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Li, S.

Publications and source records attributed to Li, S..

At least 757 records · Page 42Linked to original sources

CD4+ T cells display a spectrum of recall dynamics during re-infection with malaria parasites.

Children in malaria-endemic regions can experience multiple Plasmodium infections over a short period of time, with in vitro CD4+ T cell recall responses becoming more regulatory with increasing age and exposure. This suggests that repeated infection qualitatively changes CD4+ T cells, although the heterogeneity and dynamics of these responses await systematic analysis in vivo. Here, we examined TCR transgenic PbTII and polyclonal CD4+ T cells during Plasmodium re-infection in mice, in conjunction with scRNA-seq/TCR-seq and spatial transcriptomics at near single-cell resolution. PbTII cells gave rise to multiple antigen-experienced states in different areas of the spleen after primary infection and antimalarial treatment, including ongoing GC responses and T-cell zone memory. Upon re-infection, Th1-memory PbTII cells initiated a rapid effector response prior to proliferating, while GC Tfh cells of the same antigen specificity were entirely refractory within the same organ. Transcriptome dynamic modelling and network analysis of Th1 recall revealed a biphasic wave of RNA processing that firstly preceded immune effector transcription, and later accompanied cellular proliferation. Importantly, Th1 recall constituted a partial facsimile of primary Th1 responses, with no unique genes amongst the small subset of those upregulated upon re-infection. Finally, we noted a similar spectrum of antigen-experienced states and recall dynamics by polyclonal CD4+ T cells with diverse TCRs. Therefore, during re-infection with Plasmodium, persisting GC Tfh cells remained unaltered transcriptionally, Tcm/Tfh-like cells exhibited minimal proliferation, and Th1-memory cells displayed a rapid, proliferating IL-10-producing Tr1 response consistent with a shift towards immune-regulation. These data highlight a broad spectrum of simultaneous CD4+ T cell responses that occur in the spleen during re-infection with malaria parasites. HighlightsO_LISplenic TCR transgenic CD4+ T cells are highly heterogeneous prior to re-infection. C_LIO_LIPersisting GC Tfh cells are refractory to re-activation during re-infection. C_LIO_LITh1-memory cells rapidly upregulate RNA processing prior to effector function and proliferation. C_LIO_LITh1-recall is an imperfect but faithful facsimile of primary Th1 responses. C_LIO_LIA spectrum of recall states is observed in polyclonal CD4+ T cells with diverse TCRs. C_LI

immunology↗

A scalable, GMP-compatible, autologous organotypic cell therapy for Dystrophic Epidermolysis Bullosa

BackgroundGene editing in induced pluripotent stem (iPS) cells has been hailed to enable new cell therapies for various monogenetic diseases including dystrophic epidermolysis bullosa (DEB). However, manufacturing, efficacy and safety roadblocks have limited the development of genetically corrected, autologous iPS cell-based therapies. MethodsWe developed Dystrophic Epidermolysis Bullosa Cell Therapy (DEBCT), a new generation GMP-compatible (cGMP), reproducible, and scalable platform to produce autologous clinical-grade iPS cell-derived organotypic induced skin composite (iSC) grafts to treat incurable wounds of patients lacking type VII collagen (C7). DEBCT uses a combined high-efficiency reprogramming and CRISPR-based genetic correction single step to generate genome scar- free, COL7A1 corrected clonal iPS cells from primary patient fibroblasts. Validated iPS cells are converted into epidermal, dermal and melanocyte progenitors with a novel 2D organoid differentiation protocol, followed by CD49f enrichment and expansion to minimize maturation heterogeneity. iSC product characterization by single cell transcriptomics was followed by mouse xenografting for disease correcting activity at 1 month and toxicology analysis at 1-6 months. Culture-acquired mutations, potential CRISPR-off targets, and cancer-driver variants were evaluated by targeted and whole genome sequencing. FindingsiPS cell-derived iSC grafts were reproducibly generated from four recessive DEB patients with different pathogenic mutations. Organotypic iSC grafts onto immune-compromised mice developed into stable stratified skin with functional C7 restoration. Single cell transcriptomic characterization of iSCs revealed prominent holoclone stem cell signatures in keratinocytes and the recently described Gibbin-dependent signature in dermal fibroblasts. The latter correlated with enhanced graftability. Multiple orthogonal sequencing and subsequent computational approaches identified random and non-oncogenic mutations introduced by the manufacturing process. Toxicology revealed no detectable tumors after 3-6 months in DEBCT- treated mice. InterpretationDEBCT successfully overcomes previous roadblocks and represents a robust, scalable, and safe cGMP manufacturing platform for production of a CRISPR-corrected autologous organotypic skin graft to heal DEB patient wounds.

bioengineering↗

StereoCell enables high accuracy single cell segmentation for spatial transcriptomic dataset

BackgroundOwing to recent advances in resolution and field-of-view, spatially resolved transcriptomics sequencing, such as Stereo-seq, has emerged as a cutting-edge technology for the interpretation of large tissues at the single-cell level. To generate accurate single-cell spatial gene expression profiles from high-resolution spatial omics data, a powerful computational tool is required. FindingsWe present CellBin, an image-facilitated one-stop pipeline for high-resolution and large field-of-view spatial transcriptomic data of Stereo-seq. CellBin provides a comprehensive and systematic platform for generating high-confidence single-cell spatial gene expression profiles, which specifically includes image stitching, image registration, tissue segmentation, nuclei segmentation and molecule labeling. CellBin is user-friendly and does not require a specific level of omics and image analysis expertise. ConclusionsDuring image stitching and molecule labeling, CellBin delivers better-performing algorithms to reduce stitching error and time, in addition to improving the signal-to-noise ratio of single-cell gene expression data, in comparison with existing methods. Additionally, CellBin has been shown to obtain highly accurate single-cell spatial data using mouse brain tissue, which facilitated clustering and annotation.

bioinformatics↗

Aurora B spatial separation from its outer kinetochore substrates stabilizes chromosome biorientation when tension is applied

For correct chromosome segregation in mitosis, sister kinetochores must interact with microtubules from opposite spindle poles (biorientation). For this, aberrant kinetochore- microtubule interaction must be resolved (error correction) by Aurora B kinase. Once biorientation is formed, tension is applied across sister kinetochores, stabilizing kinetochore- microtubule interactions. The mechanism for this tension-dependent process has been debated. Here we study how localizations of Aurora B at different kinetochore sites affect the establishment and maintenance of biorientation in budding yeast. In the absence of the physiological Aurora B-INCENP recruitment mechanisms, engineered recruitment of Aurora B-INCENP to the inner kinetochore (Mif2) prior to biorientation supports the subsequent establishment of biorientation. By contrast, an engineered Aurora B-INCENP recruitment to the outer kinetochore (Ndc80) fails to support biorientation establishment. Furthermore, when the physiological Aurora B-INCENP recruitment mechanisms are present, an engineered Aurora B-INCENP recruitment to Mif2 during metaphase (after biorientation establishment) does not affect biorientation maintenance. By contrast, an engineered Aurora B-INCENP recruitment to Ndc80 during metaphase leads to disruption of biorientation, which is dependent on the kinase activity of Aurora B. Taken together, our results suggest that spatial separation of Aurora B from its outer kinetochore substrates is required to stabilize kinetochore-microtubule interaction when biorientation is formed and tension is applied on this interaction. Meanwhile, Aurora B shows dynamic turnover (or exchange) on the centromere and kinetochore during early mitosis. It has been thought that this turnover is crucial for error correction and biorientation, as it may help Aurora B reach its substrates in distance and/or may facilitate the Aurora B activation on the mitotic spindle. However, using the engineered Aurora B-INCENP recruitment to the inner kinetochore, we demonstrate that, even without such a turnover, Aurora B-INCENP can efficiently support biorientation. Altogether, our study provides important insights into how Aurora B promotes error correction and biorientation in a tension-dependent manner.

cell biology↗

Structural and mechanistic insight into ribosomal ITS2 RNA processing by nuclease-kinase machinery

Precursor ribosomal RNA (pre-rRNA) processing is a key step in ribosome biosynthesis and involves numerous RNases. A HEPN nuclease Las1 and a polynucleotide kinase Grc3 assemble into a tetramerase responsible for rRNA maturation. Here, we report the structures of full-length Saccharomyces cerevisiae and Cyberlindnera jadinii Las1-Grc3 complexes, and Cyberlindnera jadinii Las1. The Las1-Grc3 structures show that the central coiled coil domain of Las1 facilitates pre-rRNA binding and cleavage, while the Grc3 C-terminal loop motif directly binds to the HEPN active center of Las1 and regulates pre-rRNA cleavage. Structural comparison between Las1 and Las1-Grc3 complex exhibits that Grc3 binding induces conformational rearrangements of catalytic residues associated with HEPN nuclease activation. Biochemical assays identify that Las1 processes pre-rRNA at the two specific sites (C2 and C2'), which greatly facilitates rRNA maturation. Our structures and specific pre-rRNA cleavage findings provide crucial insights into the mechanism and pathway of pre-rRNA processing in ribosome biosynthesis.

biophysics↗

Spatial transcriptomics maps molecular and cellular requirements for CD4+ T cell-dependent immunity to malaria.

CD4+ T cells orchestrate adaptive immunity to circulating malaria parasites; yet cellular interactions and molecular mechanisms controlling Th1 and Tfh differentiation in the spleen remain to be fully defined in vivo. Here, using a murine model of CD4-dependent immunity, we tested if Slide-seqV2, a spatial transcriptomic method with near single-cell resolution, could determine the locations of multiple CD4+ T cell subsets and potentially interacting cellular partners in the spleen during infection. Firstly, Slide-seqV2 readily mapped splenic cellular structure and microanatomical change during infection. Next, computational integration with scRNA-seq reference datasets of splenocytes, stromal cells, and specifically of polyclonal CD4+ T cells and B cells, mapped the relative locations of multiple cell-types within this dense tissue. scRNA-seq of B cells over time mapped emergence of germinal centre B cells, red pulp-located plasmablasts and atypical B cells, and uncovered a prolonged CD4+ T-cell-independent, follicular bystander B cell response marked by Sca-1 and Ly6C upregulation. scRNA-seq of activated, polyclonal CD4+ T cells revealed their similarity to our previous TCR transgenic models. Importantly, spatial analysis revealed polyclonal Th1 cells co-localised with CXCL9/10-producing monocytes in the red pulp, while polyclonal Tfh-like cells were located close to CXCL13-expressing B cell follicles, consistent with our previous CXCR3/CXCR5 competition model of Th1/Tfh bifurcation. CRISPR/Cas9 disruption of either or both CXCR3 and CXCR5 in naive Plasmodium-specific CD4+ T cells had unexpectedly minor effects on Th1 differentiation in vivo. Instead, CXCR5 was essential for maximising clonal expansion, suggesting a role for splenic CXCL13+ cells in supporting CD4+ T cell proliferation in malaria. Thus, spatial transcriptomics at near single-cell resolution was feasible in densely packed secondary lymphoid tissue, providing multiple insights into mechanisms controlling splenic polyclonal CD4+ T cell and B cell differentiation during infection. HighlightsO_LISlide-seqV2 maps splenic microanatomy, including stromal and immune cell location. C_LIO_LIBystander activation of all follicular B cells occurs in malaria, marked by Sca-1/Ly6C upregulation. C_LIO_LISingle naive polyclonal CD4+ T cells differentiate mostly into Th1 and Tfh cells in malaria. C_LIO_LICell-cell colocalization analysis positions Th1 cells with monocytes in red pulp, and Tfh cells with Cxcl13+ B cell follicles. C_LIO_LICXCR5, but not CXCR3, supports parasite-specific CD4+ T cell clonal expansion. C_LI

immunology↗

Tenacibaculosis in wild-caught, captive Chinook salmon (Oncorhynchus tshawytscha) in British Columbia, Canada

Substantial, acute mortality was observed in wild-caught Chinook salmon (Oncorhynchus tshawytscha) of various ages and sizes, from sub-adults to returning adults, held in tanks during two holding studies carried out in August and September 2022 at the Bamfield Marine Sciences Centre (BMSC), in Bamfield, British Columbia, Canada. Within days of capture, a substantial number of fish began presenting lethargy, loss of balance, abnormal swimming behavior, and skin ulcers involving the caudal peduncle, fins, belly, trunk and mouth. Molecular testing revealed high levels of Tenacibaculum dicentrarchi in skin swabs and gills, without appreciable consistent detections of other infectious agents. T. dicentrarchi was also isolated from the skin ulcers. Histological analysis confirmed the presence of ulcerative dermatitis and myositis, associated with mats of filamentous, rod-shaped bacteria. In two individuals, the infection became systemic, with a bacterial colony (identified as T. dicentrarchi) observed in the liver of one individual. In-situ hybridization against T. dicentrarchi and T. maritimum confirmed the presence of only the former agent in the gills and skin ulcers of the affected fish. This clinical report represents the first diagnosed case of tenacibaculosis in wild-caught (captive) Chinook salmon in British Columbia. CONFLICT OF INTERESTThe authors have no conflicts of interest to report. DATA AVAILABILITY STATEMENTThe data that support the findings of this study are available from the corresponding author upon reasonable request.

pathology↗

A Metabolomics Study of Thrombosis after Cardiac Surgery in Children with Congenital Heart Disease

ObjectiveThrombosis is a major complication after cardiac surgery in children with congenital heart disease (CHD). The mechanisms underlying thrombosis development remain poorly understood. We aimed to identify novel circulating metabolites before cardiac surgery that are associated with the development of thrombosis after surgery in children with CHD. Approach and resultsAll blood samples were drawn right before surgical incision and after the induction of anesthesia, and plasma was separated immediately under 4 {degrees}C. Untargeted metabolomic data were measured by Metabolon in plasma from children (age range: 0 days-18 years) with CHD undergoing cardiac surgery. The primary outcome was thrombosis within 30 days of surgery or before discharge. Associations of individual metabolites with thrombosis were assessed with logistic regression with false discovery rate (FDR) correction for multiple comparison and adjustment for clinical characteristics; elastic net regression was used to select a prediction model. Out of 1,115 metabolites measured in samples from 203 children, 776 met the quality control criteria. In total, 26 children (12.8%) developed thrombosis. Among the 776 metabolites, 195 were significantly associated with thrombosis (FDR q-value < 0.05). The top three metabolites showing the strongest associations with thrombosis were eicosapentaenoate, steroid monosulfate C19H28O6S, and formiminoglutamate (FDR = 0.01 for all). Pathway analysis showed that the pathways of nicotinate and nicotinamide metabolism (P = 0.0007) and glycerophospholipid metabolism (P = 0.002) were enriched and had significant impacts on the development of thrombosis. In elastic net regression analysis, the area under the receiver operating-characteristic curve of a prediction model for thrombosis was 0.94 in the training sample (70% of the total sample) and 0.84 in the testing sample (the remaining 30%). ConclusionWe have identified promising novel metabolites and metabolic pathways associated with thrombosis. Future studies are warranted to confirm the findings and examine the mechanistic pathways to thrombosis.

physiology↗

E2F1 Mediates SOX17 Deficiency-Induced Pulmonary Hypertension

RationaleRare genetic variants and genetic variation at loci in an enhancer in SRY-Box Transcription Factor 17 (SOX17) are identified in patients with idiopathic pulmonary arterial hypertension (PAH) and PAH with congenital heart disease. However, the exact role of genetic variants or mutation in SOX17 in PAH pathogenesis has not been reported. ObjectivesTo investigate the role of SOX17 deficiency in pulmonary hypertension (PH) development. MethodsHuman lung tissue and endothelial cells (ECs) from IPAH patients were used to determine the expression of SOX17. Tie2Cre-mediated and EC-specific deletion of Sox17 mice were assessed for PH development. Single-cell RNA sequencing analysis, human lung ECs, and smooth muscle cell culture were performed to determine the role and mechanisms of SOX17 deficiency. A pharmacological approach was used in Sox17 deficiency mice for therapeutic implication. Measurement and Main ResultsSOX17 expression was downregulated in the lungs and pulmonary ECs of IPAH patients. Mice with Tie2Cre mediated Sox17 knockdown and EC-specific Sox17 deletion developed spontaneously mild PH. Loss of endothelial Sox17 in EC exacerbated hypoxia-induced PH in mice. Loss of SOX17 in lung ECs induced endothelial dysfunctions including upregulation of cell cycle programming, proliferative and anti-apoptotic phenotypes, augmentation of paracrine effect on pulmonary arterial smooth muscle cells, impaired cellular junction, and BMP signaling. E2F Transcription Factor 1 (E2F1) signaling was shown to mediate the SOX17 deficiency-induced EC dysfunction and PH development. ConclusionsOur study demonstrated that endothelial SOX17 deficiency induces PH through E2F1 and targeting E2F1 signaling represents a promising approach in PAH patients.

physiology↗

Comparative transcriptomics reveal differential gene expression in Plasmodium vivax geographical isolates and implications on erythrocyte invasion mechanisms

Plasmodium vivax uses Duffy binding protein (PvDBP1) to bind to the Duffy Antigen-Chemokine Receptor (DARC) to invade human erythrocytes. Individuals who lack DARC expression (Duffy-negative) are thought to be resistance to P. vivax. In recent years, P. vivax malaria is becoming more prevalent in Africa with a portion of these cases detected in Duffy-negatives. Apart from DBP1, members of the reticulocyte binding protein (RBP) and tryptophan-rich antigen (TRAg) families may also play a role in erythrocyte invasion. While the transcriptomes of the Southeast Asian and South American P. vivax are well documented, the gene expression profile of P. vivax in Africa and more specifically the expression level of several erythrocyte binding gene candidates as compared to DBP1 are largely unknown. This paper characterized the first P. vivax transcriptome in Africa and compared with those from the Southeast Asian and South American isolates. The expression of 4,404 gene transcripts belong to 12 functional groups including 43 specific erythrocyte binding gene candidates were examined. Overall, there were 10-26% differences in the gene expression profile amongst the geographical isolates, with the Ethiopian and Cambodian P. vivax being most similar. Majority of the gene transcripts involved in protein transportation, housekeeping, and host interaction were highly transcribed in the Ethiopian P. vivax. Erythrocyte binding genes including PvRBP2a and PvRBP3 expressed six-fold higher than PvDBP1and 60-fold higher than PvEBP/DBP2. Other genes including PvRBP1a, PvMSP3.8, PvMSP3.9, PvTRAG2, PvTRAG14, and PvTRAG22 also showed relatively high expression. Differential expression was observed among geographical isolates, e.g., PvDBP1 and PvEBP/DBP2 were highly expressed in the Cambodian but not the Brazilian and Ethiopian isolates, whereas PvRBP2a and PvRBP2b showed higher expression in the Ethiopian and Cambodian than the Brazilian isolates. Compared to Pvs25, the standard biomarker for detecting female gametocytes, PvAP2-G (PVP01_1440800), GAP (PVP01_1403000), and Pvs47 (PVP01_1208000) were highly expressed across geographical samples. These findings provide an important baseline for future comparisons of P. vivax transcriptomes from Duffy-negative infections and highlight potential biomarkers for improved gametocyte detection.

cell biology↗

Comprehensive Multi-omics Analysis Reveals the Core Role of Glycerophospholipid Metabolism in Rheumatoid Arthritis Development

ObjectivesRheumatoid arthritis (RA) is a chronic autoimmune disease with complex causes and recurrent attacks that can easily develop into chronic arthritis. Our study aims to elucidate potential mechanism among control, new-onset RA (NORA) and chronic RA (CRA) with multi-omics analysis. MethodsA total of 162 subjects were included in our study, 121 subjects were used for 16S rRNA, ITS sequencing and metabolomics analysis and 41 subjects were used for transcriptomics analysis. Enrichment analysis was based on significant difference metabolites and genes. Protein-protein interaction network and correlation analyses were performed to interpret the interactions among intestinal flora, metabolites and genes. We applied three models to distinguish between NORA and CRA using computational OR values, LASSO and random forest, respectively. ResultsOur results demonstrated intestinal flora disturbance in RA development, with significantly increased abundance of Escherichia-Shigella and Proteobacteria in NORA. We also found that the diversity was significantly reduced in CRA compared to NORA through fungi analysis. Moreover, we identified 28 differential metabolites between NORA and CRA. Pathway enrichment analysis revealed significant dysregulation of glycerophospholipid metabolism and phenylalanine metabolism pathways in RA patients. Next, we identified 40 differentially expressed genes between NORA and CRA, which acetylcholinesterase (ACHE) was the core gene and significantly enriched in glycerophospholipid metabolism pathway. Correlation analysis showed a strong negatively correlation between glycerophosphocholine and inflammatory characteristics. ConclusionsThese findings revealed that glycerophospholipid metabolism plays a crucial role in the development and progression of RA, providing new ideas for early clinical diagnosis and optimizing treatment strategies.

immunology↗

Cardiomyocyte-fibroblast interaction regulates ferroptosis and fibrosis after myocardial injury

Neonatal mouse hearts have transient renewal capacity which is lost in juvenile and adult hearts. After myocardial infarction (MI) in neonatal hearts, an initial loss of cardiomyocytes occurs but it is unclear through which type of regulated cell death (RCD). In the current studies, we induced MI in neonatal and juvenile mouse hearts, and show that ischemic cardiomyocytes primarily undergo ferroptosis, a non-apoptotic and iron-dependent form of RCD. We demonstrate that cardiac fibroblasts (CFs) protect cardiomyocytes from ferroptosis through paracrine factors and direct cell-cell interaction. CFs show strong resistance to ferroptosis due to high ferritin expression. Meanwhile, the fibrogenic role of CFs, typically considered detrimental to heart function, is negatively regulated by paired-like homeodomain 2 (Pitx2) signaling from cardiomyocytes. In addition, Pitx2 prevents ferroptosis in cardiomyocytes by regulating ferroptotic genes. Understanding the regulatory mechanisms of cardiomyocyte survival and death can identify potentially translatable therapeutic strategies for MI.

cell biology↗

A maize lipid droplet-associated protein is modulated by a virus to promote viral multiplication and infection

Pathogen infection induces massive reprogramming of host primary metabolism. Lipid and fatty acid metabolism is generally disrupted by pathogens and co-opted for their proliferation. Lipid droplets (LDs) that play important roles in regulating cellular lipid metabolism are utilized by a variety of pathogens in mammalian cells. However, the function of LDs during pathogenic infection in plants remains unknown. We show here that infection by rice black streaked dwarf virus (RBSDV) affects the lipid metabolism of maize, which causes elevated accumulation of C18 polyunsaturated fatty acids (PUFAs) leading to viral proliferation and symptom development. Overexpression of one of the two novel LD-associated proteins (LDAPs) of maize (ZmLDAP1 and ZmLDAP2) induces LD clustering. The core capsid protein P8 of RBSDV interacts with ZmLDAP2 and prevents its degradation through the ubiquitin-proteasome system mediated by a UBX domain-containing protein, PUX10. In addition, silencing of the ZmLDAP2 down-regulates expression of fatty acid desaturase genes in maize, leading to a decrease in C18 PUFAs levels and suppression of RBSDV accumulation. Our findings reveal that the plant virus recruits LDAP to regulate cellular fatty acid metabolism to promote viral multiplication and infection. These results expand the knowledge of the LD functions and viral infection mechanism in plants. One Sentence SummaryRice black streaked dwarf virus recruits a lipid droplet-associated protein to regulate cellular fatty acid metabolism for promoting viral multiplication and infection.

pathology↗

xTrimoDock: Rigid Protein Docking via Cross-Modal Representation Learning and Spectral Algorithm

Protein-protein interactions are the basis for the formation of protein complexes which are essential for almost all cellular processes. Knowledge of the structures of protein complexes is of major importance for understanding the biological function of these protein-protein interactions and designing protein drugs. Here we address the problem of rigid protein docking which assumes no deformation of the involved proteins during interactions. We develop a method called, xTrimoDock, which leverages a cross-modal representation learning to predict the protein distance map, and then uses a spectral initialization and gradient descent to obtain the roto-translation transformation for docking. We show that, on antibody heavy-chain and light-chain docking, and antibody-antigen docking, xTrimoDock consistently outperforms the state-of-the-art such as AlphaFold-Multimer and HDock, and can lead to as much as a 10% improvement in DockQ metric. xTrimoDock has been applied as a useful tool in protein drug design at BioMap.

bioinformatics↗

Network-based molecular subtyping of acral melanoma

Acral melanoma is more biologically aggressive with a worse prognosis compared with other melanoma subtypes. However, the molecular basis underlying the biological and clinical behavior of this cancer is still unclear. Here, using the combination of multi-omics data analysis and network-based disease gene prediction algorithm, we first demonstrate the existence of two acral melanoma subtypes which greatly differed in clinical performance, cellular and molecular mechanisms, and discovered a biomarker panel (EREG, VSIG4, FCGR3A, RAB20) that accurately distinguished these two subtypes with the AUC of 0.946, which has been verified by clinical samples. Subtype I has thinner Breslow with a better prognosis. On the contrary, subtype II is a high-risk subtype that is easier to invade the dermis. We further analyzes the intrinsic biological mechanism of the two subtypes from the cellular level, and reveals the important role of macrophages subgroups in the molecular typing of acral melanoma. Feature genes of subtype I are enriched in FCN1+ macrophages that promote inflammatory and immune responses. In contrast, feature genes of subtype II are enriched in SPP1+ macrophages which ha the greatest impact on tumor cells. The identification of the two subtypes opens up important biological and clinical perspectives for acral melanoma.

bioinformatics↗

Development of attention-based robust deep learning model for tongue diagnosis by smartphone

Compared with tongue diagnosis using tongue image analyzers, tongue diagnosis by smartphone has great advantages in convenience and cost for universal health monitoring, but its accuracy is affected by the shooting conditions of smartphones. Developing deep learning models with high accuracy and robustness to changes in the shooting environment for tongue diagnosis by smartphone and determining the influence of environmental changes on accuracy are necessary. In our study, a dataset of 9003 images was constructed after image pre-processing and labeling. Next, we developed an attention-based deep learning model (Deep Tongue) for 8 subtasks of tongue diagnosis, including the spotted tongue, teeth-marked tongue, and fissure tongue et al, which the average AUC of was 0.90, higher than the baseline model (ResNet50) by 0.10. Finally, we analyzed the objective reasons, the brightness of the environment and the hue of images, affecting the accuracy of tongue diagnosis by smartphone through a consistency experiment of direct subject inspection and tongue image inspection. Finally, we determined the influence of environmental changes on accuracy to quantify the robustness of the Deep Tongue model through simulation experiments. Overall, the Deep Tongue model achieved a higher and more stable classification accuracy of seven tongue diagnosis tasks in the complex shooting environment of the smartphone, and the classification of tongue coating (yellow/white) was found to be sensitive to the hue of the images and therefore unreliable without stricter shooting conditions and color correction.

bioinformatics↗

CALCIUM-DEPENDENT PROTEIN KINASE32 regulates cellulose biosynthesis through post-translational modification of cellulose synthase

Cellulose is an economically important source of food, paper, textiles, and biofuel. As an essential component of plant cell walls, cellulose is critical for plant cell growth. Despite its economic and biological significance, the regulation of cellulose biosynthesis is poorly understood. Phosphorylation and dephosphorylation of cellulose synthases (CESAs) were shown to impact the direction and velocity of cellulose synthase complexes (CSCs). Despite a high prevalence of phosphorylation sites in CESAs, the protein kinases that phosphorylate CESAs are largely unknown. Here, we demonstrate that CALCIUM-DEPENDENT PROTEIN KINASE32 (CPK32) regulates cellulose biosynthesis via phosphorylation of CESA3. Phosphorylation of CESA3 is important for the motility and stability of CSCs. Hence, we uncovered a new function of CPKs that regulates cellulose biosynthesis and a novel mechanism by which phosphorylation regulates the stability of CSCs.

plant biology↗

Quantitative Annotations of T-Cell Repertoire Specificity

The specificity of a T-cell receptor (TCR) repertoire determines personalized immune capacity. Existing methods have modelled the qualitative aspects of TCR specificity, while the quantitative aspects remained unaddressed. We developed a package, TCRanno, to quantify the specificity of TCR repertoires. Applying TCRanno to 4,195 TCR repertoires revealed quantitative changes in repertoire specificity upon infections, autoimmunity and cancers. Specifically, TCRanno found cytomegalovirus-specific TCRs in seronegative healthy individuals, supporting the possibility of abortive infections. TCRanno discovered age-accumulated fraction of SARS-CoV2-specific TCRs in pre-pandemic samples, which may explain the aggressive symptoms and age-related severity of COVID-19. TCRanno also identified the encounter of Hepatitis B antigens as a potential trigger of systemic lupus erythematosus. TCRanno annotations showed capability in distinguishing TCR repertoires of healthy and cancers including melanoma, lung and breast cancers. TCRanno may also facilitate single-cell TCRseq+gene expression data analyses by isolating T-cells with the specificity of interest.

bioinformatics↗