗

USP10 strikes down Wnt/β-catenin signaling by dual-wielding deubiquitinase activity and phase transition potential

Wnt/{beta}-catenin signaling is a conserved pathway crucially governing development, homeostasis and oncogenesis. Discovery of novel regulators holds great values in both basic and translational research. Through screening, we identified a deubiquitinase (DUB) USP10 as a novel and critical modulator of {beta}-catenin. Mechanistically, USP10 binds to key scaffold Axin1 via conserved motifs and stabilizes Axin1 through K48-linked deubiquitination, and surprisingly, tethers Axin1 and {beta}-catenin physically while promoting phase separation for {beta}-catenin suppression regardless of its enzymatic activity. Functionally, USP10 prominently regulates embryonic development and intestinal homeostasis by antagonizing {beta}-catenin via DUB activity. In colorectal cancer, USP10 substantially represses cancer growth mainly through physical binding compensation and phase separation promotion and correlates with Wnt/{beta}-catenin magnitude clinically. Collectively, we discovered USP10 functioning in multiple biological processes against {beta}-catenin and unearthed a novel enzyme-dependent and -independent "dual-regulating" mechanism by which USP10 utilizes parallelly and context-dependently. USP10 inhibitor was suggested in treating certain Wnt-related diseases.

cell biology↗

Protein kinase D1 phosphorylates CBX8 to facilitate the disassociation of PRC1 complex from p16 promoter and promotes cell senescence

The Polycomb group (PcG) protein chromobox 8 (CBX8) is the subunit of Polycomb repressive complex 1 (PRC1) and recognizes the trimethylation of histone H3 on Lysine 27 (H3K27me3), and coordinates with PRC2 complex to function as epigenetic gene silencer. CBX8 plays a key role in cell proliferation, stem cell biology, cell senescence, and cancer development. However, our knowledge of CBX8 post-translational modifications remains elusive. Here, we report that protein kinase D1 (PKD1) interacts and phosphorylates CBX8 at Ser256 and Ser311 in an evolutionarily conserved motif. We found that PKD1 activation triggered by serum stimulation, Nocodazole treatment and oncogene Ras-induced cell senescence (Ras OIS) all promotes CBX8 S256/311 phosphorylation. PKD1-mediated CBX8 S256/311 phosphorylation impairs PRC1 complex integrity by reducing the binding of CBX8 to other PRC1 components BMI1 and RING1B, decreases the monoubiquitination of histone H2AK119, and results in CBX8 dissociation from its target INK4a/ARF locus and the de-repression of p16, and thus ultimately facilitates cellular senescence. CBX8 S256/311 phosphorylation also compromises hepatocellular cancer cells proliferation and migration. Collectively, these results suggest that PKD1-mediated CBX8 S256/311 phosphorylation is a key mechanism governing CBX8 function, including cell senescence and cancer cell proliferation. Financial supportThis work was supported by grants from Ministry of Science and Technology of the Peoples Republic of China (2018YFC2000102), and from National Natural Science Foundation of China (31871382 and 81571369).

cell biology↗

Identifying the Biosynthetic Gene Cluster for Triacsins with an N-hydroxytriazene Moiety

Triacsins are a family of natural products containing an N-hydroxytriazene moiety not found in any other known secondary metabolites. Though many studies have examined the biological activity of triacsins in lipid metabolism, the biosynthesis of triacsins has remained unknown. Here, we report the identification of the triacsin biosynthetic gene cluster in Streptomyces aureofaciens ATCC 31442. Bioinformatic analysis of the gene cluster led to the discovery of the tacrolimus producer Streptomyces tsukubaensis NRRL 18488 as a new triacsin producer. In addition to targeted gene disruption to identify necessary genes for triacsin production, stable isotope feeding was performed in vivo to advance the understanding of N-hydroxytriazene biosynthesis.

biochemistry↗