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Shi, J.

Publications and source records attributed to Shi, J..

At least 145 records · Page 8Linked to original sources

Identify compound-protein interaction with knowledge graph embedding of perturbation transcriptomics

The emergence of perturbation transcriptomics provides a new perspective and opportunity for drug discovery, but existing analysis methods suffer from inadequate performance and limited applicability. In this work, we present PertKGE, a method designed to improve compound-protein interaction with knowledge graph embedding of perturbation transcriptomics. PertKGE incorporates diverse regulatory elements and accounts for multi-level regulatory events within biological systems, leading to significant improvements compared to existing baselines in two critical "cold-start" settings: inferring binding targets for new compounds and conducting virtual ligand screening for new targets. We further demonstrate the pivotal role of incorporating multi- level regulatory events in alleviating dataset bias. Notably, it enables the identification of ectonucleotide pyrophosphatase/phosphodiesterase-1 as the target responsible for the unique anti- tumor immunotherapy effect of tankyrase inhibitor K-756, and the discovery of five novel hits targeting the emerging cancer therapeutic target, aldehyde dehydrogenase 1B1, with a remarkable hit rate of 10.2%. These findings highlight the potential of PertKGE to accelerate drug discovery by elucidating mechanisms of action and identifying novel therapeutic compounds.

bioinformatics↗

APOBEC shapes tumor evolution and age at onset of lung cancer in smokers

APOBEC enzymes are part of the innate immunity and are responsible for restricting viruses and retroelements by deaminating cytosine residues1,2. Most solid tumors harbor different levels of somatic mutations attributed to the off-target activities of APOBEC3A (A3A) and/or APOBEC3B (A3B)3-6. However, how APOBEC3A/B enzymes shape the tumor evolution in the presence of exogenous mutagenic processes is largely unknown. Here, by combining deep whole-genome sequencing with multi-omics profiling of 309 lung cancers from smokers with detailed tobacco smoking information, we identify two subtypes defined by low (LAS) and high (HAS) APOBEC mutagenesis. LAS are enriched for A3B-like mutagenesis and KRAS mutations, whereas HAS for A3A-like mutagenesis and TP53 mutations. Unlike APOBEC3A, APOBEC3B expression is strongly associated with an upregulation of the base excision repair pathway. Hypermutation by unrepaired A3A and tobacco smoking mutagenesis combined with TP53-induced genomic instability can trigger senescence7, apoptosis8, and cell regeneration9, as indicated by high expression of pulmonary healing signaling pathway, stemness markers and distal cell-of-origin in HAS. The expected association of tobacco smoking variables (e.g., time to first cigarette) with genomic/epigenomic changes are not observed in HAS, a plausible consequence of frequent cell senescence or apoptosis. HAS have more neoantigens, slower clonal expansion, and older age at onset compared to LAS, particularly in heavy smokers, consistent with high proportions of newly generated, unmutated cells and frequent immuno-editing. These findings show how heterogeneity in mutational burden across co-occurring mutational processes and cell types contributes to tumor development, with important clinical implications.

genomics↗

2P-NucTag: on-demand phototagging for molecular analysis of functionally identified cortical neurons

Neural circuits are characterized by genetically and functionally diverse cell types. A mechanistic understanding of circuit function is predicated on linking the genetic and physiological properties of individual neurons. However, it remains highly challenging to map the molecular properties onto functionally heterogeneous neuronal subtypes in mammalian cortical circuits in vivo. Here, we introduce a high-throughput two-photon nuclear phototagging (2P-NucTag) approach for on-demand and indelible labeling of single neurons via a photoactivatable red fluorescent protein following in vivo functional characterization in behaving mice. Using this novel function-forward pipeline to selectively label and transcriptionally profile previously inaccessible place and silent cells in the hippocampus of behaving mice, we identify unexpected differences in gene expression between these hippocampal pyramidal neurons with distinct spatial coding properties. Thus, 2P-NucTag opens a new way to uncover the molecular principles that govern the functional organization of neural circuits. One-Sentence Summary2P-NucTag - A novel high-throughput on-demand phototagging approach to identify selective gene expression of functionally distinct neurons in vivo in behaving animals.

neuroscience↗

Cancer Stemness Online: A resource for investigating cancer stemness and associations with immune response

Cancer progression involves the gradual loss of a differentiated phenotype and acquisition of progenitor and stem-cell-like features, which are potential culprit in immunotherapy resistance. Although the state-of-art predictive computational methods have facilitated predicting the cancer stemness, currently there is no efficient resource that can meet various requirements of usage. Here, we presented the Cancer Stemness Online, an integrated resource for efficiently scoring cancer stemness potential at bulk and single-cell level. The resource integrates 8 robust predictive algorithms as well as 27 signature gene sets associated with cancer stemness for predicting the stemness scores. Downstream analyses were performed from five different aspects, including identifying the signature genes of cancer stemness, exploring the association with cancer hallmarks, cellular states, immune response and communication with immune cells, investigating the contributions for patient survival and the robustness analysis of cancer stemness among different methods. Moreover, the pre-calculated cancer stemness atlas for more than 40 cancer types can be accessed by users. Both the tables and diverse visualization for the analytical results are available for download. Together, Cancer Stemness Online is a powerful resource for scoring cancer stemness and going deeper and wider in the downstream functional interpretation, including immune response as well as cancer hallmark. Cancer Stemness Online is freely accessible at http://bio-bigdata.hrbmu.edu.cn/CancerStemnessOnline.

bioinformatics↗

iSORT: An Integrative Method for Reconstructing Spatial Organization of Cells using Transfer Learning

Spatial tissues exhibit complex gene expression and multicellular patterns that are difficult to dissect. Single-cell RNA sequencing (scRNA-seq) provides full coverages of genes, but lacking spatial information, whereas spatial transcriptomics (ST) measures spatial locations of individual or group of cells, with more restrictions on gene information. To integrate scRNA-seq and ST data, we introduce a transfer learning method to decipher spatial organization of cells named iSORT. iSORT trains a neural network that maps gene expressions to spatial locations using scRNA-seq data along with ST slices as references. iSORT can find spatial patterns at single-cell scale, identify key genes that drive the patterning, and infer pseudo-growth trajectories using a concept of SpaRNA velocity. Benchmarking on simulation data and comparing with multiple existing tools show iSORTs robustness and accuracy in reconstructing spatial organization. Using our own new human artery datasets, iSORT shows its capability of dissecting atherosclerosis. Applications to a range of biological systems, such as mouse embryo, mouse brain, Drosophila embryo, and human developmental heart, demonstrate that iSORT can utilize both scRNA-seq and ST datasets to uncover multilayer spatial information of single cells.

bioinformatics↗

Targeted Dab2 Restoration: A Novel Approach for Enhanced Wound Healing in Diabetic Conditions

Diabetes mellitus can cause impaired and delayed wound healing, leading to lower extremity amputations; however, the mechanisms underlying the regulation of vascular endothelial growth factor (VEGF)-dependent angiogenesis remain uncertain and could reveal new therapeutic targets. In our study, the molecular underpinnings of endothelial dysfunction in diabetes were investigated, focusing on the roles of Disabled-2 (Dab2) and Forkhead Box M1 (FoxM1) in VEGF receptor 2 (VEGFR2) signaling and endothelial cell (EC) function. Bulk RNA-sequencing analysis identified significant downregulation of Dab2 in high concentrations glucose treated primary mouse skin ECs, simulating hyperglycemic conditions in diabetes mellitus. In diabetic mice with a genetic EC deficiency of Dab2 angiogenesis was reduced in vivo and in vitro when compared with wild-type mice. Restoration of Dab2 expression by injected mRNA-containing lipid nanoparticles rescued impaired angiogenesis and wound healing in diabetic mice. At the same time, FoxM1 was downregulated in skin ECs subjected to high glucose conditions as determined by RNA-sequencing analysis. FoxM1 was found to bind to the Dab2 promoter, regulating its expression and influencing VEGFR2 signaling. The FoxM1 inhibitor FDI-6 reduced Dab2 expression and phosphorylation of VEGFR2. These findings indicate that restoring Dab2 expression through targeted therapies can enhance angiogenesis and wound repair in diabetes. To explore this therapeutic potential, we tested LyP-1-conjugated lipid nanoparticles (LNPs) containing Dab2 or control mRNAs to target ECs and found the former significantly improved wound healing and angiogenesis in diabetic mice. This study provides evidence of the crucial roles of Dab2 and FoxM1 in diabetic endothelial dysfunction and establishes targeted delivery as a promising treatment for diabetic vascular complications.

cell biology↗

Morphological and genetic analysis of inflorescence and flower development in hemp (Cannabis sativa L.)

Hemp (Cannabis sativa) is one of the oldest cultivated crops, and its myriad of uses have fascinated humans for millennia. In contemporary agriculture, the seeds are used for high-quality oil, human food, and nutritional supplements. From female inflorescences, secondary compounds (cannabinoids, terpenes, and flavonoids) are isolated that are implicated to have a wide range of medicinal applications. These elements provide hemp with significant market and research value and emphasise the need to thoroughly understand reproductive development in hemp. Here, we present a detailed morphological and molecular analysis of hemp inflorescence and flower development of the cultivar FINOLA. Hemp is unusual among flowering plants as it is dioecious, i.e. develops male and female plants. We define eight landmark events in male and female flower development and show that developmental differences between male and female plants extend beyond floral morphology, additionally comprising inflorescence structure as well as flowering time. Further, we demonstrate that the time of activation of key reproductive developmental regulators is significantly different in male and female hemp plants. Our comparison of male and female hemp plants shows that developmental pathways diverge very early, already at the two-leaf stage, laying a basis for further exploration into the genetics of sex determination of C. sativa.

plant biology↗

Dual-targeted nanoparticulate drug delivery systems for enhancing triple-negative breast cancer treatment

The efficacy of DNA-damaging agents, such as the topoisomerase I inhibitor SN38, is often compromised by the robust DNA repair mechanisms in tumor cells, notably homologous recombination (HR) repair. Addressing this challenge, we introduce a novel nano-strategy utilizing binary tumor-killing mechanisms to enhance the therapeutic impact of DNA damage and mitochondrial dysfunction in cancer treatment. Our approach employs a synergistic drug pair comprising SN38 and the BET inhibitor JQ-1. We synthesized two prodrugs by conjugating linoleic acid (LA) to SN38 and JQ-1 via a cinnamaldehyde thioacetal (CT) bond, facilitating co-delivery. These prodrugs co-assemble into a nanostructure, referred to as SJNP, in an optimal synergistic ratio. SJNP was validated for its efficacy at both the cellular and tissue levels, where it primarily disrupts the transcription factor protein BRD4. This disruption leads to downregulation of BRCA1 and RAD51, impairing the HR process and exacerbating DNA damage. Additionally, SJNP releases cinnamaldehyde (CA) upon CT linkage cleavage, elevating intracellular ROS levels in a self-amplifying manner and inducing ROS-mediated mitochondrial dysfunction. Our results indicate that SJNP effectively targets murine triple-negative breast cancer (TNBC) with minimal adverse toxicity, showcasing its potential as a formidable opponent in the fight against cancer.

cancer biology↗

Structural insights into peptidoglycan hydrolysis by the FtsEX system in Escherichia coli during cell division

Bacterial cell division relies on precise peptidoglycan (PG) remodelling, a process orchestrated by the FtsEX complex. Comprised of FtsE and FtsX, this complex collaborates with EnvC, a periplasmic lytic enzyme activator, to regulate septal PG hydrolysis by amidases like AmiB. While recent structural investigations, particularly of Pseudomonas aeruginosa FtsEX (PaeFtsEX), have shed light on complex interactions and proposed activation mechanisms, the structural intricacies governing PG degradation by the FtsEX complex and EnvC in Escherichia coli cytokinesis remain unexplored. In this study, we present a comprehensive biochemical and structural analysis of E. coli FtsEX complexes, unveiling a key role for ATP in complex stabilization that extends across bacterial species. Upon EnvC binding, ATPase activity markedly increases. High-resolution structures of EcoFtsEX, both in the presence and absence of EnvC, reveal a symmetrical conformation of EcoFtsEX capable of accommodating the inherent asymmetry of EnvC, mediated by flexible loops within the periplasmic domain. Our negative-staining imaging showcases an elongated EcoFtsEX/EnvC/AmiB complex reminiscent of the PaeFtsEX system. These findings collectively provide intricate insights into the regulation of PG cleavage by FtsEX in E. coli - a pivotal model system used in pilot genetic studies, suggesting a conserved mechanism for precise hydrolase activation in bacteria.

microbiology↗

A Comprehensive Survey of Scoring Functions for Protein Docking Models

The protein-protein docking problem is fundamental to our understanding of how proteins interact. It is also important because of its relevance to drug discovery and vaccine design. Docking methods typically involve two steps. The first step generates many possible candidate conformations, while the second step evaluates the candidates using some scoring function. Despite numerous experiments with many innovative scoring functions, a good scoring function for docking remains elusive. Deep learning models offer alternatives to using explicit empirical or mathematical functions for scoring protein-protein complexes. In this study, we perform a comprehensive survey of the state-of-the-art scoring functions by considering the most popular and highly performant approaches for scoring protein-protein complexes, evaluating their strengths and weaknesses to aid researchers in understanding progress made in this field. Our survey compares the state-of-the-art in classical and deep learning-based scoring methods.

molecular biology↗

Molecular Disambiguation of Heart Rate Control by the Nucleus Ambiguus

The nucleus ambiguus (nAmb) provides parasympathetic control of cardiorespiratory functions as well as motor control of the upper airways and esophagus. A subset of nAmb neurons innervates the heart through the vagus nerve to control cardiac function at rest and during key autonomic reflexes such as the mammalian diving reflex. Yet, how these cardiovagal nAmb neurons differ from other nAmb neurons in the adult brain remains unclear. We therefore classified adult mouse nAmb neurons molecularly, anatomically, and functionally. First, our integrated analysis of single-nucleus RNA-sequencing data predicted multiple molecular subtypes of nAmb neurons. Mapping the axon projections of one nAmb neuron subtype, Npy2r-expressing nAmb neurons, showed that they innervate cardiac ganglia but not the upper airways or esophagus. Chemogenetically stimulating Npy2r+ nAmb neurons robustly decreased heart rate through peripheral muscarinic acetylcholine receptors. Finally, Npy2r+ nAmb neurons are activated during voluntary underwater diving, consistent with a cardiovagal function for this nAmb subtype. These results together reveal the molecular organization of nAmb neurons and its control of heart rate.

neuroscience↗

Natural reversal of cavefish heart asymmetry is controlled by Sonic Hedgehog effects on the left-right organizer

The direction of left-right (L-R) visceral asymmetry is conserved in vertebrates. Deviations of the asymmetric pattern are rare, and the underlying mechanisms are not understood. Here we use the teleost Astyanax mexicanus, a single species consisting of surface fish with normal left-oriented heart asymmetry and cavefish with high levels of reversed right-oriented heart asymmetry, to explore natural changes in L-R determination. We show that Sonic Hedgehog (Shh) signaling is increased at the posterior midline, Kupffers Vesicle (KV), the teleost L-R Organizer (LRO), is enlarged and contains longer cilia, and the number of dorsal forerunner cells, the KV precursors, is increased in cavefish. Furthermore, Shh overexpression in surface fish induces KV modifications and changes in heart asymmetry resembling the cavefish phenotype. Asymmetric expression of the Nodal antagonist dand5 is equalized or reversed in the cavefish KV, and Shh overexpression in surface fish mimics changes in cavefish L-R dand5 asymmetry and shifts Nodal laterality in the lateral plate mesoderm. Our results show that naturally occurring modifications in cavefish heart asymmetry are controlled by the effects of enhanced Shh signaling on LRO function. SummaryNatural reversal of cavefish heart asymmetry is controlled by enhanced Sonic Hedgehog signaling at the posterior midline, which modifies left-right organizer function and subsequent Nodal laterality.

developmental biology↗

Bi-parental graph strategy to represent and analyze hybrid plant genomes

Hybrid plants are universally existed in wild and often exhibit greater performance of complex traits compared with their parents and other selfing plants. This phenomenon, known as heterosis, has been extensively applied in plant breeding for decades. However, the process of decoding hybrid plant genomes has seriously lagged due to the challenges in their genome assembling and the lack of proper methods to further represent and analyze them. Here we report the assembly and analysis of two hybrids: an intraspecific hybrid between two maize inbred lines and an interspecific hybrid between maize and its wild relative teosinte, based on the combination of PacBio High Fidelity (HiFi) sequencing and chromatin conformation capture sequencing data. The haplotypic assemblies are well-phased at chromosomal scale, successfully resolving the complex loci with extensive parental structural variations (SVs). By integrating into a bi-parental genome graph, the haplotypic assemblies can facilitate downstream short-reads based SV calling and allele-specific gene expression analysis, demonstrating outstanding advantages over one single linear genome. Our work provides an entire workflow which hopefully can promote the deciphering of the large numbers of hybrid plant genomes, especially those whose parents are unknown or unavailable and help to understand genome evolution and heterosis.

bioinformatics↗

Hybrid Adipocyte-Derived Exosome Nano Platform for Potent Chemo-Phototherapy in Targeted Hepatocellular Carcinoma

The high prevalence and severity of hepatocellular carcinoma (HCC) present a significant menace to human health. Despite the significant advancements in nanotechnology-driven antineoplastic agents, there remains a conspicuous gap in the development of targeted chemotherapeutic agents specifically designed for HCC. Consequently, there is an urgent need to explore potent drug delivery systems for effective HCC treatment. Here we have exploited the interplay between HCC and adipocyte to engineer a hybrid adipocyte-derived exosome platform, serving as a versatile vehicle to specifically target HCC and exsert potent antitumor effect. A lipid-like prodrug of docetaxel (DSTG) with a reactive oxygen species (ROS)-cleavable linker, and a lipid-conjugated photosensitizer (PPLA), spontaneously co-assemble into nanoparticles, functioning as the lipid cores of the hybrid exosomes (HEMPs and NEMPs). These nanoparticles are further encapsuled within adipocyte-derived exosome membranes, enhancing their affinity towards HCC cancer cells. As such, cancer cell uptakes of hybrid exosomes are increased up to 5.73-fold compared to lipid core nanoparticles. Our in vitro and in vivo experiments have demonstrated that HEMPs not only enhance the bioactivity of the prodrug and extend its circulation in the bloodstream but also effectively inhibit tumor growth by selectively targeting hepatocellular carcinoma tumor cells. Self-facilitated synergistic drug release subsequently promoting antitumor efficacy, inducing significant inhibition of tumor growth with minimal side effects. Our findings herald a promising direction for the development of targeted HCC therapeutics. Graphical abstractAn adipocyte-derived exosome nanoplatform has been developed for the combined therapy of both chemotherapy and photodynamic therapy. The hybrid adipocyte-derived exosome nanoplatform integrates the advantage of targeted co-delivery and combination therapy, which can stimulate the release of drugs under the tumor microenvironment, effectively enhanced targeted co-delivery in hepatocellular carcinoma cells, prolonged blood circulation time and improve the therapeutic effect of hepatocellular carcinoma tumors model. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=152 SRC="FIGDIR/small/567027v2_ufig1.gif" ALT="Figure 1"> View larger version (83K): org.highwire.dtl.DTLVardef@195f031org.highwire.dtl.DTLVardef@cc2b02org.highwire.dtl.DTLVardef@1bbdd9org.highwire.dtl.DTLVardef@14d147d_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

The HIV-1 capsid serves as a nanoscale reaction vessel for reverse transcription

The viral capsid performs critical functions during HIV-1 infection and is a validated target for antiviral therapy. Previous studies have established that the proper structure and stability of the capsid are required for efficient HIV-1 reverse transcription in target cells. Moreover, it has recently been demonstrated that permeabilized virions and purified HIV-1 cores undergo efficient reverse transcription in vitro when the capsid is stabilized by addition of the host cell metabolite inositol hexakisphosphate (IP6). However, the molecular mechanism by which the capsid promotes reverse transcription is undefined. Here we show that wild type HIV-1 particles can undergo efficient reverse transcription in vitro in the absence of a membrane-permeabilizing agent. This activity, originally termed "natural endogenous reverse transcription" (NERT), depends on expression of the viral envelope glycoprotein during virus assembly and its incorporation into virions. Truncation of the gp41 cytoplasmic tail markedly reduced NERT activity, indicating that gp41 permits the entry of nucleotides into virions. Protease treatment of virions markedly reduced NERT suggesting the presence of a proteinaceous membrane channel. By contrast to reverse transcription in permeabilized virions, NERT required neither the addition of IP6 nor a mature capsid, indicating that an intact viral membrane can substitute for the function of the viral capsid during reverse transcription in vitro. Collectively, these results demonstrate that the viral capsid functions as a nanoscale container for reverse transcription during HIV-1 infection.

microbiology↗

The mtDNA-derived lncMtDloop promotes mitochondrial homeostasis maintenance and implications in AD

Maintaining mitochondrial homeostasis stands as a critical factor for cell survival and the health of organisms, as evidenced by the links between mitochondrial dysfunction and a spectrum of diseases, including Alzheimers disease (AD). Here we report that lncMtDloop, a lncRNA originating from the mtDNA D-loop, upholds mitochondrial homeostasis. LncMtDloop demonstrates an affinity for mitochondrial transcription factor A (TFAM), thereby facilitating TFAMs recruitment to mtDNA promoters and enhancing gene transcription. We further observed decreased lncMtDloop expression in the brains of human AD patients and 3xTg mice. Through the introduction of allotropic lncMtDloop with the 3UTR of MRPS12, a significant improvement in mitochondrial homeostasis and a concurrent amelioration of AD-like pathology were found, which exerts a positive influence on synaptic plasticity and behavioral deficits observed in AD mice. Our study provides mechanistic insights into lncMtDloop as a regulator of mitochondrial homeostasis, shedding light on a perspective regarding its contribution to Alzheimers pathogenesis.

molecular biology↗

Elasticity of the HIV-1 Core Facilitates Nuclear Entry and Infection

HIV-1 infection requires passage of the viral core through the nuclear pore of the cell, a process that depends on functions of the viral capsid 1,2. Recent studies have shown that HIV- 1 cores enter the nucleus prior to capsid disassembly 3-5. Interactions with the nuclear pore complex are necessary but not sufficient for nuclear entry, and the mechanism by which the viral core traverses the comparably sized nuclear pore is unknown. Here we show that the HIV-1 core is highly elastic and that this property is linked to nuclear entry and infectivity. Using atomic force microscopy-based approaches, we found that purified wild type cores rapidly returned to their normal conical morphology following a severe compression. Results from independently performed molecular dynamic simulations of the mature HIV-1 capsid also revealed its elastic property. Analysis of four HIV-1 capsid mutants that exhibit impaired nuclear entry revealed that the mutant viral cores are brittle. Suppressors of the mutants restored elasticity and rescued infectivity and nuclear entry. Elasticity was also reduced by treatment of cores with the capsid-targeting compound PF74 and the antiviral drug lenacapavir. Our results indicate that capsid elasticity is a fundamental property of the HIV-1 core that enables its passage through the nuclear pore complex, thereby facilitating infection. These results provide new insights into the mechanisms of HIV-1 nuclear entry and the antiviral mechanisms of HIV-1 capsid inhibitors.

biophysics↗