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Ge, W.

Publications and source records attributed to Ge, W..

At least 37 records · Page 2Linked to original sources

Glioblastoma Neurovascular Progenitor Orchestrates Tumor Cell Type Diversity

Glioblastoma (GBM) exhibits developmental programs and marked cellular heterogeneity, yet how these features are organized into connected lineage hierarchies remains unclear. Here we identify a rare tumor-intrinsic population, termed the neurovascular progenitor (NVP), that occupies an intermediate position between the major GBM organizational axes. NVP cells co-express neural progenitor and perivascular transcriptional features, are consistently detected across independent patient cohorts, retain canonical GBM copy-number alterations, and localize in situ in both vessel-associated and parenchymal niches. Using direct-from-patient lineage tracing in a human organoid tumor transplantation system, we show that individual NVP cells clonally generate both neural-like and mesenchymal/vascular-like malignant progeny, providing a concrete lineage link between states that are commonly considered mutually exclusive. Despite comprising [~]1% of tumor cells, NVP-derived lineages account for a majority of observed tumor cell types and disproportionately contribute to cycling compartments. Orthogonally, ablation of NVP-associated programs in an in vivo GBM model remodels tumor composition, elicits compensatory progenitor states, and significantly prolongs survival. Together, these findings position NVP as a fate-restricted yet highly influential lineage intermediate that serves as a functional bridge and organizational nexus within GBM hierarchies, linking population-level lineage architecture to the behavior of a specific progenitor cell type.

cancer biology↗

Human Organoid Tumor Transplantation Identifies Functional Glioblastoma - Microenvironmental Communication Mediated by PTPRZ1

Glioblastoma, the most aggressive and deadly form of primary brain cancer, is driven by both intrinsic cellular properties and external factors from the tumor microenvironment. Here, we leverage our novel human organoid tumor transplantation (HOTT) system to explore how extrinsic cues modulate glioblastoma cell type specification, heterogeneity, and migration. We show that HOTT recapitulates the core features of major patient tumor cell types and key aspects of peritumor cell types, while providing a human microenvironment that uniquely enables perturbations in both the patient tumor and its microenvironment. Our exploration of patient tumor - microenvironmental interactions in HOTT highlighted PTPRZ1, a receptor tyrosine phosphatase implicated in tumor migration, as a key player in intercellular communication. We observed that tumor knockdown of PTPRZ1 recapitulated previously described roles in migration and maintaining progenitor identity. Unexpectedly, environmental PTPRZ1 knockdown drove opposite migration and cell fate changes in the tumor, even when the tumor was not manipulated. This previously undiscovered mode of tumor-microenvironmental communication highlights the need to study human glioblastoma in the context of a human microenvironment such as HOTT.

cancer biology↗

Role of Y box-binding protein 1 (Ybx1/ybx1) in zebrafish folliculogenesis: Promoting follicle cell proliferation via suppression of cell cycle inhibitor p21 (cdkn1a)

Y box-binding protein 1 (YB-1; Ybx1/ybx1) regulates transcription and translation of targeted genes through DNA/RNA-binding. Our research in zebrafish has revealed a high abundance of Ybx1 in the primary growth (PG) follicles in the ovary, which decreases precipitously as the follicles enter the secondary growth (SG) phase. To understand the function of Ybx1 in folliculogenesis, we created an ybx1 mutant using TALEN and observed a disruption in folliculogenesis in the mutant (ybx1-/-) during the transition from previtellogenic (PV) to early vitellogenic (EV) stage of the SG phase, resulting in underdeveloped ovaries and reduced female fertility. Transcriptome and Western blot analyses identified several differentially expressed genes between mutant (ybx1-/-) and control (ybx1+/-) ovaries. Notably, the expression of cdkn1a (p21), a cell cycle inhibitor, increased dramatically in ybx1-/- follicles. Disrupting cdkn1a gene with CRISPR/Cas9 resulted in embryonic lethality. In p21 heterozygote (cdkn1a+/-), however, follicle activation and maturation in the ovary were both advanced, contrasting with the ybx1-/- mutant. Interestingly, partial loss of p21 could alleviate the phenotype of ybx1-/-. Folliculogenesis resumed in ybx1-/-;p21+/- females with normal follicle activation (PG-PV transition) and vitellogenic growth (PV-EV transition). Interestingly, the follicle cells from the ybx1-/- mutant displayed a poor proliferative activity both in vivo and in vitro; however, the cells from the ybx1-/-;p21+/- follicles resumed normal proliferation. In conclusion, our study suggests that Ybx1 serves a pivotal role in controlling early folliculogenesis in zebrafish, and its acts, at least partly, by repressing the expression of cdkn1a, a cell cycle inhibitor.

developmental biology↗

The sterol C-24 methyltransferase encoding gene, erg6, is essential for viability of Aspergillus species.

Ergosterol is a critical component of fungal plasma membranes. Although many currently available antifungal compounds target the ergosterol biosynthesis pathway for antifungal effect, current knowledge regarding ergosterol synthesis remains incomplete for filamentous fungal pathogens like Aspergillus fumigatus. Here, we show for the first time that the lipid droplet-associated sterol C-24 methyltransferase, Erg6, is essential for A. fumigatus viability. We further show that this essentiality extends to additional Aspergillus species, including A. lentulus, A. terreus, and A. nidulans. Neither the overexpression of a putative erg6 paralog, smt1, nor the exogenous addition of ergosterol could rescue erg6 deficiency. Importantly, Erg6 downregulation results in a dramatic decrease in ergosterol and accumulation in lanosterol and is further characterized by diminished sterol-rich plasma membrane domains (SRDs) at hyphal tips. Unexpectedly, erg6 repressed strains demonstrate wild-type susceptibility against the ergosterol-active triazole and polyene antifungals. Finally, repressing erg6 expression reduced fungal burden accumulation in a murine model of invasive aspergillosis. Taken together, our studies suggest that Erg6, which shows little homology to mammalian proteins, is potentially an attractive antifungal drug target for therapy of Aspergillus infections. IMPORTANCEA. fumigatus is the most common pathogen that causes invasive aspergillosis, a life-threatening fungal infection with more than 300,000 cases reported annually. Available antifungals to treat Aspergillus-related infection are limited to three drug classes targeting the plasma membrane (ergosterol) or the cell wall, each of which suffer from either host toxicity or rising resistance levels. As ergosta-type sterols are absent in mammalian cells but are essential for fungal viability, the ergosterol biosynthesis pathway remains an enticing target for the development of new antifungals. Although ergosterol biosynthesis has been well studied in model yeast, only a few genes have been genetically characterized in A. fumigatus. Here, we characterize Erg6, one of the fungus-specific sterol biosynthesis genes, as an essential gene in Aspergillus species. We further provide in vivo evidence of the importance of Erg6 for establishment of invasive aspergillosis. Given the importance of Erg6 in other fungal systems for growth, stress resistance, and virulence, our study suggests that development of Erg6 inhibitors may be a promising strategy for developing novel broad-spectrum antifungals.

microbiology↗

AbFold -- an AlphaFold Based Transfer Learning Model for Accurate Antibody Structure Prediction

MotivationAntibodies are a group of proteins generated by B cells, which are crucial for the immune system. The importance of antibodies is ever-growing in pharmaceutics and biotherapeutics. Despite recent advancements pioneered by AlphaFold in general protein 3D structure prediction, accurate structure prediction of antibodies still lags behind, primarily due to the difficulty in modeling the Complementarity-determining regions (CDRs), especially the most variable CDR-H3 loop. ResultsThis paper presents AbFold, a transfer learning antibody structure prediction model with 3D point cloud refinement and unsupervised learning techniques. AbFold consistently produces state-of-the-art results on the prediction accuracy of the six CDR loops. The predictions of AbFold achieve an average RMSD of 1.51 [A] for both heavy and light chains and an average RMSD of 3.04 [A] for CDR-H3, bettering current models AlphaFold and IgFold. AbFold will contribute to antibody structure prediction and design processes.

bioinformatics↗

Phenotypical Rescue of Bmp15 Deficiency by Mutation of Inhibin α (inha) Provides Novel Clues to How Bmp15 Controls Zebrafish Folliculogenesis

As an oocyte-specific growth factor, bone morphogenetic protein 15 (BMP15) plays a critical role in controlling folliculogenesis. However, the mechanism of BMP15 action remains elusive. Using zebrafish as the model, we created a bmp15 mutant using CRISPR/Cas9 and demonstrated that bmp15 deficiency caused a significant delay in follicle activation and puberty onset followed by complete arrest of follicle development at previtellogenic stage without yolk accumulation. The mutant females eventually underwent female-to-male sex reversal to become functional males, which was accompanied by a series of changes in secondary sexual characteristics. Interestingly, the blockade of folliculogenesis and sex reversal in bmp15 mutant could be rescued by the loss of inhibin (inha-/-). The follicles of double mutant (bmp15-/-;inha-/-) could progress to mid-vitellogenic stage with yolk accumulation and the fish maintained their femaleness without sex reversal. Transcriptome analysis revealed up-regulation of pathways related to TGF-{beta} signaling and endocytosis in the double mutant follicles. Intriguingly, the expression of inhibin/activin {beta}Aa subunit (inhbaa) increased significantly in the double mutant ovary. Further knockout of inhbaa in the triple mutant (bmp15-/-;inha-/-;inhbaa-/-) resulted in the loss of yolk granules again in the oocytes although the follicles could continue to grow beyond the size range of previtellogenic stage. The serum levels of estradiol (E2) and vitellogenin (Vtg) both decreased significantly in bmp15 single mutant females, returned to normal in the double mutant (bmp15-/-;inha-/-), but reduced again significantly in the triple mutant (bmp15-/-;inha-/-;inhbaa-/-). E2 treatment could rescue the vitellogenic follicles in bmp15-/-, and fadrozole (a nonsteroidal aromatase inhibitor) treatment blocked yolk accumulation in bmp15-/-;inha-/- fish. In summary, the present study provided comprehensive genetic evidence for the interaction of bmp15 pathways and the activin-inhibin system in regulating folliculogenesis, in particular E2 production from the follicle, Vtg biosynthesis in the liver and its update by the developing oocytes.

developmental biology↗

Genomic heterogeneity and ploidy identify patients with intrinsic resistance to PD-1 blockade in metastatic melanoma

While the introduction of immune checkpoint blockade (ICB) has dramatically improved clinical outcomes for patients with advanced melanoma, a significant proportion of patients develop resistance to therapy, and mechanisms of resistance are poorly elucidated in most cases. Further, while combination ICB has higher response rates and improved progression free survival compared to single agent therapy in the front line setting, there is significantly increased toxicity with combination ICB, and biomarkers to identify patients who would disproportionately benefit from combination therapy vs aPD-1 ICB are poorly characterized. To understand resistance mechanisms to single vs combination ICB therapy, we analyze whole-exome-sequencing (WES) of pre-treatment tumor and matched normals of 4 cohorts (n=140) of previously ICB-naive aPD-1 ICB treated patients. We find that high intratumoral genomic heterogeneity and low ploidy identify patients with intrinsic resistance to aPD-1 ICB. Comparing to a melanoma cohort from a pre-targeted therapy and ICB time period ("untreated" cohort), we find that genomic heterogeneity specifically predicts response and survival in the ICB treated cohorts, but not in the untreated cohort, while ploidy is also prognostic of overall survival in the "untreated" (by targeted therapy or ICB) group. To establish clinically actionable predictions, we optimize a simple decision tree using genomic ploidy and heterogeneity to identify with high confidence (90% PPV) a subset of patients with intrinsic resistance to and significantly worse survival on aPD1 ICB treatment. We then validate this model in independent cohorts, and further show that a significant proportion of patients predicted to have intrinsic resistance to single agent aPD-1 ICB respond to combination ICB, which suggests that nominated patients may benefit disproportionately from combination ICB. We further show that the features and predictions of the model are independent of known clinical features and previously nominated molecular biomarkers. These findings highlight the clinical and biological importance of genomic heterogeneity and ploidy, and sets a concrete framework towards clinical actionability, broadly advancing precision medicine in oncology.

cancer biology↗

Genetic Analysis of Activin/Inhibin β Subunits in Zebrafish Development and Reproduction

Activin and inhibin are both dimeric proteins sharing the same {beta} subunits that belong to the TGF-{beta} superfamily. They are well known for stimulating and inhibiting pituitary FSH secretion, respectively, in mammals. In addition, activin also acts as a mesoderm-inducing factor in frogs. However, their functions in development and reproduction of other species are poorly defined. In this study, we disrupted all three activin/inhibin {beta} subunits ({beta}Aa, inhbaa; {beta}Ab, inhbab; and {beta}B, inhbb) in zebrafish using CRISPR/Cas9. The loss of {beta}Aa/b but not {beta}B led to a high mortality rate in the post-hatching stage. Surprisingly, the expression of fshb but not lhb in the pituitary increased in the female {beta}A mutant together with aromatase (cyp19a1a) in the ovary. The single mutant of {beta}Aa/b showed normal folliculogenesis in young females; however, their double mutant (inhbaa-/-;inhbab-/-) showed delayed follicle activation, granulosa cell hypertrophy, stromal cell accumulation and tissue fibrosis. The ovary of inhbaa-/- deteriorated progressively after 180 dpf with reduced fecundity and the folliculogenesis ceased completely around 540 dpf. In addition, tumor- or cyst-like tissues started to appear in the inhbaa-/- ovary after about one year. In contrast to females, activin {beta}Aa/b mutant males showed normal spermatogenesis and fertility. As for activin {beta}B subunit, the inhbb-/- mutant exhibited normal folliculogenesis, spermatogenesis and fertility in both sexes; however, the fecundity of mutant females decreased dramatically at 270 dpf with accumulation of early follicles. In summary, the activin-inhibin system plays an indispensable role in fish reproduction, in particular folliculogenesis and ovarian homeostasis.

physiology↗

Loss of growth differentiation factor 9 causes an arrest of early folliculogenesis in zebrafish - a novel insight into its action mechanism

Growth differentiation factor 9 (GDF9) is the best characterized growth factor released by the oocyte; however, most information about GDF9 functions comes from studies in the mouse model. In this study, we created a mutant for Gdf9 gene (gdf9-/-) in zebrafish using TALEN approach. The loss of Gdf9 caused a complete arrest of follicle development at primary growth (PG) stage. These follicles eventually degenerated, and all mutant females gradually changed to males through sex reversal, which could be prevented by mutation of the male-promoting gene dmrt1. Interestingly, the phenotypes of gdf9-/- could be rescued by mutation of inhibin (inha-/-) but not estradiol, suggesting a potential role for the activin-inhibin system in Gdf9 actions. In gdf9 null follicles, activin {beta}Aa (inhbaa) expression decreased dramatically; however, its expression rebounded in the double mutant (gdf9-/-;inha-/-). These results clearly indicate that although endocrine hormones such as follicle-stimulating hormone (FSH) are important for folliculogenesis, the activation of PG follicles requires intrinsic factors from the oocyte, such as Gdf9, which in turn works on the neighboring follicle cells to trigger follicle activation, probably via activins.

developmental biology↗

Proteomic Dynamics of Breast Cancers Identifies Potential Therapeutic Protein Targets

Treatment and relevant targets for breast cancer (BC) remain limited, especially for triple-negative BC (TNBC). We quantified the proteomes of 76 human BC cell lines using data independent acquisition (DIA) based proteomics, identifying 6091 proteins. We then established a 24-protein panel distinguishing TNBC from other BC types. Integrating prior multi-omics datasets with the present proteomic results to predict the sensitivity of 90 drugs, we found that proteomics data improved drug sensitivity predictions. The sensitivity of the 90 drugs was mainly associated with cell cytoskeleton, signal transduction and mitochondrial function. We next profiled the proteome changes of nine cell lines (five TNBC cell lines, four non-TNBC cell lines) perturbated by EGFR/AKT/mTOR inhibitors. In the TNBC cell lines, metabolism pathways were dysregulated after EGFR/mTOR inhibitors treatment, while RNA modification and cell cycle pathways were dysregulated after AKT inhibitor treatment. Our study presents a systematic multi-omics and in-depth analysis of the proteome of BC cells. This work aims to aid in prioritization of potential therapeutic targets for TNBC as well as to provide insight into adaptive drug resistance in TNBC.

systems biology↗

Integrated analyses of the single-cell ATAC-seq and RNA-seq reveal the epigenetic landscape of human ovarian aging

Studying the molecular mechanisms of ovarian aging is crucial for understanding the age-related fertility issues in females. Recently, a single-cell transcriptomic roadmap of ovarian aging based on non-human primates revealed the molecular signatures of the oocytes at different developmental stages. Herein, we present the first epigenetic landscape of human ovarian aging, through an integrated analysis of the single-cell assay for transposase-accessible chromatin using sequencing (scATAC-seq) and single-cell RNA-seq. We depicted the transcriptional profiles and chromatin accessibility of the ovarian tissues isolated from old (n=4) and young (n=2) donors. The unsupervised clustering of data revealed seven distinct cell populations in the ovarian tissues and six subtypes of oocytes, which could be distinguished by age difference. Further analysis of the scATAC-seq data from the young and old oocytes revealed that the interaction between the Notch signaling pathway and AP-1 family transcription factors may crucially determine oocyte aging. Finally, a machine-learning algorithm was applied to calculate the optimal model based on the single-cell dataset for predicting oocyte aging, which exhibited excellent accuracy with a cross-validated area under the receiver operating characteristics score of 0.99. In summary, this study provides a comprehensive understanding of human ovarian aging at both the transcriptomic and epigenetic levels, based on an integrated analysis of large-scale single-cell datasets. We believe our results will shed light on the discovery of potential therapeutic targets or diagnostic markers for age-related ovarian disorders.

genetics↗

A comprehensive mass spectral library for human thyroid tissues

Thyroid nodules occur in about 60% of the population. Current diagnostic strategies, however, often fail at distinguishing malignant nodules before surgery, thus leading to unnecessary, invasive treatments. As proteins are involved in all physio/pathological processes, a proteome investigation of biopsied nodules may help correctly classify and identify malignant nodules and discover therapeutic targets. Quantitative mass spectrometry data-independent acquisition (DIA) enables highly reproducible and rapid throughput investigation of proteomes. An exhaustive spectral library of thyroid nodules is essential for DIA yet still unavailable. This study presents a comprehensive thyroid spectral library covering five types of thyroid tissue: multinodular goiter, follicular adenoma, follicular and papillary thyroid carcinoma, and normal thyroid tissue. Our library includes 925,330 transition groups, 157,548 peptide precursors, 121,960 peptides, 9941 protein groups, and 9826 proteins from proteotypic peptides. This library resource was evaluated using three papillary thyroid carcinoma samples and their corresponding adjacent normal thyroid tissue, leading to effective quantification of up to 7863 proteins from biopsy-level thyroid tissues.

systems biology↗

Optimization of Spectral Library Size Improves DIA-MS Proteome Coverage

Efficient peptide and protein identification from data-independent acquisition mass spectrometric (DIA-MS) data typically rely on an experiment-specific spectral library with a suitable size. Here, we report a computational strategy for optimizing the spectral library for a specific DIA dataset based on a comprehensive spectral library, which is accomplished by a priori analysis of the DIA dataset. This strategy achieved up to 44.7% increase in peptide identification and 38.1% increase in protein identification in the test dataset of six colorectal tumor samples compared with the comprehensive pan-human library strategy. We further applied this strategy to 389 carcinoma samples from 15 tumor datasets and observed up to 39.2% increase in peptide identification and 19.0% increase in protein identification. In summary, we present a computational strategy for spectral library size optimization to achieve deeper proteome coverage of DIA-MS data.

bioinformatics↗

Gonadectomy and blood sampling procedures in small size teleost models

Sex steroids, produced by the gonads, play an essential role in the neuroendocrine control of reproduction in all vertebrates by providing feedback to the brain and pituitary. Sex steroids also play an important role in tissue plasticity by regulating cell proliferation in several tissues including the brain and the pituitary. Therefore, investigating the role of sex steroids and mechanisms by which they act is crucial to better understand both feedback mechanism and tissue plasticity. Teleost fish, which possess a higher degree of tissue plasticity and variations in reproduction strategies compared to mammals, appear to be useful models to investigate these questions. The removal of the main source of sex steroid production using gonadectomy together with blood sampling to measure steroid levels, have been well-established and fairly feasible in bigger fish and are powerful techniques to investigate the role and effects of sex steroids. However, small fish such as zebrafish and medaka, which are particularly good model organisms considering the well-developed genetic toolkit and the numerous protocols available to investigate their biology and physiology, raise challenges for applying such protocols due to their small size. Here, we demonstrate the step-by-step procedure of gonadectomy in both males and females followed by blood sampling in a small sized teleost model, the Japanese medaka (Oryzias latipes). The use of these procedures combined with the other advantages of using these small teleost models will greatly improve our understanding of feedback mechanisms in the neuroendocrine control of reproduction and tissue plasticity provided by sex steroids in vertebrates. SUMMARYThe article describes a quick protocol to gonadectomize and sample blood from small teleost fish, using medaka (Oryzias latipes) as a model, to investigate the role of sex steroids in animal physiology.

physiology↗

Genome-Wide Association for Itraconazole Sensitivity in Non-Resistant Clinical Isolates of Aspergillus fumigatus

Aspergillus fumigatus is a potentially lethal opportunistic pathogen that infects over [~]200,000 people and causes [~]100,000 deaths per year globally. Treating A. fumigatus infections is particularly challenging because of the recent emergence of azole-resistance. The majority of studies focusing on the molecular mechanisms underlying azole resistance have examined azole-resistant isolates. However, isolates that are susceptible to azoles also display variation in their sensitivity, presenting a unique opportunity to identify genes contributing to azole sensitivity. Here, we used genome-wide association (GWA) analysis to identify loci involved in azole sensitivity by analyzing the association between 68,853 SNPs and itraconazole (ITCZ) minimum inhibitory concentration (MIC) in 76 clinical isolates of A. fumigatus from Japan. Population structure analysis suggests the presence of four distinct populations, with ITCZ MICs distributed relatively evenly across populations. We independently conducted GWA when treating ITCZ MIC as a quantitative trait and a binary trait and identified two SNPs with strong associations that were identified in both analyses. These SNPs fell within the coding regions of Afu2g02220 and Afu2g02140. We functionally validated Afu2g02220 by knocking it out using a CRISPR/Cas-9 approach, because orthologs of this gene are involved in sterol modification and ITCZ targets the ergosterol pathway. Knockout strains displayed no difference in growth compared to the parent strain in minimal media, yet a minor but consistent inhibition of growth in the presence of 0.15 ug/ml ITCZ. Our results suggest that GWA paired with efficient gene deletion is a powerful and unbiased strategy for identifying the genetic basis of complex traits in A. fumigatus. ImportanceAspergillus fumigatus is a pathogenic mold that can infect and kill individuals with compromised immune systems. The azole class of drugs provide antifungal activity against A. fumigatus infections and have become an essential treatment strategy. Unfortunately, A. fumigatus azole resistance has recently emerged and rapidly risen in frequency making treatment more challenging. Our understanding of the molecular basis of azole sensitivity has been shaped mainly through candidate gene studies. Unbiased approaches are necessary to understand the full repertoire of genes and genetic variants underlying azole resistance and sensitivity. Here, we provide the first application of genome-wide association analysis in A. fumigatus in the identification of a gene (Afu2g02220) that contributes to itraconazole susceptibility. Our approach, which combines association mapping and CRISPR/Cas-9 for functional validation of candidate genes, has broad application for investigating the genetic basis of complex traits in fungal systems.

genomics↗

DENV NS1 and MMP-9 cooperate to induce vascular leakage by altering endothelial cell adhesion and tight junction

Dengue virus (DENV) is a mosquito-borne pathogen that causes a spectrum of diseases including life-threatening dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). Vascular leakage is a common clinical crisis in DHF/DSS patients which is closely associated with increased endothelial permeability. The presence of vascular leakage causes hypotension, circulatory failure or disseminated intravascular coagulation as the disease progresses, which can lead to death under such conditions. However, the mechanisms by which DENV infection caused the vascular leakage are not fully understood. This study reveals a distinct mechanism by which DENV induces endothelial permeability and vascular leakage in human endothelial cells and mice tissues. We initially show that DENV2 promotes the matrix metalloproteinase-9 (MMP-9) expression and secretion in DHF patient serum, peripheral blood mononuclear cells (PBMCs) and macrophages, and further reveal that DENV non-structural protein 1 (NS1) induces MMP-9 expression through activating the nuclear factor {kappa}B (NF-{kappa}B) signaling pathway. Additionally, NS1 inhibits TIMP-1 expression to facilitates the MMP-9 enzymatic activity which alters the adhesion and tight junctions and vascular leakage in human endothelial cells and mouse tissues. Moreover, NS1 recruits MMP-9 to interact with {beta}-catenin and Zona occludins protein-1/2 to degrade the important adhesion and tight junction proteins, thereby inducing endothelial hyperpermeability and vascular leakage in human endothelial cells and mouse tissues. Thus, we reveal that DENV NS1 and MMP-9 cooperatively induce vascular leakage by impairing endothelial cell adhesion and tight junction, and suggest that MMP-9 may serve as a potential target for the treatment of hypovolemia in DSS/DHF patients. Author SummaryDENV is the most common mosquito-transmitted viral pathogen in humans. In general, DENV-infected patients are either asymptomatic or have flu-like symptoms with fever and rash. However, in severe cases of DENV infection, the disease may progress to dengue hemorrhagic fever (DHF) or dengue shock syndrome (DSS), the leading causes of morbidity and mortality in school-age children in tropical and subtropical regions. DENV-induced vascular leakage is characterized by enhanced vascular permeability without morphological damage to the capillary endothelium. We found that a distinct mechanism of DENV NS1 and MMP-9 cooperatively induce vascular leakage is the main reason leading to death in severe dengue patients. Also, NS1 recruits MMP-9 to degrade {beta}-catenin, ZO-1, ZO-2 to intervene endothelial hyperpermeability in human endothelial cells and mouse vascular. Finally, we reveal that DENV activating NF-{kappa}B signaling pathway induces MMP-9 expression, in patients, mice, PBMC and macrophages though the viral NS1 protein. This study would provide new in signs into the pathogenesis caused by DENV infection, and suggest that MMP-9 may acts as a drug target for the prevention and treatment of DENV-associated diseases.

microbiology↗

Daily mitochondrial dynamics in cone photoreceptors

Cone photoreceptors in the retina are exposed to intense daylight, and have higher energy demands in darkness. Cones produce energy using a large cluster of mitochondria. Mitochondria are susceptible to oxidative damage, and healthy mitochondrial populations are maintained by regular turnover. Daily cycles of light exposure and energy consumption suggest that mitochondrial turnover is important for cone health. We investigated the 3-D ultrastructure and metabolic function of zebrafish cone mitochondria throughout the day. At night cones undergo a mitochondrial biogenesis event, corresponding to an increase in the number of smaller, simpler mitochondria and increased metabolic activity. In the daytime, ER and autophagosomes associate more with mitochondria, and mitochondrial size distribution across the cluster changes. We also report dense material shared between cone mitochondria that is extruded from the cell in darkness, sometimes forming extracellular structures. Our findings reveal an elaborate set of daily changes to cone mitochondrial structure and function. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=143 SRC="FIGDIR/small/030262v1_ufig1.gif" ALT="Figure 1"> View larger version (48K): org.highwire.dtl.DTLVardef@101b1f9org.highwire.dtl.DTLVardef@4b79eeorg.highwire.dtl.DTLVardef@1320df3org.highwire.dtl.DTLVardef@131edf5_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

A single-cell transcriptome atlas during Cashmere goat hair follicle morphogenesis

Cashmere, also known as soft gold, is produced from the secondary hair follicles in Cashmere goats and its therefore of significance to investigate the molecular profiles during Cashmere goat hair follicle development. However, our current understanding of the machinery underlying Cashmere goat hair follicle remains largely unexplored and researches regarding hair follicle development mainly used the mouse as a research model. To provides comprehensively understanding on the cellular heterogeneity and cell lineage cell fate decisions, we performed single-cell RNA sequencing on 19,705 single cells from induction (embryonic day 60), organogenesis (embryonic day 90) and cytodifferentiation (embryonic day 120) stages of fetus Cashmere goat dorsal skin. Unsupervised clustering analysis identified 16 cell clusters and their corresponding cell types were also unprecedentedly characterized. Based on the lineage inference, we revealed detailed molecular landscape along the dermal and epidermal cell lineage developmental pathways. Notably, by cross-species comparasion of single cell data with murine model, we revelaed conserved programs during dermal condensate fate commitment and the heterochrony development of hair follicle development between mouse and Cashmere goat were also discussed here. Our work here delineate unparalleled molecular profiles of different cell populations during Cashmere goat hair follicle morphogenesis and provide a valuable resource for identifying biomarkers during Cashmere goat hair follicle development.

developmental biology↗