Biology subjects

Su, J.

Publications and source records attributed to Su, J..

At least 145 records · Page 8Linked to original sources

bioRxiv2021

Simultaneous in vivo Pharmacokinetics and Pharmacodynamics of TDF Intravaginal Ring during High-dose Vaginal SHIV Challenge in Pigtail Macaques

The demonstration of complete protection of macaques in a repeated low dose virus challenge by a tenofovir disoproxil fumarate (TDF) intravaginal ring (IVR) and the success of the dapivirine IVR in clinical trials highlighted the potential of IVRs as pre- exposure prophylaxis against HIV. Efficacy of TDF ring was not investigated in sexually active women. Our understanding of the mechanisms of protection is limited. To address this knowledge gap, we performed simultaneous pharmacokinetic and pharmacodynamic analysis of a TDF-IVR at the site of SIV challenge in pigtail macaques at the anatomical and cellular level. Specifically, we challenged TDF-IVR administered pigtail macaques with a single high dose of a non-replicative SIV-based vector containing a dual reporter system that helped us to identify the earliest targets of SIV infection within the mucosa. Two and three days after challenge, the macaques were euthanized and tenofovir (TFV) concentrations were measured in the female reproductive tract (FRT) by HPLC-MS/MS to correlate drug concentrations and SIV-vector transduction efficiency. TFV formed a gradient through the mucosal tissue, with the highest concentrations near the ring, in the upper vagina and endocervix. Despite this, several transduction events were identified with the most common sites being in the ovaries. Moreover, proviral DNA was detected in the cervix and vagina. Thus, our studies demonstrate an uneven distribution of TFV in the FRT of macaques after release from a TDF-IVR that leads to incomplete FRT protection from high viral dose challenge.

pharmacology and toxicology↗

bioRxiv2021

Multiview super-resolution microscopy

We enhance the performance of confocal microscopy over imaging scales spanning tens of nanometers to millimeters in space and milliseconds to hours in time, improving volumetric resolution more than 10-fold while simultaneously reducing phototoxicity. We achieve these gains via an integrated, four-pronged approach: 1) developing compact line-scanners that enable sensitive, rapid, diffraction-limited imaging over large areas; 2) combining line-scanning with multiview imaging, developing reconstruction algorithms that improve resolution isotropy and recover signal otherwise lost to scattering; 3) adapting techniques from structured illumination microscopy, achieving super-resolution imaging in densely labeled, thick samples; 4) synergizing deep learning with these advances, further improving imaging speed, resolution and duration. We demonstrate these capabilities on more than twenty distinct fixed and live samples, including protein distributions in single cells; nuclei and developing neurons in Caenorhabditis elegans embryos, larvae, and adults; myoblasts in Drosophila wing imaginal disks; and mouse renal, esophageal, cardiac, and brain tissues.

bioengineering↗

bioRxiv2021

Integrative molecular and clinical profiling of acral melanoma identifies LZTR1 as a key tumor promoter and therapeutic target

Acral melanoma, the most common melanoma subtype among non-Caucasian individuals, is associated with poor prognosis. However, its key molecular drivers remain obscure. Here, we performed integrative genomic and clinical profiling of acral melanomas from a cohort of 104 patients treated in North America or China. We found that recurrent, late-arising amplifications of cytoband chr22q11.21 are a leading determinant of inferior survival, strongly associated with metastasis, and linked to downregulation of immunomodulatory genes associated with response to immune checkpoint blockade. Unexpectedly, LZTR1 - a known tumor suppressor in other cancers - is a key candidate oncogene in this cytoband. Silencing of LZTR1 in melanoma cell lines caused apoptotic cell death independent of major hotspot mutations or melanoma subtypes. Conversely, overexpression of LZTR1 in normal human melanocytes initiated processes associated with metastasis, including anchorage-independent growth, formation of spheroids, and increased levels of MAPK and SRC activities. Our results provide new insights into the etiology of acral melanoma and implicate LZTR1 as a key tumor promoter and therapeutic target.

cancer biology↗

bioRxiv2021

The entorhinal cortex modulates trace fear memory formation and neuroplasticity in the lateral amygdala via cholecystokinin

Although the neural circuitry underlying fear memory formation is important in fear-related mental disorders, it is incompletely understood. Here, we utilized trace fear conditioning to study the formation of trace fear memory. We identified the entorhinal cortex (EC) as a critical component of sensory signaling to the amygdala. Moreover, we used the loss of function and rescue experiments to demonstrate that release of the neuropeptide cholecystokinin (CCK) from the EC is required for trace fear memory formation. We discovered that CCK-positive neurons extend from the EC to the lateral nuclei of the amygdala (LA), and inhibition of CCK-dependent signaling in the EC prevented long-term potentiation of sensory signals to the LA and formation of trace fear memory. Altogether, we suggest a model where sensory stimuli trigger the release of CCK from EC neurons, which potentiates sensory signals to the LA, ultimately influencing neural plasticity and trace fear memory formation.

neuroscience↗

bioRxiv2021

Regulation of Brain Primary Cilia Length by MCH Signaling: Evidence from Pharmacological, Genetic, Optogenetic and Chemogenic Manipulations

The melanin concentrating hormone (MCH) system is involved in numerous functions including energy homeostasis, food intake, sleep, stress, mood, aggression, reward, maternal behavior, social behavior, and cognition. MCH acts on a G protein-coupled receptor MCHR1, which expresses ubiquitously in the brain and localizes to neuronal primary cilia. Cilia act as cells antennas and play crucial roles in cell signaling to detect and transduce external stimuli to regulate cell differentiation and migration. Cilia are highly dynamic in terms of their length and morphology; however, it is not known if cilia length is causally regulated by MCH system activation in-vivo. In the current work, we examined the effects of the activation and inactivation of MCH system on cilia lengths by using different methodologies, including pharmacological (MCHR1 agonist and antagonist GW803430), germline and conditional genetic deletion of MCHR1 and MCH, optogenetic, and chemogenetic (Designer Receptors Exclusively Activated by Designer Drugs (DREADD)) approaches. We found that stimulation of MCH system either directly through MCHR1 activation, or indirectly through optogenetic and chemogenetic- mediated excitation of MCH neurons, causes cilia shortening. Contrarily, inactivation of MCH signaling through pharmacological MCHR1 blockade or through genetic manipulations - germline deletion of MCHR1 and conditional ablation of MCH neurons - induces cilia lengthening. Our study is the first to uncover the causal effects of the MCH system in the regulation of the length of brain neuronal primary cilia. These findings place MCH system at a unique position in the ciliary signaling in physiological and pathological conditions, and implicate cilia MCHR1 as a potential therapeutic target for the treatment of pathological conditions characterized by impaired cilia function.

molecular biology↗

bioRxiv2021

SARS-CoV-2 variant B.1.1.7 caused HLA-A2+ CD8+ T cell epitope mutations for impaired cellular immune response

The rapid spreading of the newly emerged SARS-CoV-2 variant, B.1.1.7, highlighted the requirements to better understand adaptive immune responses to this virus. Since CD8+ T cell responses play an important role in disease resolution and modulation in COVID-19 patients, it is essential to address whether these newly emerged mutations would result in altered immune responses. Here we evaluated the immune properties of the HLA-A2 restricted CD8+ T cell epitopes containing mutations from B.1.1.7, and furthermore performed a comprehensive analysis of the SARS-CoV-2 specific CD8+ T cell responses from COVID-19 convalescent patients and SARS-CoV-2 vaccinees recognizing the ancestral Wuhan strain compared to B.1.1.7. First, most of the predicted CD8+ T cell epitopes showed proper binding with HLA-A2, while epitopes from B.1.1.7 had lower binding capability than those from the ancestral strain. In addition, these peptides could effectively induced the activation and cytotoxicity of CD8+ T cells. Our results further showed that at least two site mutations in B.1.1.7 resulted in a decrease in CD8+ T cell activation and a possible immune evasion, namely A1708D mutation in ORF1ab1707-1716 and I2230T mutation in ORF1ab2230-2238. Our current analysis provides information that contributes to the understanding of SARS-CoV-2-specific CD8+ T cell responses elicited by infection of mutated strains or vaccination. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=172 SRC="FIGDIR/small/437363v2_ufig1.gif" ALT="Figure 1"> View larger version (29K): org.highwire.dtl.DTLVardef@b9f2cdorg.highwire.dtl.DTLVardef@1f39e3dorg.highwire.dtl.DTLVardef@119c313org.highwire.dtl.DTLVardef@565388_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

bioRxiv2021

RENET2: High-Performance Full-text Gene-Disease Relation Extraction with Iterative Training Data Expansion

BackgroundRelation extraction is a fundamental task for extracting gene-disease associations from biomedical text. Existing tools have limited capacity, as they can extract gene-disease associations only from single sentences or abstract texts. ResultsIn this work, we propose RENET2, a deep learning-based relation extraction method, which implements section filtering and ambiguous relations modeling to extract gene-disease associations from full-text articles. We designed a novel iterative training data expansion strategy to build an annotated full-text dataset to resolve the scarcity of labels on full-text articles. In our experiments, RENET2 achieved an F1-score of 72.13% for extracting gene-disease associations from an annotated full-text dataset, which was 27.22%, 30.30% and 29.24% higher than the best existing tools BeFree, DTMiner and BioBERT, respectively. We applied RENET2 to (1) ~1.89M full-text articles from PMC and found ~3.72M gene-disease associations; and (2) the LitCovid articles set and ranked the top 15 proteins associated with COVID-19, supported by recent articles. ConclusionRENET2 is an efficient and accurate method for full-text gene-disease association extraction. The source-code, manually curated abstract/full-text training data, and results of RENET2 are available at https://github.com/sujunhao/RENET2.

bioinformatics↗

bioRxiv2021

A cell-ECM mechanism for connecting the ipsilateral eye to the brain

Information about features in the visual world are parsed by circuits in the retina and are then transmitted to the brain by distinct subtypes of retinal ganglion cells (RGCs). Axons from RGC subtypes are stratified in retinorecipient brain nuclei, such as the superior colliculus (SC), to provide a segregated relay of parallel and feature-specific visual streams. Here, we sought to identify the molecular mechanisms that direct the stereotyped laminar targeting of these axons. We focused on ipsilateral-projecting subtypes of RGCs (ipsiRGCs) whose axons target a deep SC sublamina. We identified an extracellular glycoprotein, Nephronectin (NPNT), whose expression is restricted to this ipsiRGC-targeted sublamina. SC-derived NPNT and integrin receptors generated by ipsiRGCs are both required for the targeting of ipsiRGC axons to the deep sublamina of SC. Thus, a cell-extracellular matrix (ECM) recognition mechanism specifies precise laminar targeting of ipsiRGC axons and the assembly of eye-specific parallel visual pathways. Significance StatementDistinct features of the visual world are transmitted from the retina to the brain through anatomically segregated circuits. Despite this being an organizing principle of visual pathways in mammals, we lack an understanding of the signaling mechanisms guiding axons of different types of retinal neurons into segregated layers of brain regions. We explore this question by identifying how axons from the ipsilateral retina innervate a specific lamina of the superior colliculus. Our studies reveal a unique cell-extracellular matrix (ECM) recognition mechanism that specifies precise targeting of these axons to the superior colliculus. Loss of this mechanism not only resulted in the absence of this eye-specific visual circuit, but it led to an impairment of innate predatory visual behavior as well.

neuroscience↗

bioRxiv2021

CD8+ T cell epitope variations suggest a potential antigen presentation deficiency for spike protein of SARS-CoV-2

COVID-19 is caused by a newly identified coronavirus, SARS-CoV-2, and has become a pandemic around the world. The illustration of the immune responses against SARS-CoV-2 is urgently needed for understanding the pathogenesis of the disease and its vaccine development. CD8+ T cells are critical for virus clearance and induce long lasting protection in the host. Here we identified specific HLA-A2 restricted T cell epitopes in the spike protein of SARS-CoV-2. Seven epitope peptides (n-Sp1, 2, 6, 7, 11, 13, 14) were confirmed to bind with HLA-A2 and potentially be presented by antigen presenting cells to induce host immune responses. Tetramers containing these peptides could interact with specific CD8+ T cells from convalescent COVID-19 patients, and one dominant epitope (n-Sp1) was defined. In addition, these epitopes could activate and generate epitope-specific T cells in vitro, and those activated T cells showed cytotoxicity to target cells. Meanwhile, all these epitopes exhibited high frequency of variations. Among them, n-Sp1 epitope variation 5L>F significantly decreased the proportion of specific T cell activation; n-Sp1 epitope 8L>V variant showed significantly reduced binding to HLA-A2 and decreased the proportion of n-Sp1-specific CD8+ T cell, which potentially contributes to the immune escape of SAR-CoV-2.

immunology↗

bioRxiv2021

MMpred: a distance-assisted multimodal conformation sampling for de novo protein structure prediction

MotivationThe mathematically optimal solution in computational protein folding simulations does not always correspond to the native structure, due to the imperfection of the energy force fields. There is therefore a need to search for more diverse suboptimal solutions in order to identify the states close to the native. We propose a novel multimodal optimization protocol to improve the conformation sampling efficiency and modeling accuracy of de novo protein structure folding simulations. ResultsA distance-assisted multimodal optimization sampling algorithm, MMpred, is proposed for de novo protein structure prediction. The protocol consists of three stages: The first is a modal exploration stage, in which a structural similarity evaluation model DMscore is designed to control the diversity of conformations, generating a population of diverse structures in different low-energy basins. The second is a modal maintaining stage, where an adaptive clustering algorithm MNDcluster is proposed to divide the populations and merge the modal by adjusting the annealing temperature to locate the promising basins. In the last stage of modal exploitation, a greedy search strategy is used to accelerate the convergence of the modal. Distance constraint information is used to construct the conformation scoring model to guide sampling. MMpred is tested on a large set of 320 non-redundant proteins, where MMpred obtains models with TM-score[≥]0.5 on 268 cases, which is 20.3% higher than that of Rosetta guided with the same set of distance constraints. The results showed that MMpred can help significantly improve the model accuracy of protein assembly simulations through the sampling of multiple promising energy basins with enhanced structural diversity. AvailabilityThe source code and executable versions are freely available at https://github.com/iobio-zjut/MMpred. Contactzgj@zjut.edu.cn or zhng@umich.edu or sujz@wmu.edu.cn

bioinformatics↗

bioRxiv2021

Fission yeast Rad8/HLTF facilitates Rad52-dependent chromosomal rearrangements through PCNA lysine 107 ubiquitination

Rad52 recombinase can cause gross chromosomal rearrangements (GCRs). However, the mechanism of Rad52-dependent GCRs remains unclear. Here, we show that fission yeast Rad8/HLTF facilitates Rad52-dependent GCRs through the ubiquitination of lysine 107 (K107) of PCNA, a DNA sliding clamp. Loss of Rad8 reduced isochromosomes resulting from centromere inverted repeat recombination. Rad8 HIRAN and RING finger mutations reduced GCRs, suggesting that Rad8 facilitates GCRs through 3 DNA-end binding and ubiquitin ligase activity. Mms2 and Ubc4 but not Ubc13 ubiquitin-conjugating proteins were required for GCRs. Consistent with this, PCNA K107R but not K164R mutation greatly reduced GCRs. Rad8-dependent PCNA K107 ubiquitination facilitates Rad52-dependent GCRs, as PCNA K107R, rad8, and rad52 mutations epistatically reduced GCRs. Remarkably, K107 is located at the interface between PCNA subunits, and an interface mutation D150E bypassed the requirement of PCNA K107 ubiquitination for GCRs. This study uncovers the role of Rad8-dependent PCNA K107 ubiquitination in Rad52-dependent GCRs.

genomics↗

bioRxiv2020

The transcription factor Rreb1 regulates epithelial architecture and invasiveness in gastrulating mouse embryos

Ras-responsive element-binding protein 1 (Rreb1) is a zinc-finger transcription factor downstream of RAS signaling. Rreb1 has been implicated in cancer but little is known about its role in mammalian non-disease states. Here, we found that Rreb1 is essential for mouse embryonic development. Loss of Rreb1 led to a reduction in the expression of vasculogenesis factors, cardiovascular defects and embryonic lethality. During gastrulation, the absence of Rreb1 also resulted in the upregulation of cytoskeleton-associated genes, a change in the organization of F-ACTIN and adherens junctions within the pluripotent epiblast, and perturbed epithelial architecture characterized by irregular tissue folding and abnormal accumulations of cells. Moreover, Rreb1 mutant cells ectopically exited the epiblast epithelium through the underlying basement membrane, paralleling cell behaviors observed during metastasis. Thus, disentangling the function of Rreb1 in development could shed light on its role in cancer and other diseases involving loss of epithelial integrity.

developmental biology↗

bioRxiv2020

A Mycobacterium tuberculosis effector protein attacks host innate immunity by acting as an unusual ubiquitinating enzyme

Protein kinase G (PknG), a eukaryotic type serine-threonine protein kinase (STPK) in Mycobacterium tuberculosis (Mtb), is secreted into the cytosol of infected macrophages to promote intracellular survival of mycobacteria and has been considered as a promising therapeutic target for tuberculosis (TB) treatment. However, the molecular details of Mtb PknG-host intracellular interactions remain obscure. Here, we demonstrate that PknG serves as both the ubiquitin-activating enzyme (E1) and the ubiquitin ligase (E3) to promote ubiquitination and degradation of tumor necrosis factor receptor-associated factor 2 (TRAF2) and TGF-{beta}-activated kinase 1 (TAK1), and thus inhibits the NF-{kappa}B-mediated host innate immune responses. Surprisingly, PknG promotes the attachment of ubiquitin (Ub) to ubiquitin-conjugating enzyme (E2) UbcH7 via an isopeptide bond (UbcH7 K82-Ub), instead of a usual C86-Ub thiol-ester bond, and then promotes the discharge of Ub from UbcH7 by acting as an isopeptidase before attaching Ub to its substrates TRAF2 and TAK1. These results demonstrate that Mtb PknG promotes ubiquitination of the key components of the host innate immunity by acting as an unusual ubiquitinating enzyme to suppress innate immunity. Our findings provide a potential TB treatment via targeting unconventional ubiquitinating activities of PknG. SignificanceMycobacterium tuberculosis (Mtb) protein kinase G (PknG), which is critical for Mtb intracellular survival, is a promising target for tuberculosis (TB) treatment. However, the molecular mechanisms underlying PknG-host interactions remain largely unclear. Here we demonstrate that PknG serves as both the ubiquitin-activating enzyme and the ubiquitin ligase to promote the ubiquitination and degradation of tumor necrosis factor receptor-associated factor 2 (TRAF2) and TGF-{beta}-activated kinase 1 (TAK1), thus inhibiting NF-{kappa}B signaling activation. PknG promotes the attachment of ubiquitin to ubiquitin-conjugating enzyme UbcH7 via an isopeptide bond, instead of a usual thiol-ester bond, and releases the ubiquitin from UbcH7 by acting as an isopeptidase. These findings provide important information for rational development of TB treatment via targeting unconventional ubiquitinating activity of PknG.

microbiology↗

bioRxiv2020

DSTG: Deconvoluting Spatial Transcriptomics Data through Graph-based Artificial Intelligence

Recent development of spatial transcriptomics (ST) is capable of associating spatial information at different spots in the tissue section with RNA abundance of cells within each spot, which is particularly important to understand tissue cytoarchitectures and functions. However, for such ST data, since a spot is usually larger than an individual cell, gene expressions measured at each spot are from a mixture of cells with heterogenous cell types. Therefore, ST data at each spot needs to be disentangled so as to reveal the cell compositions at that spatial spot. In this study, we propose a novel method, named DSTG, to accurately deconvolute the observed gene expressions at each spot and recover its cell constitutions, thus achieve high-level segmentation and reveal spatial architecture of cellular heterogeneity within tissues. DSTG not only demonstrates superior performance on synthetic spatial data generated from different protocols, but also effectively identifies spatial compositions of cells in mouse cortex layer, hippocampus slice, and pancreatic tumor tissues. In conclusion, DSTG accurately uncovers the cell states and subpopulations based on spatial localization.

bioinformatics↗

bioRxiv2020

Airway bacterial and fungal microbiome in chronic obstructive pulmonary disease

BackgroundLittle is known about airway mycobiome, and its relationship with bacterial microbiome in chronic obstructive pulmonary disease (COPD). MethodsHere we report the first simultaneous characterization of sputum bacterial and fungal microbiome in 84 stable COPD and 29 healthy subjects, using 16S ribosomal DNA and fungal internal transcribed spacer DNA sequencing. ResultsAscomycota predominated over Basidiomycota in fungal microbiome both in COPD patients and healthy controls. Meyerozyma, Candida, Aspergillus and Schizophyllum were most abundant at the genus level. There was a significant inverse correlation between bacterial and fungal microbial diversity, both of which altered in opposite directions in COPD patients versus controls, and in frequent versus non-frequent exacerbators. An enhanced bacterial-fungal ecological interaction was observed in COPD patients, which was characterized by higher proportion of co-occurrence intrakingdom interactions and co-exclusive interkingdom interactions. In COPD, four mutually co-occurring fungal operational taxonomic units (OTUs) in Candida palmioleophila, Aspergillus and Sordariomycetes exhibited co-exclusive relationships with other fungal OTUs, which was specifically present in frequent exacerbators but not in non-frequent exacerbators. Conversely, the mutual co-occurrence interactions between bacterial OTUs in Rothia mucilaginosa, Streptococcus, Veillonella and Prevotella, showed up in non-frequent exacerbators but not in frequent exacerbators. The perturbed bacterial-fungal interactions in COPD were associated with increased airway inflammatory mediators such as IL-6 and IL-8. InterpretationThe disruption of airway bacterial-fungal community balance, characterized by the loss of commensal bacterial taxa and enriched pathogenic fungal taxa, is implicated in COPD. The airway mycobiome is an important cofactor mediating COPD pathogenic infection and host inflammation. Clinical Trial Registrationwww.clinicaltrials.gov (NCT 03240315).

microbiology↗

bioRxiv2020

Evaluation method of ecosystem service value under complex ecological environment: A case study of Gansu Province, China

Scientific assessment of regional ecosystem service value (ESV) is helpful to make scientific ecological protection plan and compensation policy. The evaluation method has not been established that is adapted to the complex and diverse characteristics of the ecological environment. This paper takes Gansu Province as an example, on the basis of fully considering the regional differences of ecosystem service function, the five correction index of value equivalent factor per unit area were constructed in the provincial scale, and the regional difference adjustment index of 11 kinds of ES was constructed in regional scale, in the way, the value evaluation model based on regional difference was established. The results show that in 2015, the total ESV reached 2239.555 billion Yuan in Gansu Province, ESV gradually increased from the northeast to the southwest, and the high-value areas of service function located in Qilian Mountain and Longnan Mountain, of which the forest and grassland ecosystem contributed the most to the value. From the perspective of value composition, local climate regulation and biodiversity maintenance function are the main service functions of Gansu Province. From 2000 to 2015, ESV increased by 3.426 billion Yuan in Gansu Province, the value of forest and urban ecosystem continued increasing, while the value of cultivated land ecosystem continue decreasing. From the spatial characteristics of service value change, the area of value reduction gradually moved from the central part of Gansu Province to the surrounding area. In general, although this study needs further improvement, the constructed evaluation method provides a relatively comprehensive evaluation scheme for the spatiotemporal dynamic evaluation of ESV in Gansu Province. This study provided a more overall research idea for the evaluation of ESV under complex ecological environment.

ecology↗

bioRxiv2020

The role of miR-31-5p in the development of intervertebral disk degeneration and its therapeutic potential

Intervertebral disc degeneration (IDD) refers to the abnormal response of cell-mediated progressive structural failure. In order to understand the molecular mechanism of the maintenance and destruction of the intervertebral disc, new IDD treatment methods are developed. Here, we first analyzed the key regulators of IDD through miRNA microarrays. The cell structure and morphology were discovered by Histological and radiographic. Then, the level of miR-31-5p was disclosed by qRT-PCR. The association between miR-31-5p and SDF-1/CXCR7 axis was discovered by 3'-Untranslated region (UTR) cloning and luciferase assay. The apoptosis of cells under different treatments was disclosed by Flow cytometer. The cell proliferation was discovered by EdU assay. Finally, the protein levels of SDF-1, CXCR7, ADAMTS-5, Col II, Aggrecan and MMP13 were discovered by Western blot. The results show that miR-31-5p is a key regulator of IDD and its level is down-regulated in IDD. Overexpression of miR-31-5p facilitates NP cell proliferation, inhibits apoptosis, facilitates ECM formation and inhibits the level of matrix degrading enzymes in NP cells. The SDF-1/CXCR7 axis is the direct target of miR-31-5p. miR-31-5p acts on IDD by regulating SDF-1/CXCR7. In vitro experiments further verified that the up-regulation of miR-31-5p prevented the development of IDD. In conclusion, overexpression of miR-31-5p can inhibit IDD by regulating SDF-1/CXCR7.

molecular biology↗

bioRxiv2020

scGCN: a Graph Convolutional Networks Algorithm for Knowledge Transfer in Single Cell Omics

Single-cell omics represent the fastest-growing genomics data type in the literature and the public genomics repositories. Leveraging the growing repository of labeled datasets and transferring labels from existing datasets to newly generated datasets will empower the exploration of the single-cell omics. The current label transfer methods have limited performance, largely due to the intrinsic heterogeneity and extrinsic differences between datasets. Here, we present a robust graph-based artificial intelligence model, single-cell Graph Convolutional Network (scGCN), to achieve effective knowledge transfer across disparate datasets. Benchmarked with other label transfer methods on totally 30 single cell omics datasets, scGCN has consistently demonstrated superior accuracy on leveraging cells from different tissues, platforms, and species, as well as cells profiled at different molecular layers. scGCN is implemented as an integrated workflow as a python software, which is available at https://github.com/QSong-github/scGCN.

bioinformatics↗