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Wang, R.

Publications and source records attributed to Wang, R..

At least 145 records · Page 8Linked to original sources

A Set of Novel Far-Red Fluorescent Proteins for Temporal Domain Multiplexing and Super-Resolution Imaging

The diverse spectral and photochemical properties of fluorescent proteins enable a variety of imaging applications in cell biology, ranging from cellular and organelle labeling to super-resolution microscopy and multiplexed live cell imaging. Here, we report a set of novel far-red fluorescent proteins, named mfRFP, mfRFP-A, and mCardinal-A, which are characterized by similar fluorescence spectra with excitation/emission at [~]600/660 nm while exhibiting distinct photobleaching rates. Differences in photostability allowed us to perform per-pixel unmixing of the three far-red FPs imaged simultaneously by employing a recently introduced temporal domain multiplexing approach. We demonstrated the application of the temporal domain multiplexing approach with different combinations of far-red fluorescent proteins possessing nearly identical emission spectra by acquiring BrainBow-like images of cellular populations and distinguishing subcellular structures in mammalian cells using a single imaging channel without applying any hardware modifications to the conventional microscope. Unlike previous temporal domain multiplying approaches employing photophysical properties of fluorescent proteins, the current approach is a wide range of microscopy modalities, including 3D imaging with a spinning disk and point scanning confocal microscopy. The most photostable fluorescent protein in the set, mfRFP, was further benchmarked against spectrally similar FPs and applied for super-resolution imaging of structural proteins in mammalian cells and for neuroimaging of model organisms, including mice, zebrafish, and C. elegans.

biochemistry↗

Neural Spectral Prediction for Structure Elucidation with Tandem Mass Spectrometry

Structural elucidation using untargeted tandem mass spectrometry (MS/MS) has played a critical role in advancing scientific discovery [1, 2]. However, differentiating molecular fragmentation patterns between isobaric structures remains a prominent challenge in metabolomics [3-10], drug discovery [11-13], and reaction screening [14-17], presenting a significant barrier to the cost-effective and rapid identification of unknown molecular structures. Here, we present a geometric deep learning model, ICEBERG, that simulates high-energy collision-induced dissociation in mass spectrometry to generate chemically plausible fragments and their relative intensities with awareness of collision energies and polarities. We utilize ICEBERG predictions to facilitate structure elucidation by ranking a set of candidate structures based on the similarity between their predicted in silico MS/MS spectra and an experimental MS/MS spectrum of interest. This integrated elucidation pipeline enables state-of-the-art performance in compound annotation, with 40% top-1 accuracy on the NIST20 [M+H]+ adduct subset and with 92% of correct structures appearing in the top ten predictions in the same dataset. It achieves 46% top-1 and 86% top-10 accuracies when tested on the open-access MassSpecGym benchmark, and outperforms SIRIUS on a recently released test set with previously uncharacterized structures. We demonstrate several real-world case studies, including identifying clinical biomarkers of depression and tuberculous meningitis, annotating an aqueous abiotic degradation product of the pesticide thiophanate methyl, disambiguating isobaric products in pooled reaction screening, and annotating biosynthetic pathways in Withania somnifera. Overall, this deep learning-based paradigm for structural elucidation enables rapid molecular annotation from complex mixtures, driving discoveries across diverse scientific domains.

bioinformatics↗

A resource and computational approach for quantifying gene editing allelism at single-cell resolution

CRISPR-Cas9-based gene editing is a powerful approach to developing gene and cell therapies for several diseases. Engineering cell therapies requires accurate assessment of gene editing allelism because editing patterns can vary across cells leading to genotypic heterogeneity. This can hinder development of robust cell therapies. Droplet-based targeted single-cell DNA sequencing (scDNAseq) has been used to genotype targeted loci across thousands of cells enabling high-throughput assessment of gene editing efficiency. Here, we constructed a "ground truth" gene editing single-cell DNAseq atlas, along with an artifact-aware computational workflow called GUMM (Genotyping Using Mixture Models) to systematically infer single-cell allelism from these data. This resource was created by expanding CRISPR-Cas9-edited HL-60 clones that harbored distinct insertion-deletion (indel) profiles in CLEC12A and mixing them at pre-defined ratios to create artificial cocktails that mimic the potential editing diversity of a CRISPR-Cas9 experiment. This enabled assessment of technical artifacts that confound interpretation of allelism in the readouts of gene edited cells. GUMM was able to accurately genotype cells and infer the original clonal composition of the artificial cocktails even in the presence of artifacts.

bioinformatics↗

Intravenous BCG immunization drives naive CD4+ T cell to Th1 differentiation via CD4+ T cell epigenetic reprogramming

Intravenous (IV) administration of live Bacille Calmette-Guerin (BCG) boosts potent immunity through coordinated interactions of innate immune response and adaptive immune response for BCG antiviral activity. The underlying mechanisms by which BCG initiates CD4+ T response remain incompletely understood. Here, we show that IV administration of BCG drives naive CD4+ T cell differentiation to Th1 cell through epigenetic reprogramming. Single-cell transcriptomic and epigenomic analyses revealed that IV BCG immunization induced metabolic reprogramming in monocytes and increased the proportion of T cells. The immunization induced chromatin openness for transcription factors regulating naive CD4+ T cells differentiation into Th1 cells. Importantly, we observed increases in Stat1, Irf1 and interferon-stimulated genes such as Igtp in Th1 cells, leading to upregulation of interferon related gene expression for antiviral response by BCG immunization. Activated transcription factors like Irf1 in CD4+ T cells promotes Il12rb1 expression to facilitate IL-12 signaling and drive naive CD4+ T cells differentiation into Th1 cells. We showed that BCG immunization reduced respiratory syncytial virus (RSV) infection. Thus, transcription regulation through epigenetic reprogramming plays a critical role in BCG-induced CD4+ T cell differentiation and to the broad antiviral activity. SignificanceBacille Calmette-Guerin (BCG) vaccination confers nonspecific protection against heterologous pathogens. Recent work demonstrated that coordinated interactions of innate immune and persistent CD4+ T cell response plays a critical role in BCG induced antiviral activity. In our study, we investigated BCG immunization on epigenetic reprogramming of CD4+ T cells and found that BCG immunization elicited antiviral activity by provoking T cell proliferation. We observed chromatin openness favoring naive T cell differentiation to Th1 response. Importantly, we observed STAT1 and interferon regulatory factor-1 (Irf1) activation. These findings provide mechanistic insights into BCG-induced Th1 response through epigenetic reprogramming and highlight the potential of BCG in offering a long-term protection against emerging and reemerging pathogens. Graphic abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=181 SRC="FIGDIR/small/655674v1_ufig1.gif" ALT="Figure 1"> View larger version (53K): org.highwire.dtl.DTLVardef@1c3cb94org.highwire.dtl.DTLVardef@16a8e8forg.highwire.dtl.DTLVardef@b58b88org.highwire.dtl.DTLVardef@dbc994_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIIntravenous BCG immunization drives naive CD4+ T cell differentiation to Th1 response; C_LIO_LIBCG alters chromatin accessibility for transcriptional factor expression favoring Th1 response through a Irf1-Il12rb1-IL12 feedback loop; C_LIO_LIThe immunization elicits antiviral activity against RSV infection; C_LI

immunology↗

PLK1-mediated phosphorylation of PHGDH reprograms serine metabolism in advanced prostate cancer

Metabolic reprogramming is a hallmark of cancer, enabling tumor cells to meet their increased biosynthetic and energetic demands. While cells possess the capacity for de novo serine biosynthesis, most transformed cancer cells heavily depend on exogenous serine uptake to sustain their growth, yet the regulatory mechanisms driving this metabolic dependency remain poorly understood. Here, we uncover a novel mechanism by which Polo-like kinase 1 (PLK1), often overexpressed in prostate cancer, orchestrates a metabolic shift in serine and lipid metabolism through the phosphorylation of phosphoglycerate dehydrogenase (PHGDH), the rate-limiting enzyme of the serine synthesis pathway (SSP). We demonstrate that PLK1 phosphorylates PHGDH at three specific sites (S512, S513, S517), leading to a marked reduction in its protein level and enzymatic activity. This downregulation of SSP forces cancer cells to increase their reliance on exogenous serine uptake via the ASCT2 transporter, which, in turn, fuels the biosynthesis of lipids, including sphingolipids essential for tumor growth and survival. Targeting the SSP, serine uptake, or downstream lipid biosynthetic pathways may offer promising therapeutic avenues in PLK1-high advanced cancers.

cancer biology↗

Cryo-EM structure of plant urea transporter DUR3 reveals essential role of C-terminal domain in tetramer assembly and insights into proton-coupled transport

Nitrogen pollution, caused by the overuse of nitrogen-fertilizers such as urea in agricultural production, has become a serious problem that threatens both the environment and human health. Improving the nitrogen use efficiency of crops is an important approach to reduce fertilizer use. DUR3, a high-affinity urea transporter, enables plants to acquire urea from natural or agricultural soils with low urea concentrations and has been proposed as a promising target for engineering crops to improve nitrogen-fertilizer use efficiency. Despite extensive studies for more than 20 years, the structure, substrate recognition and transport mechanism of DUR3 have remained unknown. Here we report the cryo-EM structure of maize DUR3 (ZmDUR3) at 3.41 [A] resolution. ZmDUR3 adopts an amino acid-polyamine-organocation (APC) superfamily fold and is structurally distinct from animal facilitative urea transporters. Our structure provides important insights into urea recognition by DUR3 and suggests that a pair of acidic residues is potentially involved in proton coupling during urea transport. Furthermore, our structural and functional studies indicate that DUR3 assembles into a tetramer and tetramer formation is important for its function. Our results pave the way for engineering plant DUR3 protein for applications in sustainable agricultural production.

plant biology↗

Cell Type-Specific Effects of miR-21 Loss Attenuate Tumor Progression in MYC-Driven Prostate Cancer

Aberrant microRNA expression is common in cancer, yet cell-type-specific microRNA activity in the tumor microenvironment (TME) remains poorly understood. Here, we show that germline deletion of miR-21 significantly attenuated the progression of MYC-driven prostate cancer (PCa), reducing prostate weight, tumor burden, and proliferation index in Hi-Myc mice. In situ hybridization revealed elevated miR-21 expression in multiple cell types during disease progression. Inflammatory and premalignant lesions in mouse and human prostate showed increased miR-21 in both stroma and epithelium, with further enrichment in the stroma of invasive adenocarcinoma. In Hi-Myc mice, single cell RNA-sequencing revealed miR-21 gene regulation in neoplastic, stromal, and immune cells in a cell-type-specific manner, impacting both direct and indirect targets. Notably, miR-21 deletion reduced immune infiltration into the prostate TME, particularly Trem2-expressing macrophages and regulatory T cells. The Timp1-fibroblast gene signature in MYC-driven PCa was suppressed in miR-21 knockout prostates. Cell-cell communication analysis showed that miR-21 suppressed TGF-beta signaling in the TME, partially through Ski and Smad7 suppression in cancer-associated fibroblasts. These findings underscore the crucial role of miR-21 in PCa and provide some of the first in situ insights into cell-type-specific miRNA activity in solid tumors.

cancer biology↗

A synergistic generative-ranking framework for tailored design of therapeutic single-domain antibodies

Single-domain antibodies (sdAbs) have emerged as powerful therapeutic agents due to their small size, high stability, and superior tissue penetration. However, unlike conventional monoclonal antibodies (mAbs), sdAbs lack an Fc domain, limiting their functional versatility and manufacturability. To address this challenge, we developed TFDesign-sdAb, a deep learning-based generative-ranking framework that enables rational engineering of sdAbs with tailored functionalities. Our framework integrates a structure-aware diffusion model (IgGM) for large-scale candidate generation and a fine-tuned sorter (A2binder) that evaluates and prioritizes them based on predicted functionality. Unlike traditional CDR-focused approaches, TFDesign-sdAb optimizes both complementarity-determining regions (CDRs) and framework regions (FRs), allowing sdAbs to acquire new functional properties while maintaining antigen specificity. We validated our approach by conferring Protein A binding to human VHs and nanobodies that originally lacked this feature, achieving high expression rates, strong binding affinities, and successful purification via industry-standard Protein A affinity chromatography. High-resolution structural characterization (1.49 [A] and 2.0 [A]) of the redesigned sdAb-Protein A complexes revealed conserved FR-mediated binding motifs that recapitulate natural Fc-Protein A interactions, validating the accuracy of our model. Furthermore, our pipeline streamlined the antibody engineering process, achieving a 100% success rate in generating Protein A-binding sdAbs while maintaining their original antigen-binding affinity. This work demonstrates the power of AI-driven design in overcoming long-standing limitations in antibody engineering and presents a scalable, generalizable solution for enhancing sdAb functionality.

bioinformatics↗

SANTON: Sequencing Analysis Toolkits for Off-target Nomination

BackgroundGenome-wide off-target nomination and screening sequencing methods, such as synthetic oligonucleotide-based sequencing and whole genome-based sequencing, evaluate the precision and safety of gene-editing technologies. However, there remains a lack of comprehensive bioinformatics tools for analyzing the sequencing data generated by off-target nomination assays for various gene editors, including Cas9, Cas12a, and base editors. ResultsWe introduce a Sequencing Analysis Toolkits for Off-target Nomination (SANTON) for the identification and quantification of potential off-target sites using datasets generated from synthetic oligonucleotide-based sequencing and whole genome-based sequencing (e.g., Digenome-seq) methods. By applying SANTON to a Cas9 treated oligo synthesization-based sequencing data, a comprehensive set of potential off-target sites are evaluated in which the top off-target sites displayed highly constituency with a published study using in vivo method (e.g, GUIDE-seq). Utilizing SANTON to previously published Digenome-seq datasets, we identified more potential off-target regions than previous studies, including ones showing significantly higher cleavage level than the on-target site. To the best of our knowledge, SANTON is the first public package capable of analyzing synthetic oligonucleotide-based sequencing data and the first to specific optimized for the analysis of whole genome-based sequencing analysis for Cas12a and base editors. We demonstrated the capability of SANTON to effectively analyze complex cleavage patterns by a diverse editing system. ConclusionsSANTON provides a powerful computational solution to support genome editing research, facilitating more reliable and comprehensive off-target profiling.

bioinformatics↗

scGenAI: A generative AI platform with biological context embedding of multimodal features enhances single cell state classification

SummarySingle-cell sequencing has advanced the understanding of cellular heterogeneity, yet traditional cell type annotation tools struggle with increasingly complex datasets and multimodal integration. Recent large language models (LLMs) offer improved accuracy but rely on pre-trained models with limited gene vocabularies and lack of biological contextualization. These constraints make it challenging to effectively fine-tune pre-trained models, especially for novel datasets, non-human species, or disease-specific studies where unique gene expression patterns are critical. To address these constraints, we developed scGenAI, an LLM-based tool that supports straightforward and flexible de novo training, allowing researchers to incorporate genomic and biofunctional contexts to improve accuracy and interpretability on the prediction of cell states. Here, we demonstrate that scGenAI outperforms conventional models in tasks such as cell type prediction and acute myeloid leukemia (AML) malignant cell states identification, making it a powerful tool for single-cell analysis workflows. Availability and implementationscGenAI (DOI: 10.5281/zenodo.14927611) is distributed as an open-source Python package, with source code and comprehensive documentation accessible on GitHub at https://github.com/VOR-Quantitative-Biology/scGenAI.

bioinformatics↗

Neural organoids protect engineered heart tissues from glucolipotoxicity by transferring versican in a co-culture system

Metabolic disorders could cause dysregulated glucose and lipid at the systemic level, but how inter-tissue/organ communications contribute to glucolipotoxicity is difficult to dissect in animal models. To solve this problem, myocardium and nerve tissues were modeled by 3D engineered heart tissues (EHTs) and neural organoids (NOs), which were co-cultured in a generalized medium with normal or elevated glucose/fatty acid contents. Morphology, gene expression, cell death and functional assessments detected no apparent alterations of EHTs and NOs in co-culture under normal conditions. By contrast, NOs significantly ameliorated glucolipotoxicity in EHTs. Transcriptomic and protein secretion assays identified the extracellular matrix protein versican as a key molecule that was transferred from NOs into EHTs in the high-glucose/fatty acid condition. Recombinant versican protein treatment was sufficient to reduce glucolipotoxicity in EHTs. Adeno-associated virus-delivered versican overexpression was sufficient to ameliorate cardiac dysfunction in a murine model of diabetic cardiomyopathy. These data provide the proof-of-concept evidence that inter-tissue/organ communications exist in the co-culture of engineered tissues and organoids, which could be systemically studied to explore potential pathological mechanisms and therapeutic strategies for multi-organ diseases in vitro.

cell biology↗

Inflammasome Activation in Cutaneous Squamous Cell Carcinoma

Epithelia maintain their barrier function by exploiting the proliferative and plastic properties of stem cells to promote continual tissue regeneration. Consequently, however, these features make epithelia prone to tumorigenesis. Skin is the largest epithelial barrier and the source of cutaneous cancers, the deadliest of which are cutaneous squamous cell carcinomas (cSCCs). Despite the pervasiveness of these cancers, however, the molecular mechanisms employed by stem cells and their microenvironment to promote skin tumor development remain poorly defined. Our previous work revealed that genotoxic damage to normal skin activates inflammasome signaling crosstalk between epidermal epithelia and fibroblasts to promote epithelial stem cell hyperproliferation and fate misspecification. We hypothesized that these phenomena would also be featured during skin cancer development. Using mouse and human skin disease specimens, we determined that in vivo stem cell misspecification is a generalizable feature across diverse pathophysiological skin conditions, including cutaneous cancers, but is not present in normal high proliferative contexts. Strikingly, in vivo inflammasome activation was observed in both the epithelial and dermal compartments of cSCC tumors but was not evident in other skin pathologies. Probing further into the mechanism, we revealed that inflammasome pathway activation in cSCC is epithelial autonomous but non-cell autonomous. Furthermore, fibroblasts juxtaposed to the cSCC epithelial tumor interface exhibited population expansion as well as IL-1 signaling activation, which was absent in overlying epithelia. Based on these findings, we propose a model whereby epithelial-to-fibroblast inflammasome crosstalk initiates a fibroblast feed-forward IL-1 signaling loop that augments the tumor-promoting cSCC milieu.

cell biology↗

Stretchable, hair-compatible, and long-term stable wearable EEG system

Electroencephalography (EEG) is a cornerstone in both neuroscience research and clinical diagnostics. However, conventional EEG monitoring faces hardware limitations, particularly its adaptability and stability. Headsets either require complicated wiring or do not have enough stretchability and wearability to comply with the diverse head anthropometry and hair conditions of the user population. Additionally, there is an inherent tradeoff between wet and dry electrodes in capturing high-fidelity signals from hair-covered scalp regions while ensuring continuous and long-term recording quality. Here, we present a Mesh-integrated, Stretchable, and Hair-compatible EEG system engineered to overcome these limitations. By incorporating a kirigami-inspired mesh design and stretchable eutectic Gallium-Indium interconnects, MindStretcH adapts to various head sizes and allows for easy wearing and removal. Moreover, its uniquely designed porous, conical, soft 3D-printed mold, embedded with hydrogel electrodes, effectively penetrates hair layers to deliver low impedance and sustained signal integrity with minimal discomfort. We validate MindStretcH through offline and online EEG-based brain-computer interface tasks over a month, demonstrating its exceptional stability in continuous monitoring and dynamic applications. These results mark a promising advance toward non-invasive neural interfaces in both clinical and everyday use.

bioengineering↗

Chromosome-Specific Aneuploidy Engineering via dCas9-Induced Centromeric Chromatin Relaxation

Aneuploidy, the gain or loss of chromosomes, is prevalent in both normal and disease conditions, however, experimental approaches to engineer and study aneuploidy remain limited, leaving its functional significance under-characterized. Here, we present CRISPR-Taiji (CRISPRt), an efficient method for inducing chromosome-specific mis-segregation and aneuploidy generation across all 24 human chromosomes via dead Cas9 (dCas9)-induced centromeric chromatin relaxation. Using CRISPRt with scRNA-seq, we generated the first comprehensive transcriptomic alteration landscape of nearly all autosomal aneuploidies at chromosome-arm resolution. This genotype-phenotype map provides causal evidence linking recurrent aneuploidies in clear cell renal cell carcinoma (ccRCC) to molecular and clinical phenotypes observed in patient tumors. Notably, chromosome 3(p) loss, the ccRCC initiating event, specifically drives strong interferon signaling activation, offering novel insights into ccRCC tumorigenesis and immune modulation. Overall, we establish CRISPRt as a simple, efficient and scalable approach for chromosome-specific aneuploidy engineering and characterization in preclinical models to advance aneuploidy research across diverse biological contexts.

genomics↗

Single and Multiple Buds Form characteristics in Amorphophallus muelleri

This study compared the physiological characteristics and transcriptomic profiles of single-budded and multi-budded corms, as well as developmental stages of foliar bulbils in Amorphophallus muelleri, to reveal regulatory mechanisms underlying bud development. Hormonal analysis showed that the IAA/CTK ratio was significantly higher in single-budded corms (1.9060 vs 1.5753), while multi-budded corms exhibited higher CTK (0.2766 g/g), BR (0.8692 p mol/g), and SLs (0.5090 ng/g) levels. During foliar bulbils development, ABA content peaked at 41.54 ng/g in the G2 stage, and sucrose reached maximum levels (6.86 mg/g) in the G1 stage. Transcriptomic sequencing identified 742 differentially expressed transcription factors, with over 80% of CRE1 and AHP genes in CTK signaling pathways significantly upregulated. KEGG pathway analysis highlighted starch/sucrose metabolism (215 DEGs) and plant hormone signal transduction (243 DEGs) as key regulatory networks. The study demonstrated that CTK signaling activation and carbohydrate metabolic reprogramming promoted multi-bud formation, while foliar bulbils development displayed stage-specific gene expression patterns, providing theoretical insights for improving konjac propagation coefficient.

physiology↗

DTMol: Pocket-based Molecular Docking using Diffusion Transformers

In computational chemistry, molecular docking--predicting the binding structure of a small molecule ligand to a protein--is vital for understanding interactions between small molecules and their protein targets, with broad applications in drug discovery (Morris and Lim-Wilby, 2008). Traditional docking methods rely on energy-based scoring functions and optimization algorithms to identify ligand-binding structures. However, these methods are often slow and inaccurate due to the extensive search space for binding structures and the complexity of scoring function landscapes (Corso et al., 2023). Deep learning techniques have emerged as promising alternatives for molecular docking. These methods harness the power of neural networks to understand the complex interactions between protein pockets and ligands from large datasets. They can be classified into two categories: regression-based methods (Stark et al., 2022; Lu et al., 2022), which offer greater computational efficiency compared to traditional docking methods but have yet to offer substantial improvements in accuracy (Corso et al., 2023); and generative models, particularly diffusion models (Corso et al., 2023; Qiao et al., 2024; Nakata et al., 2023; Lu et al., 2024; Schneuing et al., 2024), which lead to significant accuracy improvements compared to regression-based methods. Most diffusion-based docking methods aim to address the blind docking problem, where the ligand is docked without prior knowledge of the specific protein pocket--a site of the protein with potential ligand-binding capabilities--and only the overall protein structure is provided (Yim et al., 2024). However, in many drug discovery cases, specific pockets have already been identified (Zheng et al., 2013), meaning that the docking process only needs to determine how the ligand binds to the pocket. This defines the pocket-based docking problem. Pocket-based docking leverages the physical and chemical information of protein side chains around the pocket, significantly reducing the search space for ligand binding structures and improving the understanding of atomic-level interactions. Additionally, focusing on the local protein substructure rather than the global structure enhances computational efficiency, which allows for the use of more complex neural architectures. We introduce DTMol, a novel diffusion model designed to tackle the pocket-based docking problem. Our model integrates a pretrained molecular representation framework with a diffusion transformer architecture. The advantages of this design are twofold: first, the molecular representation models we employ are pretrained on separate datasets of small molecules and protein pockets, which are larger than the datasets of ligand-pocket interactions. Consequently, these pretrained models encode typical structural features of both elements, enhancing our models ability to represent them and predict binding structures. Second, the transformer architecture used in our diffusion model is more capable of effectively capturing all-atom interactions between the pocket and the ligand. We test our method on the docking benchmark PDBBind v2020 and PoseBuster, and compare it with other methods. DTMol achieves 77.65% top-1 success rate (RMSD {inverted exclamation} 2[A]) on PoseBuster, outperforms the second-best docking software Gnina (65.65%) We also test the performance of our method on a real-world virtual screening task using Janus kinase 2 (PDB ID: 6BBV) as the target protein. A TR-FRET screening experiment is performed on the union of top ligands identified via physics-based docking and the diffusion model, in order to measure their inhibitory activity against the JAK2 protein. The results shows that our model achieved the only positive rank correlation score compared to other traditional docking methods and machine learning-based methods. To summarize, the main contributions of this work are: - We introduce DTMol, a novel diffusion model designed to address the pocket-based docking problem. This model represents the first application of the diffusion transformer architecture in solving pocket-based molecular docking. - We propose a novel SE(3)-equivariant transformer architecture with an SE(3)-invariant and a parallel SE(3)-equivariant flow, which is straightforward to implement and train while achieving excellent performance. - We achieve new state-of-the-art results on both the PDBBind and PoseBuster pocket-based docking benchmarks, obtaining top-1 prediction rates of 45.05% and 77.65%, respectively, at RMSD < 2[A]. - Doing virtual screening on Janus kinase 2, DTMol is able to achieve the only positive rank score; and identifies 2 new experimentally effective JAK2 inhibitors.

bioinformatics↗

DNA Methylation in Sex Chromosomes and Genes under Selection Underpins the Emergence of Sexual Size Dimorphism

Sexual size dimorphism (SSD) refers to the differences in body size between males and females. Epigenetics such as methylation contribute to shaping phenotypes, nevertheless, their role in SSD is still unclear. Here, we used Cynoglossus semilaevis, a species with larger females known as female-biased SSD, as a model to investigate the role of methylation in the emergence and regulation of SSD. Methylomes and transcriptomes were constructed in four tissues (brain, liver, muscle, and gonad) from three key life stages: juveniles (3-months post fertilization), male mature stage (1-year post fertilization; ypf), and female mature stage (3 ypf). In 1 ypf and 3 ypf females showed lower methylation, while the number of differentially methylated regions between sexes increased during the lifetime. Genes at the top of the growth hormone/insulin-like growth factor (GH/IGF) axis and hypothalamus-pituitary-gonadal axis (gh1, igf1, gnrhr2r-like, err{gamma}, etc.) showed differential methylation between sexes, consistent with sex-related differences in growth. The female-specific W chromosome showed higher methylation than the autosomes or the Z chromosome. Genes of the IGF signaling network that negatively regulate growth and located on W chromosome were hyper-methylated than their Z homologs. Furthermore, genes with a faster evolutionary rate in C. semilaevis exhibited lower methylation levels than the background genes, suggesting an important evolutionary role for DNA methylation in shaping SSD. Our results provide a comprehensive depiction of methylation regulation of SSD in vertebrates, and improve our understanding of how methylation regulation can help organisms to respond to natural selection, and allocate resources between the sexes.

developmental biology↗

Novel Strategy against AML by Rescuing Loss of Phase Separation of Pathogenic NPM1c

Nucleophosmin (NPM1) is a nucleolar protein that participates in many biological processes through phase separation. In acute myeloid leukemia (AML), nearly one-third of cases harbor NPM1c mutations. Previous studies mainly focused on the contribution of the additional NES in NPM1c mislocalization and AML development; however, the mechanisms underlying the relationship between aberrant localization and phase separation of NPM1c remain poorly understood. In this study, we demonstrate that loss of phase separation (LoPS) with RNA is associated with NPM1c mislocalization, which uncovers a new strategy for therapeutic targeting of NPM1c. Leveraging high-throughput screening, we identify a potent small molecule capable of rescuing NPM1c LoPS in vitro and effectively restoring the nucleolar localization of NPM1c within cells. Remarkably, this compound demonstrates anti-leukemia activity in both AML cell lines and patient-derived blasts. Overall, these findings indicate a promising avenue for developing new AML therapies against NPM1c by reinstating its phase separation capabilities. One-Sentence SummaryRescuing the lost phase separation capacity of NPM1c unveils a promising AML therapy.

cancer biology↗