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Nguyen, C.

Publications and source records attributed to Nguyen, C..

At least 37 records · Page 2Linked to original sources

Network-aware self-supervised learning enables high-content phenotypic screening for genetic modifiers of neuronal activity dynamics

High-throughput phenotypic screening has historically relied on manually selected features, limiting our ability to capture complex cellular processes, particularly neuronal activity dynamics. While recent advances in self-supervised learning have revolutionized the ability to study cellular morphology and transcriptomics, dynamic cellular processes have remained challenging to phenotypically profile. To address this limitation, we developed Plexus, a self-supervised model specifically designed to capture and quantify network-level neuronal activity dynamics. Unlike existing phenotyping tools that focus on static readouts, Plexus leverages a network-level cell encoding method, which enables it to efficiently encode dynamic neuronal activity data into rich representational embeddings. In turn, Plexus achieves state of the art performance in detecting phenotypic changes in neuronal activity. We validated Plexus using a comprehensive GCaMP6m simulation framework and demonstrated its enhanced ability to classify distinct neuronal activity phenotypes compared to traditional signal-processing approaches. To enable practical application, we integrated Plexus with a scalable experimental system utilizing human iPSC-derived neurons equipped with the GCaMP6m calcium indicator and CRISPR interference machinery. This integrated platform successfully identified nearly seventeen times as many distinct phenotypic changes in response to genetic perturbations compared to conventional signal processing methods, as demonstrated in a 52-gene CRISPRi screen across multiple iPSC lines. Using this framework, we identified potential genetic modifiers of aberrant neuronal activity in frontotemporal dementia, illustrating its utility for understanding complex neurological disorders.

bioinformatics↗

T cells are necessary for development of PCOS reproductive symptoms in a letrozole-induced mouse model of PCOS

Polycystic ovary syndrome (PMOS) is a complex reproductive disorder with clear genetic susceptibilities that impact the heterogeneous clinical presentation of symptoms and severity through unknown mechanisms. Chronic inflammation is linked to PMOS, but a clear cause-and-effect relationship between immune mediators and PMOS phenotypes has yet to be demonstrated. This study employed a comprehensive systems immunology approach, utilizing a letrozole-induced PMOS mouse model to identify changes in inflammatory factors associated with PMOS symptoms. By analyzing immune cells and secreted cytokines from 22 different mouse strains, we identified T cells and TNF-{beta} as associated with PMOS-like phenotypes, regardless of genetic background. We used a knockout of TCR to show that functional T cells are necessary for development of pathologically elevated luteinizing hormone (LH) in letrozole-treated female mice. In women with PMOS, we observed elevated TNF-{beta} transcripts in immune cells from women with PMOS. Finally, we demonstrate that TNF-{beta} increased Lhb mRNA in a female mouse gonadotrope-derived cell line, suggesting that TNF-{beta} may directly modulate gonadotrope gene expression and may contribute to elevated LH in PMOS-like conditions. These findings support a requirement for functional {beta} T cells in LET-induced LH elevation in a PMOS-like mouse model and identify TNF-{beta} as a candidate immune mediator for further investigation. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=190 SRC="FIGDIR/small/631835v2_ufig1.gif" ALT="Figure 1"> View larger version (90K): org.highwire.dtl.DTLVardef@14dcf2aorg.highwire.dtl.DTLVardef@15bdc67org.highwire.dtl.DTLVardef@1e2f718org.highwire.dtl.DTLVardef@1cc5c16_HPS_FORMAT_FIGEXP M_FIG C_FIG One Sentence SummaryFunctional {beta} T cells are linked to LET-induced LH elevation in a PMOS-like mouse model, uncovering candidate immune mechanisms for further study.

immunology↗

Nicotine engages a VTA-NAc feedback loop to inhibit amygdala-projecting dopamine neurons and induce anxiety.

Nicotine activates ventral tegmental area (VTA) dopaminergic (DA) neurons projecting to the nucleus accumbens (NAc) to drive its reinforcing effects. Simultaneously, it inhibits those projecting to the amygdala (Amg) to mediate anxiety through a process that remains unknown. Here we show that NAc- and Amg-projecting DA neurons respond with similar polarities to ethanol and nicotine, suggesting a shared network-based mechanism underlying the inhibitory effect of these otherwise pharmacologically-distinct drugs. Selective activation of NAc-projecting DA neurons, using genetic or optogenetic strategies, produced inhibition of Amg-projecting DA neurons, through a GABAergic feedback loop. Furthermore, optogenetically silencing this feedback loop prevented nicotine from inducing both inhibition of DA neurons and anxiety-like behavior. Therefore, nicotine-induced inhibition of the VTA-Amg DA pathway results from a VTA-NAc inhibitory feedback loop, mediating anxiety.

neuroscience↗

Natural Selection in a Synthetic Yeast Endosymbiont Promotes Stable Coexistence

Bacteria engulfment by a higher order host is believed to be the beginning of an evolutionary process that ultimately formed mitochondria. In an effort to experimentally elucidate the early effects of natural selection on bacteria resident in a eukaryotic host, a synthetic endosymbiont model system has been exploited. Here we describe a reproducible series of mutations that were observed after Escherichia coli was passaged within Saccharomyces cerevisiae for >8 passages which led to enhanced coexistence of bacteria within the yeast. These naturally selected mutations, formed by gene acquisition of trans-posable elements in rcsC, cpxA, and idnK, result in both functional and non-functional protein products with phenotypic effects on the bacteria that promote endosymbiont stability.

synthetic biology↗

N6-methyladenosine in DNA promotes genome stability

DNA base lesions, such as incorporation of uracil into DNA or base mismatches, can be mutagenic and toxic to replicating cells. To discover factors in repair of genomic uracil, we performed a CRISPR knockout screen in the presence of floxuridine, a chemotherapeutic agent that incorporates uracil and fluoro-uracil into DNA. We identified known factors, such as uracil DNA N-glycosylase (UNG), and unknown factors, such as the N6-adenosine methyltransferase, METTL3, as required to overcome floxuridine-driven cytotoxicity. Visualized with immunofluorescence, the product of METTL3 activity, N6-methyladenosine, formed nuclear foci in cells treated with floxuridine. The observed N6-methyladenosine was embedded in DNA, called 6mA, and these results were confirmed using an orthogonal approach, liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). METTL3 and 6mA were required for repair of lesions driven by additional base damaging agents, including raltitrexed, gemcitabine, and hydroxyurea. Our results establish a role for METTL3 and 6mA in promoting genome stability in mammalian cells, especially in response to base damage.

molecular biology↗

Genetically modifying the protein matrix of macroscopic living materials to control their structure and rheological properties

The field of engineering living materials (ELMs) seeks to engineer cells to form macroscopic materials with tailorable structures and properties. While centimeter-scale ELMs can be grown from Caulobacter crescentus engineered to secrete a protein matrix, how the sequence of the protein matrix affects structural and rheological properties remains poorly understood. Here, we explore how changing the elastin-like polypeptide (ELP) length impacts ELM microstructure and viscoelastic behavior. We demonstrate that shortening ELP produces fibers almost 2x thicker than other variants, resulting in a stiffer material at rest. Interestingly, the mid-length ELP forms a complex structure with globules and multidirectional fibers with increased yield stress under flow conditions. Lengthening ELP creates thinner strands between cells with similar storage and loss moduli to the mid-length ELP. This study indicates that sequence-structure-property relationships in these ELMs are complex with few parallels to other biocomposite models. Furthermore, it highlights that fine-tuning genetic sequences can create significant differences in rheological properties, uncovering new design principles of ELMs.

synthetic biology↗

Lcn2 protects from cisplatin induced AKI by regulating DNA damage response via EGFR activation

BackgroundLipocalin 2 (Lcn2), a small-secreted protein, is an established sensitive biomarker of kidney injury. In Cisplatin (CDDP) induced acute kidney injury (AKI), Lcn2 expression is swiftly and strongly increased in suffering renal medullary tubules. While recent reports correlates Lcn2 expression in cancer cells with CDDP resistance, the role of Lcn2 in kidney tubule damaged by CDDP remains unknown. MethodsTo better understand the role of Lcn2 in CDDP-induced AKI, experiments on Lcn2+/+ or Lcn2-/- mice as well as immortalized kidney cells knock-down (KD) for Lcn2 were conducted. Kidney function and injury were assessed using standard techniques. Cellular and molecular mechanisms were studied in WT and Lcn2 KD cells in combination with pathways inhibitors in order to gain insight Lcn2 driven mechanisms. ResultsIn animal injected with CDDP, Lcn2 was upregulated mostly in kidney inner medulla collecting duct while it was reabsorbed in the proximal tubules. Lcn2-/- in mice significantly decreased kidney function compare to WT mice, while it increased parenchymal damage due to increased cell death and cast formation. Interestingly, while little to no damage were present in the medulla of CDDP injected WT animal, a clear increase of medulla tubular lesions was observed in Lcn2-/- mice. Using Inner Medullary Collecting Duct cells (mIMDC-3), we showed that Lcn2 KD induces a p53-dependent apoptosis upon Cisplatin exposure while no effect on necrosis was observed. Finally, we demonstrated that Lcn2 drives CDDP resistance to apoptosis through the activation of the pro-survival EGFR pathway. ConclusionsWe established that Lcn2 is a renoprotective protein in CDDP-induced AKI via the activation of EGFR pathway. This new mechanism might represent a new approach for the treatment of AKI.

cell biology↗

Circadian rhythm disruption alters mammary gland morphology and accelerates cold aggressive tumorigenesis through a LILRB4-dependent pathway

Epidemiological studies have shown that circadian rhythm disruption (CRD) is associated with the risk of breast cancer. However, the role of CRD in mammary gland morphology and aggressive basal mammary tumorigenesis and the molecular mechanisms underlying CRD and cancer risk remain unknown. To investigate the effect of CRD on aggressive tumorigenesis, a genetically engineered mouse model that recapitulates the human basal type of breast cancer was used for this study. The effect of CRD on mammary gland morphology was investigated using wild-type mice model. The impact of CRD on the tumor microenvironment was investigated using the tumors from LD12:12 and CRD mice via scRNA seq. ScRNA seq was substantiated by multiplexing immunostaining, flow cytometry, and realtime PCR. The effect of LILRB4 immunotherapy on CRD-induced tumorigenesis was also investigated. Here we identified the impact of CRD on basal tumorigenesis and mammary gland morphology and identified the role of LILRB4 on CRD-induced lung metastasis. We found that chronic CRD disrupted mouse mammary gland morphology and increased tumor burden, and lung metastasis and induced an immunosuppressive tumor microenvironment by enhancing LILRB4a expression. Moreover, CRD increased the M2-macrophage and regulatory T-cell populations but decreased the M1-macrophage, and dendritic cell populations. Furthermore, targeted immunotherapy against LILRB4 reduced CRD-induced immunosuppressive microenvironment and lung metastasis. These findings identify and implicate LILRB4a as a link between CRD and aggressive mammary tumorigenesis. This study also establishes the potential role of the targeted LILRB4a immunotherapy as an inhibitor of CRD-induced lung metastasis.

cancer biology↗

Decellularized Banana Leaves: Eco-Friendly Scaffolds for Cell-Based Seafood

Cellular agriculture, as an emerging food production system, holds potential to address sustainability, food security, and agricultural resilience. Within the cell-based meat supply chain, one of the key steps is scaffolding. In this study, we assessed decellularized banana leaves, various coating materials, and different cell seeding strategies to determine their effects on cell viability, cell growth, cell alignment, and the response of the materials to thermal processing. The efficiency of decellularization was verified through DNA quantification, which decreased from 445 ng/mg in fresh banana leaves to non-detectable levels in the decellularized samples. This was further confirmed by FTIR and PCA modeling. Cell viability exceeded 98% on uncoated, soy-coated, and gelatin-coated samples of the decellularized banana leaves. Alignment of cells on gelatin-coated samples was the highest among the samples, with a dominant orientation of 65.8{degrees}, compared to soy-coated and uncoated samples with dominant orientations of 9.2{degrees} and -6.3{degrees}, respectively. In terms of quality attributes, the kinetics of shrinkage indicated that coating with soy and the presence of cells increased the activation energy due to the higher energy required for protein denaturation. Moreover, the kinetics of area changes in plain scaffolds without cells followed a first-order pattern, while with seeded cells a second-order pattern was followed. In summary, decellularized banana leaves present a sustainable and suitable biomaterial to support cells towards future needs related to meat production.

synthetic biology↗

Nicotine in adolescence freezes dopamine circuits in an immature state

Nicotine use during adolescence is largely associated with negative long-term outcomes, including addiction to nicotine in adulthood. How nicotine acts on developing neurocircuitry in adolescence remains largely unknown, but may hold the key for informing more effective intervention efforts. We found transient nicotine exposure in early adolescence was sufficient for adult mice to show a marked vulnerability to nicotine. Brain-wide activity mapping showed that these mice had an enhanced response to an acute nicotine injection and widespread disruption of functional connectivity in comparison to controls, particularly within dopaminergic networks. Neurophysiological analysis further revealed that their ventral tegmental area (VTA) dopamine neurons show an immature basal plasticity signature and an adolescent-like imbalance in nicotine-induced activity between nucleus accumbens (NAc) and amygdala (AMG)-projecting pathways, known to respectively produce the reinforcing and anxiogenic effects of nicotine. The anxiogenic effect of nicotine is abolished in adult mice treated with nicotine in adolescence, strongly resembling the normal phenotype of young mice. Together these results suggest that nicotine exposure in adolescence somehow "froze" both their neural circuit and behavioral reaction to nicotine, carrying an adolescent-like vulnerability to the drug into adulthood. Finally, we are able to "thaw" the behavioral response to acute nicotine in adolescent-exposed mice by chemogenetically resetting the balance between the underlying NAc- and AMG-projecting dopamine circuits, restoring a mature anxiety-like response to acute nicotine. Together, our results highlight how diverse dopamine pathways can be impacted by experience in adolescence, and further suggest that the perseverance of a developmental imbalance between dopamine pathways may alter vulnerability profiles for later dopamine-dependent psychopathologies.

neuroscience↗

Individual variations in reward-seeking adaptability emerge among isogenic mice living in a micro-society and predict their response to nicotine

Individual animals differ in their traits and preferences, which shape their social interactions, survival, and susceptibility to disease, including addiction. Nicotine use is highly heterogenous, and has been linked to the expression of personality traits. Although these relationships are well-documented, we have limited understanding of the neurophysiological mechanisms that give rise to distinct personalities and their connection to nicotine susceptibility. To address this question, we conducted a study using a semi-natural and social environment called "Souris-City" to observe the long-term behavior of individual mice. Souris-City provided both a communal living area and a separate test area where mice engaged in a reward-seeking task isolated from their peers. Mice developed individualistic reward-seeking strategies when choosing between water and sucrose in the test compartment, which, in turn, predicted how they adapted to the introduction of nicotine as a reinforcer. Moreover, mouse profiles in isolation also extended to correlate with their behavior within the social environment, linking decision-making strategies to the expression of behavioral traits. Neurophysiological markers of adaptability within the dopamine system were apparent upon nicotine challenge, and were associated with specific profiles. Our findings suggest that environmental adaptations influence behavioral traits and sensitivity to nicotine by acting on dopaminergic reactivity in the face of nicotine exposure, potentially contributing to addiction susceptibility. These results further emphasize the importance of understanding inter-individual variability in behavior to gain insight into the mechanisms of decision making and addiction.

neuroscience↗

The interpeduncular nucleus blunts the rewarding effect of nicotine

Nicotine, by stimulating ventral tegmental area (VTA) dopaminergic neurons, has a rewarding effect that drives tobacco consumption. In turn, the interpeduncular nucleus (IPN) is thought to become activated at high nicotine doses to restrict drug intake. However, the dynamics of the IPN response to nicotine and its impact on the rewarding effect of the drug remain unknown. To address this issue, we have developed a genetically-modified mouse model, in which a "suicide" antagonist of nicotinic acetylcholine receptors (nAChRs) selectively attaches to a designer {beta}4 nAChR subunit. By locally infusing this antagonist in the IPN, we achieved pharmacologically-specific and sustained antagonism of nAChRs containing the {beta}4 subunit. By combining this chemogenetic method with in vivo electrophysiology, we show that even at low doses, nicotine activates and inhibits two different populations of IPN neurons, and that {beta}4-containing nAChRs are only involved in the activation response. Furthermore, blocking the response to nicotine selectively in the IPN increased both the sensitivity of the VTA to the drug and its rewarding effect in a conditioned place preference paradigm. These findings indicate that the IPN is engaged across a large range of nicotine doses and acts as a regulatory brake on the nicotine reward circuit.

neuroscience↗

Collecting-Gathering Biophysics of the Blackworm L. variegatus

Many organisms exhibit collecting and gathering behaviors as a foraging and survival method. Certain benthic macroinvertebrates are classified as collector-gatherers due to their collection of particulate matter as a food source, such as the aquatic oligochaete Lumbriculus variegatus (California blackworms). Blackworms demonstrate the ability to ingest organic and inorganic materials, including microplastics, but previous work has only qualitatively described their possible collecting behaviors for such materials. The mechanism through which blackworms consolidate discrete particles into a larger clumps remains unexplored quantitatively. By analyzing a group of blackworms in a large arena with an aqueous algae solution, we discover that their relative collecting efficiency is proportional to population size. Examining individual blackworms under a microscope reveals that both algae and microplastics physically adhere to the worms body due to external mucus secretions, which cause the materials to clump around the worm. We observe that this clumping reduces the worms exploration of its environment, potentially due to thigmotaxis. To validate the observed biophysical mechanisms, we create an active polymer model of a worm moving in a field of particulate debris with a short-range attractive force on its body to simulate its adhesive nature. We find that the attractive force increases gathering efficiency. This study offers insights into the mechanisms of collecting-gathering behavior, informing the design of robotic systems, as well as advancing our understanding the ecological impacts of microplastics on benthic invertebrates.

ecology↗

Cradle to production gate life cycle assessment of cultured meat growth media: A comparison of Essential 8™ and Beefy-9

There is an increasing interest in use of biotechnology as a means of sustainable food manufacturing; however, biotechnology processing is considerably resource and energy intensive. Recent interest in animal cell-based meat (ACBM) has prompted scientific and engineering questions about the economic and environmental viability of these proposed ACBM products. This study provides an environmental assessment of two proposed growth mediums (Essential 8TM and Beefy-9) for ACBM production. The study found that the addition of antibiotics/antimycotics (10,000 g/mL) to the growth media increased the environmental metrics, such as the cumulative energy demand and global warming potential, by two orders of magnitude. To account for additional processing for animal cell culture, a scenario analysis was conducted to assess the potential environmental impacts of growth medium production with varying level of refinement required for the input components. The study indicates that the heavy refinement of the growth medium components is likely to undermine the potential sustainability of future ACBM products.

ecology↗

Environmental impacts of cultured meat: A cradle-to-gate life cycle assessment

Interest in animal cell-based meat (ACBM) or cultured meat as a viable environmentally conscious replacement for livestock production has been increasing, however a life cycle assessment for the current production methods of ACBM has not been conducted. Currently, ACBM products are being produced at a small scale and at an economic loss, however ACBM companies are intending to industrialize and scale-up production. This study assesses the potential environmental impact of near term ACBM production. Updated findings from recent technoeconomic assessments (TEAs) of ACBM and a life cycle assessment of Essential 8 were utilized to perform a life cycle assessment of near-term ACBM production. A scenario analysis was conducted utilizing the metabolic requirements examined in the TEAs of ACBM and a purification factor from the Essential 8 life cycle assessment was utilized to account for growth medium component processing. The results indicate that the environmental impact of near-term ACBM production is likely to be orders of magnitude higher than median beef production if a highly refined growth medium is utilized for ACBM production.

ecology↗

Ancient Fish Lineages Illuminate Toll-Like Receptor Diversification in Early Vertebrate Evolution

Since its initial discovery over 50 years ago, understanding the evolution of the vertebrate adaptive immune response has been a major area of research focus for comparative geneticists. However, how the evolutionary novelty of an adaptive immune response impacted the diversity of receptors associated with the innate immune response has received considerably less attention until recently. Here we investigate the diversification of vertebrate Toll-like receptors (TLRs), one of the most ancient and well conserved innate immune receptor families found across the Tree of Life, integrating genomic data that represent all major vertebrate lineages with new transcriptomic data from Polypteriformes, the earliest diverging ray-finned fish lineage. Our analyses reveal TLR sequences that reflect the 6 major TLR subfamilies, TLR1, TLR3, TLR4, TLR5, TLR7, and TLR11, and also currently unnamed, yet phylogenetically distinct TLR clades. We additionally recover evidence for a pulse of gene gain coincident with the rise of the adaptive immune response in jawed vertebrates, followed by a period of rapid gene loss during the Cretaceous. These gene losses are primarily concentrated in marine teleost fish and synchronous with the mid Cretaceous anoxic event, a period of rapid extinction for marine species. Finally, we reveal a mismatch between phylogenetic placement and gene nomenclature for up to 50% of TLRs found in clades such as ray-finned fishes, cyclostomes, amphibians, and elasmobranchs. Collectively these results provide an unparalleled perspective of TLR diversity, and offer a ready framework for testing gene annotations in non-model species.

evolutionary biology↗

Host genetic variation guides hepacivirus clearance, chronicity, and liver fibrosis in mice

Background & AimsHuman genetic variation is thought to guide the outcome of hepatitis C virus (HCV) infection but model systems within which to dissect these host genetic mechanisms are limited. Norway rat hepacivirus (NrHV), closely related to HCV, causes chronic liver infection in rats but causes acute self-limiting hepatitis in typical strains of laboratory mice, which resolves in two weeks. The Collaborative Cross (CC) is a robust mouse genetics resource comprised of a panel of recombinant inbred strains, which model the complexity of the human genome and provide a system within which to understand diseases driven by complex allelic variation. Approach & ResultsWe infected a panel of CC strains with NrHV and identified several that failed to clear virus after 4 weeks. Strains displayed an array of virologic phenotypes ranging from delayed clearance (CC046) to chronicity (CC071, CC080) with viremia for at least 10 months. Body weight loss, hepatocyte infection frequency, viral evolution, T-cell recruitment to the liver, liver inflammation and the capacity to develop liver fibrosis varied among infected CC strains. ConclusionsThese models recapitulate many aspects of HCV infection in humans and demonstrate that host genetic variation affects a multitude of virus and host phenotypes. These models can be used to better understand the molecular mechanisms that drive hepacivirus clearance and chronicity, the virus and host interactions that promote chronic disease manifestations like liver fibrosis, therapeutic and vaccine performance, and how these factors are affected by host genetic variation.

microbiology↗

A mathematical model of the disruption of glucose homeostasis in cancer patients

In this paper we investigate the disruption of the glucose homeostasis at the whole-body level by the presence of cancer disease. Of particular interest are the potentially different responses of patients with or without hyperglycemia (including Diabetes Mellitus) to the cancer challenge, and how tumor growth, in turn, responds to hyperglycemia and its medical management. We propose a mathematical model that describes the competition between cancer cells and glucosedependent healthy cells for a shared glucose resource. We also include the metabolic reprogramming of healthy cells by cancer-cell-initiated mechanism to reflect the interplay between the two cell populations. We parametrize this model and carry out numerical simulations of various scenarios, with growth of tumor mass and loss of healthy body mass as endpoints. We report sets of cancer characteristics that show plausible disease histories. We investigate parameters that change cancer cells aggressiveness, and we exhibit differing responses in diabetic and non-diabetic, in the absence or presence of glycemic control. Our model predictions are in line with observations of weight loss in cancer patients and the increased growth (or earlier onset) of tumor in diabetic individuals. The model will also aid future studies on countermeasures such as the reduction of circulating glucose in cancer patients.

cancer biology↗