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Wu, C.-Y.

Publications and source records attributed to Wu, C.-Y..

At least 19 recordsLinked to original sources

Machine Learning-Guided Discovery of Bacterial-Selective Membrane-Active Compounds Reveals Mechanistic Bias in Antibiotic Training Datasets

The rise of antibiotic resistance necessitates the discovery of antibacterial compounds with novel mechanisms of action (MoAs). Recent machine learning approaches have shown promise in antibacterial compound discovery, but often identify derivatives of known antibiotic classes rather than mechanistically novel compounds. Previous approaches applied Tanimoto similarity filters at the end of screening pipelines, but this method has substantial drawbacks: Tanimoto similarity can be misleading in chemical space, and post-hoc filtering does not influence what activity models learn to prioritize. Here, we present a machine learning pipeline that addresses chemical novelty upfront by employing an XGBoost-based MoA classifier to explicitly prioritize compounds predicted to have mechanisms distinct from known antibiotic classes, combined with graph neural networks for antibacterial activity and toxicity prediction. Applied to the Zinc20 database, our approach successfully identified non-toxic antibacterial compounds structurally distinct from known antibiotics. Notably, the majority of these hits exhibited membrane-targeting activity with selectivity for bacterial cells over mammalian cells, suggesting potential for next-generation membrane-active antibiotics. However, we did not identify compounds with novel protein targets. Systematic analysis revealed that this limitation stems from mechanistic bias in training data rather than model architecture. Specifically, our activity model learned to preferentially score compounds similar to specific groups in the training data, thus overrepresenting certain MoA classes including membrane-active compounds. Even substantial model architecture and training data enhancements did not overcome this constraint. Our findings demonstrate that the primary bottleneck for discovering mechanistically novel antibiotics is the scarcity of diverse, mechanistically-annotated training data. This work provides both a methodological framework for mechanism-aware screening and critical insights into data requirements for genuinely novel antibiotic discovery.

bioinformatics↗

A comparison of scalable approaches for the pairwise analysis of large pathogen genomic and spatial datasets: an application to studying Mycobacterium tuberculosis transmission

Pairwise analysis of genomic and spatial data offers opportunities to identify and estimate the associations between covariates and the transmission of pathogens between individuals. However, such pairwise analyses are computationally intensive, and may not be feasible to conduct given the high dyad count in even moderately sized datasets. Here we compare two approaches to increase the efficiency of pairwise analysis for large datasets. We quantify and compare the performance of divide-and-conquer Bayesian model fitting and pairwise case-control approaches for estimating associations between individual- and pair-level covariates and shared membership in a transmission cluster. We utilize a large dataset (n=4,154) of spatially-referenced, genomically-sequenced Mycobacterium tuberculosis isolates collected from a single city for this analysis. We find that the case-control approach produces unbiased estimates of effect sizes with expected credible interval coverage and is more robust than the divide-and-conquer method when effect sizes are large. Thus, we recommend using the case-control approach with at least three controls per case to downscale datasets for pairwise analysis when analysis of the entire dataset is not possible. This approach mitigates the computational challenges of pairwise Bayesian modeling on datasets that require significant computational resources while maintaining desired inferential properties. Author SummaryPairwise analyses of large datasets to study pathogen transmission are computationally demanding because they typically require simultaneous analysis of each possible pair of individuals in a dataset; as datasets become larger these analyses often are not feasible to conduct even with access to high-performance computing resources. In this work, we compare a case-control approach and divide-and-conquer approaches for more efficient pairwise analysis of large datasets. Using a large dataset of Mycobacterium tuberculosis isolates including genetic and spatial data, we investigate the performance of each method for estimating the associations between host covariates and genetic clustering of isolates. We find that the case-control approach is generally preferred over methods which first divide the data into subsets and then combine results. While additional extensions of these analyses are needed to test the generality of these findings to other data settings, this work provides a practical way forward for the pairwise analysis of large datasets to study pathogen transmission.

microbiology↗

TIGIT-NECTIN2/3 signaling preserves ignorant CD8⁺ T cells for favorable immune checkpoint outcomes in HBV-related hepatocellular carcinoma

BackgroundImmune checkpoint inhibitors (ICIs) have revolutionized cancer therapy by restoring anti-tumor immunity. However, persistent antigen exposure drives T cell exhaustion, limiting the effectiveness of ICIs. Ignorant T cells are antigen-specific T cells that maintain a naive state by regaining stem-like properties, allowing them to remain fully responsive to subsequent immunization. Virus-related hepatocellular carcinoma (HCC) demonstrates superior responses to ICIs compared to non-viral HCC, prompting us to investigate whether immunologically ignorant T cells exist in HBV-associated HCC and represent a promising target for improving immunotherapy outcomes. MethodsSingle-cell RNA sequencing (scRNA-seq) was performed on tumor tissues from patients with HBV-associated HCC. For validation, immunostaining was conducted on the discovery cohort and an independent cohort of 16 non-B non-C HCC and 22 HBV HCC. The enrichment of TIGIT and NECTIN3 in the proposed ignorant T cell was further validated using the TCGA database. ResultsscRNA-seq identified distinct HBV-infected HCC populations and revealed NECTIN3 upregulation in HBV-enriched subsets. CellChat analysis uncovered a novel NECTIN3-TIGIT tumor-immune interaction in HBV-enriched subsets, which shifted toward TIGIT-NECTIN2 as viral transcription declines. Trajectory analysis revealed the emergence of ignorant CD8 T cells following T cell exhaustion. TIGIT-NECTIN2/3 interactions deliver a weak exhaustion signal. This allows T cells to survive and regain naive-like properties as ignorant cells. Integration of bulk RNA-seq data identified CD24, STMN1, and EZH2 as potential biomarkers of ignorant CD8 T cells. ConclusionsTIGIT-NECTIN2/3 interactions present a promising axis for preserving immunologically ignorant T cells and sustaining ICI responsiveness in HBV-associated HCC.

immunology↗

Phloiokeratosis - a new ichthyosiform hyperkeratotic cornification disorder in dogs with SUV39H1 variants

The continuous renewal of healthy epidermis depends on the finely regulated proliferation of basal keratinocytes and subsequent differentiation as the newly formed cells move upwards through the different layers of the epidermis. Perturbations in keratinocyte differentiation may lead to cornification disorders. We investigated seven dogs of different breeds belonging to four independent families that showed striking multifocal tree bark-like skin lesions. Histopathologically, lesional skin was characterized by pronounced epidermal and infundibular hyperkeratosis with epidermal and sebaceous gland hyperplasia. We therefore tentatively termed the phenotype phloiokeratosis, derived from the Greek word phloios for tree bark and keratosis indicating abnormal keratinization. Whole genome sequencing of DNA from affected dogs revealed four independent variants in the SUV39H1 gene encoding the SUV39H1 histone lysine methyltransferase, an H3K9 methyltransferase, which is involved in epigenetic silencing of chromatin. Phloiokeratosis is inherited as an X-chromosomal semi-dominant trait. Four of the affected dogs in our study were heterozygous females and had lesion patterns reminiscent of Blaschko lines. In two of them, trio analyses experimentally confirmed de novo mutation events in the SUV39H1 gene. Previously, Suv39h1-/- knockout mice had been reported to have normal skin. So far, no human patients with SUV39H1 loss-of-function variants have been reported. The findings in SUV39H1 mutant dogs with phloiokeratosis for the first time link SUV39H1 deficiency to a heritable skin phenotype. Our study highlights the essential role of SUV39H1-mediated epigenetic silencing during normal keratinocyte differentiation and provides a unique model for further investigations. Author SummaryThe integrity of the skin depends on a balanced equilibrium of keratinocyte proliferation, differentiation, and sloughing of terminally differentiated cells into the environment requiring finely regulated changes in the global transcriptome of differentiating keratinocytes. We investigated seven dogs belonging to four different families with a new disorder of cornification characterized by tree bark-like outgrowths of the epidermis. Histopathological examinations confirmed that the outermost layer of the epidermis was thickened in affected dogs. The genetic analysis yielded four different SUV39H1 loss-of-function variants in the affected dogs from the four families. The SUV39H1 gene encodes an enzyme that is involved in the epigenetic silencing of chromatin. The newly characterized inherited skin disease in dogs is the first clinical phenotype that has been linked to SUV39H1 deficiency. Most likely, SUV39H1 deficiency leads to delayed epigenetic silencing and consequently delayed differentiation of keratinocytes. Dogs with this rare skin disease provide an improved understanding of the essential role of SUV39H1 in the epigenetic control of gene expression in skin.

genetics↗

Mitochondrial COX4I2 drives pericyte-dependent inflammation and emphysema

Chronic obstructive pulmonary disease (COPD) is characterized by neutrophilic inflammation, emphysema, and mild pulmonary hypertension (PH). Oxidative/nitrosative stress are key drivers, but specific mitochondrial mechanisms remain unclear. We show increased expression of the regulatory mitochondrial cytochrome c oxidase subunit 4 isoform 2 (COX4I2) in an early murine model and human COPD. After 8 months of cigarette smoke exposure, Cox4i2-/- mice were completely protected from emphysema but not from PH, associated with reduced nitrosative stress, inflammation, and apoptosis. Using a novel Cox4i2 reporter mouse and in situ hybridization of human lungs, COX4I2 was detected in precapillary ACTA2+ cells and capillary pericytes. COX4I2 promotes mitochondrial reactive oxygen species (mtROS) production in these cells, thereby enhancing neutrophil migration and alveolar type II cell apoptosis, and modulates angiogenesis. In contrast to Cox4i2-/-, mitochondria-targeted antioxidant MitoQ reversed emphysema and PH, suggesting pericyte-specific regulation of COPD pathologies and mtROS inhibition as a therapeutic approach in COPD. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=124 SRC="FIGDIR/small/703513v1_ufig1.gif" ALT="Figure 1"> View larger version (39K): org.highwire.dtl.DTLVardef@83bca4org.highwire.dtl.DTLVardef@d5ebaborg.highwire.dtl.DTLVardef@632d1borg.highwire.dtl.DTLVardef@1267a13_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

Innovative Methods for Prenatal Cannabis Exposure: Vapor Inhalation Chamber and Metabolite Quantification in Prairie Voles and Rats

The increasing prevalence of cannabis use, including among pregnant women, highlights the critical need for a deeper understanding of prenatal cannabis exposure. This study aimed to develop a standardized cross-species inhalation exposure protocol to administer the principal psychoactive component of cannabis, {Delta}9-tetrahydrocannabinol (THC), to prairie voles (Microtus ochrogaster) and laboratory rats (Rattus norvegicus), and to investigate the distribution of THC in maternal and fetal tissues following prenatal exposure. Using an established e-cigarette system for delivering vaporized THC, we administered THC to pregnant prairie voles and rats. THC concentrations were measured in maternal plasma and fetal brain tissue using LC-MS/MS (Liquid Chromatography coupled with Tandem Mass Spectrometry). In both species, THC levels were compared across groups to evaluate the impact of fetal position on THC uptake. We found that THC readily crossed the placental barrier in both species, resulting in significantly higher concentrations of THC in the fetal brain within the THC-exposed groups compared to the vehicle controls. Interspecies comparison revealed higher THC concentrations in rat fetal brain tissue compared to prairie voles. No significant effects of fetal position on THC levels were found for either species. The findings confirm placental transfer of THC and reveal species-specific patterns of THC distribution. Additional studies were then carried out in voles to compare plasma and brain THC levels in maternal and virgin adult prairie voles. Maternal brain THC concentrations were significantly higher than fetal brain concentrations in prairie voles. Strong positive correlations were observed between plasma and brain THC concentrations in both maternal and virgin adult prairie voles. This study establishes a translational model for investigating prenatal cannabis exposure using an aerosolized administration method in voles compared to established methods in rats. The standardized protocol and results provide a foundation for future research into the developmental consequences of prenatal cannabis exposure and offer crucial insights for informing public health policies and clinical practices in response to the global increase in cannabis use.

neuroscience↗

Cigarette smoking upregulates vascular expression of the novel atherosclerosis risk factor ADAMTS-7

BackgroundCigarette smoking is an established risk factor for coronary artery disease (CAD) and myocardial infarction. Genetic variants in the extracellular matrix protease ADAMTS-7 were also identified to increase CAD risk. Notably, ADAMTS7 represents the only genomic locus that revealed a gene-environment interaction with smoking. The underlying mechanisms of this interaction remain unclear. Methods and ResultsIn a murine model, cigarette smoke exposure (CSE) led to an upregulation of vascular ADAMTS7 expression in wild type (WT) C57BL/6J mice. ADAMTS7 upregulation was also found in carotid plaques from ever-smokers undergoing carotid endarterectomy in humans. Bulk RNA sequencing of lung tissues from WT mice exposed to CS revealed a downregulation of 20 and an upregulation of 173 transcripts. Among upregulated transcripts in smoking-exposed lungs, we found C-C motif chemokine ligand 17 (CCL17), which was likewise upregulated in plasma from smoking mice and humans. In vitro, recombinant CCL17 upregulated ADAMTS7 expression in primary vascular smooth muscle cells (VSMC), which was inhibited secondary to silencing of CCL17s bona fide receptor C-C Motif Chemokine Receptor 4 (CCR4). Conditioned media from CCL17-stimulated VSMC lacking ADAMTS-7 showed reduced release of inflammatory cytokines by endothelial cells (EC), reduced EC activation, and monocyte-to-EC adhesion. In proatherogenic Apoe-/- mice exposed to CS, more numerous neutrophils, inflammatory monocytes, and macrophages were found in atherosclerotic plaques as compared to room air exposition. This effect was blunted in Apoe-/-Adamts7-/- mice. ConclusionsFor the first time, our findings link CSE to vascular inflammation via CCL17-mediated upregulation of the CAD risk factor ADAMTS7 and provide a mechanistic explanation for the gene-environment interaction between CS and ADAMTS7 in CAD. Targeting ADAMTS-7 might be a promising therapeutic strategy irrespective of smoking status. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=85 SRC="FIGDIR/small/685237v1_ufig1.gif" ALT="Figure 1"> View larger version (16K): org.highwire.dtl.DTLVardef@1d8366eorg.highwire.dtl.DTLVardef@1dda3feorg.highwire.dtl.DTLVardef@39a4bcorg.highwire.dtl.DTLVardef@6e58b6_HPS_FORMAT_FIGEXP M_FIG C_FIG

physiology↗

Mobilization of nuclear antiviral factors by Exportin XPO1 via the actin network inhibits RNA virus replication

The intricate interplay between +RNA viruses and their hosts involves the exploitation of host resources to build virus-induced membranous replication organelles (VROs) in cytosol of infected cells. Previous genome- and proteome-wide approaches have identified numerous nuclear proteins, including restriction factors that affect replication of tomato bushy stunt virus (TBSV). However, it is currently unknown how cells mobilize nuclear antiviral proteins and how tombusviruses manipulate nuclear-cytoplasmic communication. The authors discovered that XPO1/CRM1 exportin plays a central role in TBSV replication in plants. Based on knockdown, chemical inhibition, transient expression and in vitro experiments, we show that XPO1 acts as a cellular restriction factor against TBSV. XPO1 is recruited by TBSV p33 replication protein into the cytosolic VROs via direct interaction. Blocking nucleocytoplasmic transport function of XPO1 inhibits delivery of several nuclear antiviral proteins into VROs resulting in dampened antiviral effects. The co-opted actin network is critical for XPO1 to deliver nuclear proteins to VROs for antiviral activities. We show that XPO1 and XPO1-delivered restriction factors accumulate in vir-condensates associated with membranous VROs. Altogether, the emerging theme on the role of vir-condensates is complex: we propose that vir-condensate serves as a central battleground between virus and the host for supremacy in controlling virus infection. It seems that the balance between co-opted pro-viral and antiviral factors within vir-condensates associated with membranous VROs could be a major determining factor of virus replication and host susceptibility. We conclude that XPO1 and nuclear antiviral cargos are key players in nuclear-cytoplasmic communication during cytosolic +RNA virus replication. SignificanceTomato bushy stunt virus (TBSV), similar to other (+)RNA viruses, replicates in the cytosol and exploits organellar membrane surfaces to build viral replication organelles (VROs) that represent the sites of virus replication. The authors discovered that XPO1 exportin nuclear shuttle protein inhibited TBSV replication in plants. The conserved XPO1 is a central protein interaction nod, which propelled nucleocytoplasmic transport of several viral restriction factors into the cytosolic VROs that restricted tombusviruses replication. The delivered virus restriction factors provided inhibitory functions within virus-induced condensates associated with membranous VROs. The authors propose that the VRO-associated condensate serves as a central battleground between virus and the host for supremacy in controlling virus infection. Altogether, XPO1 is a critical protein interaction hub with major implications in viral replication. The authors conclude that XPO1 and its nuclear antiviral cargos are key players in nuclear-cytoplasmic communication during cytosolic (+)RNA virus replication.

microbiology↗

A spontaneous mutation in ADIPOR1 causes retinal degeneration in mice

Adiponectin receptor 1 (ADIPOR1) is a transmembrane protein necessary for normal anatomy and physiology in the retina. In a recent study of complement factor H knockout mice (Cfh-/-), our lab discovered a flecked retina phenotype and retinal thinning by fundus imaging and optical coherence tomography (OCT), respectively. The phenotype was observed in a subset (50%) of Cfh-/- mice. The thinning observed in vivo is due to an early degeneration of rod photoreceptors. This phenotype has not been reported in published studies of Cfh-/- mice. AdipoR1 knockout mice (AdipoR1-/-) and mice deficient in Membrane Frizzled Related Protein (MFRP) exhibit this phenotype, suggesting an involvement in the emergence of the retinal degeneration observed in a subset of Cfh-/- mice. Cfh and AdipoR1 are located in close proximity on mouse Chromosome 1 (Chr1) and a complementation cross between Cfh and AdipoR1 mice with retinal degeneration produced 100% progeny with retinal degeneration. Sequencing of the Cfh-/- mice revealed a c.841 C > T mutation in AdipoR1. Furthermore, one Cfh wildtype (of Cfh+/+) and 2 heterozygous (of Cfh+/-) mice exhibited retinal degeneration and were homozygous for the point mutation. The c.841 C > T mutation results in a proline to serine conversion at position 281 (P281S) in ADIPOR1. This residue is critical for ADIPOR1 open and closed conformations in the membrane. In silico modeling of candidate ADIPOR1 ligands, 11-cis-retinaldehyde and docosahexaenoic acid (DHA), that are deficient in AdipoR1-/-, suggests that ADIPOR1 is involved in trafficking retinoids and fatty acids and their combined deficiency in the ADIPOR1 mutant retinas might explain the retinal degeneration phenotype.

neuroscience↗

Identification of Novel Biomarkers for Alzheimer's Disease and Related Dementias Using Unbiased Plasma Proteomics

Alzheimers disease (AD) and related dementias (ADRD) is a complex disease with multiple pathophysiological drivers that determine clinical symptomology and disease progression. These diseases develop insidiously over time, through many pathways and disease mechanisms and continue to have a huge societal impact for affected individuals and their families. While emerging blood-based biomarkers, such as plasma p-tau181 and p-tau217, accurately detect Alzheimer neuropthology and are associated with faster cognitive decline, the full extension of plasma proteomic changes in ADRD remains unknown. Earlier detection and better classification of the different subtypes may provide opportunities for earlier, more targeted interventions, and perhaps a higher likelihood of successful therapeutic development. In this study, we aim to leverage unbiased mass spectrometry proteomics to identify novel, blood-based biomarkers associated with cognitive decline. 1,786 plasma samples from 1,005 patients were collected over 12 years from partcipants in the Massachusetts Alzheimers Disease Research Center Longitudinal Cohort Study. Patient metadata includes demographics, final diagnoses, and clinical dementia rating (CDR) scores taken concurrently. The ProteographTM Product Suite (Seer, Inc.) and liquid-chromatography mass-spectrometry (LC-MS) analysis were used to process the plasma samples in this cohort and generate unbiased proteomics data. Data-independent acquisition (DIA) mass spectrometry results yielded 36,259 peptides and 4,007 protein groups. Linear mixed effects models revealed 138 differentially abundant proteins between AD and healthy controls. Machine learning classification models for AD diagnosis identified potential candidate biomarkers including MBP, BGLAP, and APoD. Cox regression models were created to determine the association of proteins with disease progression and suggest CLNS1A, CRISPLD2, and GOLPH3 as targets of further investigation as potential biomarkers. The Proteograph workflow provided deep, unbiased coverage of the plasma proteome at a speed that enabled a cohort study of almost 1,800 samples, which is the largest, deep, unbiased proteomics study of ADRD conducted to date.

neuroscience↗

A shift in the host web occupancy of dew-drop spiders associated with genetic divergence in the Southwest Pacific

AimWe assessed the population genetic structure of the kleptoparasitic spider Argyrodes bonadea across the Southwestern Pacific islands. Our focus is on assessing the impact of overseas distances and, in particular, the Kerama gap, as potential drivers of genetic differentiation. We found that the spider kleptoparasites switch to a specific host species is associated with significant genetic variation at fine scales, whereas the same species adoption of a generalist host strategy has likely facilitated its broad dispersal, colonization, and recent range expansion across the southwestern Pacific, and is associated with a lack of geographically- structured genetic variation in these latter, subsequently-colonized landmasses. LocationSouthwestern Pacific Islands TaxonArgyrodes bonadea MethodsWe used mitochondrial Cytochrome Oxidase 1 (CO1) gene sequences, and Restriction Site-associated DNA Sequencing (RAD-seq) for our analyses. ResultsTwo strongly supported lineages, an Amami-Okinawa Lineage (AOL) and an Austral-Asia Lineage (AAL) correspond to two separate clades, roughly divided by the Kerama Gap, in phylogenetic trees estimated here. However, species delimitation led to the interpretation of only a single species present. The AOL exhibits complex, geographically-structured host web spider species specificity, wherein the Amami population utilizes Cyrtophora, but AOL samples in Okinawa associates exclusively with Nephila--and yet all broadly distributed AAL populations show no evidence of host web spider species specificity. Main conclusionThe population boundary between AOL and AAL likely results from local adaptation to novel hosts--instead of isolation by the Kerama Gap--following long-distance dispersal and range expansion. Our results suggest kleptoparasitic spiders have the capacity to overcome permanent deep-sea barriers and colonize distant landmasses. Whereas peripheral populations (AOL) demonstrate the capacity for specialization to a single host, which may have contributed to genetic differentiation and isolation, the broadly-distributed AAL persists and has successfully expanded its geographical range as a host generalist, which may contribute to ongoing gene flow inferred in this study.

evolutionary biology↗

The heparin-binding domain of VEGF165 directly binds to integrin αvβ3 and plays a critical role in signaling.

VEGF-A is a key cytokine in tumor angiogenesis and a major therapeutic target for cancer. VEGF165 is the predominant isoform and is the most potent angiogenesis stimulant. VEGFR2/KDR domains 2 and 3 (D2D3) bind to the N-terminal domain (NTD, residues 1-110) of VEGF165. Since removal of the heparin-binding domain (HBD, residues 111-165) markedly reduced the mitogenic activity of VEGF165, it has been proposed that the HBD plays a critical role in the mitogenicity of VEGF165. Integrin v{beta}3 has been shown to bind to VEGF165, but the role of integrin v{beta}3 in VEGF165 signaling are unclear. Here we describe that v{beta}3 specifically bound to the isolated HBD, but not to the NTD. We identified several critical amino acid residues in HBD for integrin binding (Arg-123, Arg-124, Lys-125, Lys-140, Arg-145, and Arg-149) by docking simulation and mutagenesis, and generated full-length VEGF165 that is defective in integrin binding by including mutations in the HBD. The full-length VEGF165 mutant defective in integrin binding (R123A/R124A/K125A/K140A/R145A/R149A) was defective in ERK1/2 phosphorylation, integrin {beta}3 phosphorylation, and KDR phosphorylation, although the mutation did not affect KDR binding to VEGF165. We propose a model in which VEGF165 induces KDR (through NTD)-VEGF165 (through HBD)-integrin v{beta}3 ternary complex formation on the cell surface and this process is critically involved in potent mitogenicity of VEGF165.

biochemistry↗

Successive responses of three coral holobiont components (coral hosts, symbiotic algae, and bacteria) to daily temperature fluctuations

Coral reef ecosystems support over a quarter of the worlds marine life and play important ecological and economic roles. However, the increasingly severe weather events associated with ocean warming and climate change are believed to be rapidly altering the functions of coral reefs and their ecosystems. Corals and their associated microbiota form a "holobiont," which includes symbiotic algae and other associated microbiota dominated by bacteria. These microbiota have a direct relationship with the health of the coral host. Their composition is influenced by various environmental factors, such as increasing sea water temperatures. Previous studies of the effects of temperature changes on coral physiology and associated bacterial communities have been conducted based on stable water temperatures set by mean temperatures, or by slowly increasing/decreasing temperatures. However, the daily temperature fluctuations that corals experience in nature are not stable. Rather, there may be significant differences of up to 6{degrees}C in a single day. The current understanding of the effects of large daily temperature fluctuations on coral and associated bacterial community dynamics is limited. Hence, in this study, we conducted a four-week tank experiment using different large daily temperature fluctuations accompanied by continuous warming conditions to investigate the effects on two common reef-building corals, Stylophora pistillata and Pocillopora acuta, in Taiwan. During the experiment, the activity of coral host catalase was measured, the photosynthetic ability of symbiotic algae was recorded, and the variation in bacterial communities was analyzed using the V6-V8 region of 16S rDNA. According to the results, different parts of the holobionts of different coral species exhibited varying response rates to the continuous warming conditions and diurnal temperature fluctuations. Additionally, it was found that diurnal temperature fluctuations may mitigate the heat stress on the host and reduce the changes in bacterial response to warming. Furthermore, the holobionts of different coral species may adopt different adaptation and survival strategies in response to diurnal temperature fluctuations and warming. Finally, based on the response of these two coral species under the conditions of diurnal temperature fluctuations and continuous warming, Acinetobacter and Rhodobacteraceae were identified as potential indicator coral-associated bacteria. This is the first study to investigate the tripartite dynamic response of coral, symbiotic algae and bacteria to daily temperature fluctuations.

microbiology↗

Niche differential gene expression analysis in spatial transcriptomics data identifies context-dependent cell-cell interactions

Single cells influence, and are shaped by, their local spatial niche. Technologies for in situ measurement of gene expression at the transcriptome scale have enabled the detailed profiling of the spatial distributions of cell types in tissue as well as the interrogation of local signaling patterns between cell types [1]. Towards these goals, we propose a new statistical procedure called niche-differential expression (niche-DE) analysis. Niche-DE identifies cell-type specific niche-associated genes, defined as genes whose expression within a specific cell type is significantly up- or down-regulated, in the context of specific spatial niches. We develop effective and interpretable measures for global false discovery control and show, through the analysis of data sets generated by myriad protocols, that the method is robust to technical issues such as over-dispersion and spot swapping. Niche-DE can be applied to low-resolution spot- and ROI-based spatial transcriptomics data as well as data that is single-cell or subcellular in resolution. Based on niche-DE, we also develop a procedure to reveal the ligand-receptor signaling mechanisms that underlie niche-differential gene expression patterns. When applied to 10x Visium data from liver metastases of colorectal cancer, niche-DE identifies marker genes for cancer-associated fibroblasts and macrophages and elucidates ligand-receptor crosstalk patterns between tumor cells, macrophages and fibroblasts. Co-detection by indexing (CODEX) was performed on the same patient samples, to corroborate the niche-DE results.

bioinformatics↗

Ultrastructural characterization of a viral RNA and G-protein containing, membranous organelle formed in respiratory syncytial virus infected cells

Withdrawal statementThe authors have withdrawn their manuscript because since deposition of this preprint, they have become aware of the possibility that the findings reported may be an artefact. Carter et al. (J Struct Biol 2018 Jan;201(1):15-25. doi: 10.1016/j.jsb.2017.10.009) have reported that multilamellar bodies exhibit autofluorescence under cryogenic conditions. Thus, there is a possibility that stress induced by virus infection may stimulate formation of the features reported in this article, and autofluorescence, rather than specific labelling led them to identify the puncta as compartments containing RSV proteins or genomes. They are working to address these issues. Therefore, the authors do not wish this work to be cited as reference for the project. If you have any questions, please contact the corresponding author.

microbiology↗

In-vivo characterization of glutamine metabolism identifies therapeutic targets in clear cell renal cell carcinoma

Targeting metabolic vulnerabilities has been proposed as a therapeutic strategy in renal cell carcinoma (RCC). Here, we analyzed metabolism in patient-derived xenografts (tumorgrafts) from diverse forms of RCC. Tumorgrafts from VHL-mutant clear cell RCC (ccRCC) retained metabolic features of human ccRCC and engage in oxidative and reductive glutamine metabolism. We used several approaches to suppress glutamine metabolism and test the effect on tumor growth. Genetic silencing of isocitrate dehydrogenase-1 or -2 impaired reductive labeling of TCA cycle intermediates and suppressed tumor growth. Glutaminase inhibition resulted in modest growth suppression and variable effects on glutamine metabolism in vivo. Infusions with [amide-15N]glutamine revealed persistent amidotransferase activity during glutaminase inhibition, and blocking these activities with the amidotransferase inhibitor JHU-083 also reduced tumor growth. We conclude that ccRCC tumorgrafts catabolize glutamine via multiple pathways, perhaps explaining why it has been challenging to achieve therapeutic responses in patients by inhibiting glutaminase. TeaserGlutamine fuels the TCA cycle and amidotransferase pathways in clear cell renal cell carcinoma.

cancer biology↗

Anti-PF4 (heparin-independent)/PF4 complex induces allosteric activation of integrins αIIbβ3 and αvβ3, a potential mechanism of vaccine-induced thrombotic thrombocytopenia (VITT) and autoimmune diseases

The classical immune-mediated heparin-induced thrombocytopenia (HIT) is induced by autoantibody against platelet-factor 4 (PF4)/heparin complex. Vaccine-induced thrombotic thrombocytopenia (VITT) and autoimmune HIT (aHIT) are induced by anti-PF4 in a heparin-independent manner. Activation of platelet integrin IIb{beta}3 is a key event that leads to IIb{beta}3 binding to fibrinogen and platelet aggregation, but is not involved in current models of HIT or VITT. Anti-PF4 (heparin-independent) is also detected in autoimmune diseases (e.g., SLE). However, the role of anti-PF4 in these diseases is unknown. Previous studies showed that several pro-inflammatory chemokines potently activated integrins by binding to the allosteric site (site 2). PF4 is known to be inhibitory since it inhibits angiogenesis and tumor growth. Here we describe that PF4 was predicted to bind to site 2 of IIb{beta}3 by docking simulation, but did not activate it. However, PF4/anti-PF4 mAb (RTO, heparin-independent) complex potently activated it at biological concentrations of PF4 (<1 g/ml), but anti-PF4/heparin (KKO) did not. This indicates that RTO changed the phenotype of PF4. We generated PF4 mutants defective in site 2 binding to integrin by introducing mutations in the predicted site 2 binding site of PF4. A PF4 mutant/RTO complex was defective in activating integrins. Furthermore, this PF4 mutant acted as an antagonist of PF4/RTO-induced integrin activation. We obtained similar results with vascular integrin v{beta}3. We propose that a potential mechanism, in which PF4/RTO complex binds to site 2 and activates integrins and triggers thrombocytopenia or autoimmune diseases. The inhibitory PF4 mutant may have potential as a therapeutic.

immunology↗

Cancer subclone detection based on DNA copy number in single cell and spatial omic sequencing data

In cancer, somatic mutations such as copy number alterations (CNAs) accumulate during disease progression and lead to functional intra-tumor heterogeneity that can influence the efficacy of cancer therapy. Therefore, studying the functional characteristics and spatial distribution of genetically distinct subclones is crucial to the understanding of tumor evolution and the design of cancer treatment. Here, we present Clonalscope, a method for subclone detection using copy number profiles that can be applied to spatial transcriptomics (ST) data and data from single-cell sequencing platforms such as scRNA-seq and scATAC-seq. Clonalscope implements a nested Chinese restaurant process to identify de novo subclones within one or multiple samples from the same patient. Clonalscope incorporates prior information from paired whole-genome or whole-exome sequencing (WGS/WES) data to achieve more reliable subclone detection and malignant cell labeling. On scRNA-seq and scATAC-seq data from four gastrointestinal tumor samples, Clonalscope successfully labeled malignant cells and identified genetically different subclones, which were validated in detail using matched scDNA-seq data. On ST data from a squamous cell carcinoma and two invasive ductal carcinoma samples, Clonalscope successfully labelled malignant spots, traced subclones between associated datasets, and identified spatially segregated subclones expressing genes associated with drug resistance and survival.

bioinformatics↗