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Song, W.

Publications and source records attributed to Song, W..

At least 55 records · Page 3Linked to original sources

Control of spatiotemporal activation of organ-specific fibers in the vagus nerve by intermittent interferential current stimulation

Vagus nerve stimulation (VNS) is emerging as potential treatment for several chronic diseases, however, limited control of fiber activation to promote desired effects over side effects restricts clinical translation. Here we describe a new VNS method that relies on intermittent, interferential sinusoidal current stimulation (i2CS) through implanted, multi-contact epineural cuffs. In swine, i2CS elicits specific nerve potentials and end organ responses, distinct from equivalent non-interferential sinusoidal stimulation. Comparing experimental results with anatomical trajectories of nerve fascicles from end organs to the stimulation electrode indicates that i2CS activates organ-specific fascicles rather than the entire nerve. Experimental results and anatomically realistic, physiologically validated biophysical models of the vagus nerve demonstrate that i2CS reduces fiber activation at the focus of interference. Current steering and repetition frequency determine spatiotemporal pattern of vagal fiber activation, allowing tunable and precise control of neural and organ responses. In experiments in a cohort of anesthetized swine, i2CS has improved selectivity for a desired effect, mediated by smaller bronchopulmonary fibers, over a side effect, mediated by larger laryngeal fibers, compared to non-interferential sinusoidal or square pulse VNS.

neuroscience↗

A percolation-type criticality threshold controls immune protein coating of surfaces

When a material enters the body, it is immediately attacked by hundreds of proteins, organized into complex networks of binding interactions and reactions. How do such complex systems interact with a material, "deciding" whether to attack? We focus on the "complement" system of [~]40 blood proteins that bind microbes, nanoparticles, and medical devices, initiating inflammation. We show a sharp threshold for complement activation upon varying a fundamental material parameter, the surface density of potential complement attachment points. This sharp threshold manifests at scales spanning single nanoparticles to macroscale pathologies, shown here for diverse engineered and living materials. Computational models show these behaviors arise from a minimal subnetwork of complement, manifesting percolation-type critical transitions in the complement response. This criticality switch explains the "decision" of a complex signaling network to interact with a material, and elucidates the evolution and engineering of materials interacting with the body.

biophysics↗

Omicron-specific ultra-potent SARS-CoV-2 neutralizing antibodies targeting the N1/N2 loop of Spike N-terminal domain

A multitude of functional mutations continue to emerge on the N-terminal domain (NTD) of the spike protein in SARS-CoV-2 Omicron subvariants. Understanding the immunogenicity of Omicron NTD and the properties of antibodies elicited by it is crucial for comprehending the impact of NTD mutations on viral fitness and guiding vaccine design. In this study, we find that most of NTD-targeting antibodies isolated from individuals with BA.5/BF.7 breakthrough infection (BTI) are ancestral (wildtype or WT)-reactive and non-neutralizing. Surprisingly, we identified five ultra-potent neutralizing antibodies (NAbs) that can only bind to Omicron but not WT NTD. Structural analysis revealed that they bind to a unique epitope on the N1/N2 loop of NTD and interact with the receptor-binding domain (RBD) via the light chain. These Omicron-specific NAbs achieve neutralization through ACE2 competition and blockage of ACE2-mediated S1 shedding. However, BA.2.86 and BA.2.87.1, which carry insertions or deletions on the N1/N2 loop, can evade these antibodies. Together, we provided a detailed map of the NTD-targeting antibody repertoire in the post-Omicron era, demonstrating their vulnerability to NTD mutations enabled by its evolutionary flexibility, despite their potent neutralization. These results highlighted the importance of considering the immunogenicity of NTD in vaccine design. Author SummaryCOVID-19 pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues to be a major global public health concern four years after its emergence. The N-terminal domain (NTD) is a critical component of the spike glycoprotein, which is pivotal for SARS-CoV-2 cellular entry and serves as a primary target for antibody therapeutics and vaccine development. Characterizing the properties of antibodies elicited by NTD of Omicron sublineages is crucial for understanding viral evolution and guiding vaccine design. Here, we show that Omicron infection after vaccination induces majorly non-neutralizing NTD antibodies. Still, we identified a class of ultra-potent neutralizing antibodies (NAbs) which specifically bind to the NTD of Omicron sublineages. These NAbs neutralize the virus by competing with ACE2 and blocking ACE2-mediated S1 shedding. Structural analyses reveal that these antibodies target a unique epitope on the N1/N2 loop of NTD, and intriguingly interact with the receptor-binding domain (RBD) of spike glycoprotein. This class of NAbs with the special binding pattern, are escaped by BA.2.86 and BA.2.87.1 sublineages, shedding light on the role of recently emerged mutations in the N1/N2 loop of NTD. Our findings provide fresh insights into the immunogenicity of Omicron NTD, highlighting its capacity for antibody evasion due to its evolutionary flexibility. This underscores the importance of carefully considering the NTD component in vaccine design.

immunology↗

Unraveling Lineage Roadmaps and Cell Fate Determinants to Postnatal Neural Stem Cells and Ependymal cells in the Developing Ventricular Zone

The ventricular zone (VZ) is made up of adult neural stem cells (NSCs) and multi-ciliated ependymal cells (EPCs). Both NSCs and EPCs are derived from radial glial cells (RGCs). To date, the transcriptomic dynamics and the molecular mechanisms guiding the cell fate commitment during the differentiation remain poorly understood. In this study, we analysed the developing VZ at the single-cell resolution and identified three distinct cellular states of RGCs: bipotent glial progenitor cells (bGPCs), neonatal NSC-neuroblasts (nNSC-NBs) and neonatal EPCs (nEPCs). The differentiation from bGPCs to nNSC-NBs and nEPCs forms a continuous bifurcating trajectory. Further molecular analysis along the NSC branch unveiled a novel intermediate state of cells expressing oligodendrocyte precursor cell (OPC) and neuroblast (NB) marker genes. Several transcription factors (TFs) were proved to be essential for the EPC-lineage differentiation, with TFEB emerging as a key regulator dictating the bGPC fate. The activation of TFEB promoted differentiation towards NSC-NBs while restrained the trajectory towards EPCs. Our findings offer detailed insights into further understanding VZ development and lay the groundwork for investigating potential therapeutic strategies against VZ-related disorders, such as hydrocephalus and neurodegenerative diseases (NDDs).

genomics↗

Dysfunctional S1P/S1PR1 signaling in the dentate gyrus drives vulnerability of chronic pain-related memory impairment

Memory impairment in chronic pain patients is substantial and common, and few therapeutic strategies are available. Chronic pain-related memory impairment has susceptible and unsusceptible features. Therefore, exploring the underlying mechanisms of its vulnerability is essential for developing effective treatments. Here, combining two spatial memory tests (Y-maze test and Morris water maze), we segregated chronic pain mice into memory impairment-susceptible and -unsusceptible subpopulations in a chronic neuropathic pain model induced by chronic constrictive injury of the sciatic nerve. RNA-seq analysis and gain/loss-of-function study revealed that S1P/S1PR1 signaling is a determinant for vulnerability to chronic pain-related memory impairment. Knockdown of the S1PR1 in the DG promoted a susceptible phenotype and led to structural plasticity changes of reduced excitatory synapse formation and abnormal spine morphology as observed in susceptible mice, while overexpression of the S1PR1 and pharmacological administration of S1PR1 agonist in the DG promoted an unsusceptible phenotype and prevented the occurrence of memory impairment, and rescued the morphological abnormality. Finally, GO enrichment analysis and biochemical evidence indicated that down-regulation of S1PR1 in susceptible mice may impair DG structural plasticity via interaction with actin cytoskeleton rearrangement-related signaling pathways including Itga2 and its downstream Rac1/Cdc42 signaling and Arp2/3 cascade. These results reveal a novel mechanism and provide a promising preventive and therapeutic molecular target for vulnerability to chronic pain-related memory impairment.

neuroscience↗

Single-cell dissection of prognostic architecture and immunotherapy response in Helicobacter pylori infection associated gastric cancer

Most of the gastric cancer (GC) worldwide are ascribed to Helicobacter pylori (H. pylori) infections, which have a detrimental effect on the immunotherapys efficacy. Comprehensively dissecting the key cell players and molecular pathways associated with cancer immunotherapies is critical for developing novel therapeutic strategies against H. pylori infection associated GC. We performed a comprehensive single-cell transcriptome analysis of nine GC with current H. pylori infection (HpGC), three GC with previous H. pylori infection (ex-HpGC), six GC without H. pylori infection (non-HpGC), and six healthy controls (HC). We also investigated key cell players and molecular pathways associated with GC immunotherapy outcomes. We revealed the molecular heterogeneity of different cell components in GC including epithelium, immune cells, and cancer-associated fibroblasts (CAFs) at the single-cell level. The malignant epithelium of HpGC exhibited high expression level of inflammatory and epithelial-mesenchymal transition (EMT) signature, HpGC and ex-HpGC were enriched with VEGFA+ angiogenic tumor-associated macrophages (Angio-TAM) and IL11+ inflammatory CAF (iCAF), characterized by high expression levels of NECTIN2 and VEGFA/B. Additionally, we found significant correlations between the abundance of iCAF with Angio-TAM and TIGIT+ suppressive T cells, and iCAF interacted with Angio-TAM through the VEGF and ANGPTL angiogenic pathways. We also developed an immune signature and angiogenic signature and demonstrated that the iCAF abundance and angiogenic signature could predict poor immunotherapy outcomes in GC. We revealed the transcriptome characteristics and heterogeneity of various cellular constituents of HpGC and demonstrated that a synergistic combination of immunotherapy and anti-angiogenic targeted therapy may be an effective therapeutic modality for HpGC.

cancer biology↗

Neisseria gonorrhoeae induces local secretion of IL-10 at the human cervix to promote asymptomatic colonization

Gonorrhea, caused by the human-restricted pathogen Neisseria gonorrhoeae, is a commonly reported sexually transmitted infection. Since most infections in women are asymptomatic, the true number of infections is likely much higher than reported. How gonococci (GC) colonize womens vaginocervix without triggering symptoms remains elusive. Using a human cervical tissue explant model, we found that GC inoculation increased the local secretion of both pro- (IL-1{beta} and TNF-) and anti-inflammatory (IL-10) cytokines during the first 24-h. Cytokine induction required GC expression of an Opa isoform that binds the host receptors carcinoembryonic antigen-related cell adhesion molecules (CEACAMs). GC inoculation induced NF-{kappa}B activation in both cervical epithelial and subepithelial cells. However, inhibition of NF-{kappa}B activation, which reduced GC-induced IL-1{beta} and TNF-, did not affect GC colonization. Neutralizing IL-10 or blocking IL-10 receptors by antibodies reduced GC colonization by increasing epithelial shedding and epithelial cell-cell junction disassembly. Inhibition of the CEACAM downstream signaling molecule SHP1/2, which reduced GC colonization and increased epithelial shedding, reduced GC-induced IL-10 secretion. These results show that GC induce local IL-10 secretion at the cervix by engaging the host CEACAMs to prevent GC-colonizing epithelial cells from shedding while suppressing inflammation activation, providing a potential mechanism for GC asymptomatic infection in women.

cell biology↗

Omicron-specific naive B cell maturation alleviates immune imprinting induced by SARS-CoV-2 inactivated vaccine

SARS-CoV-2 ancestral strain-induced immune imprinting poses great challenges to vaccine updates. Studies showed that repeated Omicron exposures could override immune imprinting induced by inactivated vaccines but not mRNA vaccines, a disparity yet to be understood. Here, we analyzed the underlying mechanism of immune imprinting alleviation in inactivated vaccine (CoronaVac) cohorts. We observed in CoronaVac-vaccinated individuals who experienced BA.5/BF.7 breakthrough infection (BTI), the proportion of Omicron-specific memory B cells (MBCs) substantially increased after an extended period post-Omicron BTI, with their antibodies displaying enhanced somatic hypermutation and neutralizing potency. Consequently, the neutralizing antibody epitope distribution encoded by MBCs post-BA.5/BF.7 BTI after prolonged maturation closely mirrors that in BA.5/BF.7-infected unvaccinated individuals. Together, these results indicate the activation and expansion of Omicron-specific naive B cells generated by first-time Omicron exposure helped to alleviate CoronaVac-induced immune imprinting, and the absence of this process should have caused the persistent immune imprinting seen in mRNA vaccine recipients. HighlightsO_LILongitudinal MBC profiling of CoronaVac-vaccinated individuals following BA.5 BTI C_LIO_LIOmicron-specific MBC proportion rises greatly after extended period post-BA.5 BTI C_LIO_LIOmicron-specific naive B cell maturation reduces ancestral strain immune imprinting C_LI

immunology↗

Persistent lung inflammation and alveolar-bronchiolization due to Notch signaling dysregulation in SARS-CoV-2 infected hamster

Long COVID or Post-acute sequalae of COVID-19 (PASC) defines the persistent signs, symptoms, and conditions long after initial SARS-CoV-2 infection which affecting over 10% of COVID-19 patients, with 40% of them affecting respiratory system. The lung histopathological changes and underlying mechanism remain elusive. Here we systemically investigate histopathological and transcriptional changes at 7, 14, 42, 84 and 120 days-post-SARS-CoV-2-infection (dpi) in hamster. We demonstrate persistent viral residues, chronic inflammatory and fibrotic changes from 42dpi to 120dpi. The most prominent lung histopathological lesion is multifocal alveolar-bronchiolization observed in every animal from 14dpi until 120dpi. However, none of the above are observed in hamsters recovered from influenza A infection. We show airway progenitor CK14+ basal cells actively proliferate, differentiate into SCGB1A+ club cell or Tubulin+ ciliated cells, leading to alveolar-bronchiolization. Most importantly, Notch pathway is persistently upregulated. Intensive Notch3 and Hes1 protein expression are detected in alveolar-bronchiolization foci, suggesting the association of sustained Notch signaling with dysregulated lung regeneration. Lung spatial transcriptomics show upregulation of genes positively regulating Notch signaling is spatially overlapping with alveolar-bronchiolization region. To be noted, significant upregulation of tumor-related genes was detected in abnormal bronchiolization region by spatial transcriptomics analysis, indicating possible risk of lung carcinoma. Collectively, our data suggests SARS-CoV-2 infection caused chronic inflammatory and fibrotic tissue damages in hamster lung, sustained upregulation of Notch pathway signaling contributed to the dysregulated lung regeneration and CK14+ basal cells-driven alveolar-bronchiolization. The study provides important information for potential therapeutic approaches and probable long-term surveillance of malignancy in PASC management.

microbiology↗

Humoral immunogenicity comparison of XBB and JN.1 in human infections

The continuous evolution of SARS-CoV-2, particularly the emergence of the BA.2.86/JN.1 lineage replacing XBB lineages, necessitates re-evaluation of current vaccine compositions. Here, we provide a comprehensive analysis of the humoral immune response to XBB and JN.1 human exposures, emphasizing the need for JN.1-lineage-based boosters. We demonstrate the antigenic distinctiveness of XBB and JN.1 lineages in SARS-CoV-2-naive individuals but not in those with prior vaccinations or infections, and JN.1 infection elicits superior plasma neutralization titers against its subvariants. We highlight the strong immune evasion and receptor binding capability of KP.3, supporting its foreseeable prevalence. Extensive analysis of the BCR repertoire, isolating [~]2000 RBD-specific monoclonal antibodies (mAbs) with their targeting epitopes characterized by deep mutational scanning (DMS), underscores the systematic superiority of JN.1-elicited memory B cells (MBCs). Notably, Class 1 IGHV3-53/3-66-derived neutralizing antibodies (NAbs) contribute majorly within wildtype (WT)-reactive NAbs against JN.1. However, KP.2 and KP.3 evade a substantial subset of them, even those induced by JN.1, advocating for booster updates to KP.3 for optimized enrichment. JN.1-induced Omicron-specific antibodies also demonstrate high potency across all Omicron lineages. Escape hotspots of these NAbs have mainly been mutated in Omicron RBD, resulting in higher immune barrier to escape, considering the probable recovery of previously escaped NAbs. Additionally, the prevalence of broadly reactive IGHV3-53/3-66- encoding antibodies and MBCs, and their capability of competing with all Omicron-specific NAbs suggests their inhibitory role on the de novo activation of Omicron-specific naive B cells, potentially explaining the heavy immune imprinting in mRNA-vaccinated individuals. These findings delineate the evolving antibody response to Omicron antigenic shift from XBB to JN.1, and highlight the importance of developing JN.1 lineage, especially KP.3-based vaccine boosters, to enhance humoral immunity against current and future SARS-CoV-2 variants.

immunology↗

A generalized framework to identify SARS-CoV-2 broadly neutralizing antibodies

Monoclonal antibodies (mAbs) targeting the SARS-CoV-2 receptor-binding domain (RBD) are used to treat and prevent COVID-19. However, the rapid evolution of SARS-CoV-2 drives continuous escape from therapeutic mAbs. Therefore, the ability to identify broadly neutralizing antibodies (bnAbs) against future variants is needed. Here, we use deep mutational scanning (DMS) to predict viral RBD evolution and to select for mAbs neutralizing both existing and prospective variants. A retrospective analysis of 1,103 SARS-CoV-2 wildtype-elicited mAbs shows that this method can increase the probability of identifying effective bnAbs against the XBB.1.5 strain from 1% to 40% in an early pandemic setup. Among these bnAbs, BD55-1205 exhibited potent activity against all tested variants. Cryo-EM structural analyses revealed the receptor mimicry of BD55-1205, explaining its broad reactivity. Delivery of mRNA-LNPs encoding BD55-1205-IgG in mice resulted in ~5,000 serum NT50 against XBB.1.5, HK.3.1, and JN.1 variants. Combining bnAb identification using viral evolution prediction with the versatility of mRNA delivery technology can enable rapid development of next-generation antibody-based countermeasures against SARS-CoV-2 and potentially other pathogens with pandemic potential.

immunology↗

Pro-renin Receptor Inhibited ABCA1/G1 Expression Associated with Low HDL-c and Promoted Atherosclerosis

Background(Pro)renin receptors [(P)RR] binding both renin and its inactive proenzyme for prorenin induce increasing the efficiency of angiotensin I conversion and the production of angiotensin II (Ang II). Recently, (P)RR was reported to played a pathological role in diabetic renal disease independent of Ang II. Ang II is involved in lipid metabolism and atherosclerosis, but the (P)RR participation in atherosclerosis remains unclear. Thus, the objective of this study was to examine the relative importance of Ang II-independent actions of (P)RR and its mechanism in the development of atherosclerosis. MethodsClinical demographic characteristics and laboratory profile data of 1189 essential hypertensive were collected. Patients were divided into four groups based on the quartiles of plasma renin activity (PRA). The plasma lipoprotein levels of four groups were compared. Furthermore, we examined serum and liver lipoprotein levels, as well as ATP-binding cassette transporter A1 (ABCA1) and ATP-binding cassette transporter G1 (ABCG1) expression in ApoE-/- mice treated with prorenin. ABCA1 and ABCG1 expression and their function in mediating cholesterol efflux were evaluated in THP-1 cells by prorenin treatment. Agonists of the peroxisome proliferator-activated receptor-{gamma} (PPAR-{gamma}) and liver X receptor (LXR) were used to investigate the mechanism involved in vitro. ResultsPlasma TC, TG, LDL-c, and apoB were significantly increased, and HDL-c and apoA were dramatically decreased with a trend of higher plasma renin activity (PRA) ( all P < 0.05) in hypertensive patients. Prorenin accelerated atherosclerosis by inhibiting mRNA and protein expression of ABCA1/ABCG1 in the liver of ApoE-/- mice. Prorenin binding to (P)RR inhibited the functions of ABCA1- and ABCG1-mediated cholesterol efflux. Furthermore, Prorenin reduced ABCA1/G1 expression of THP-1 cells through PPAR{gamma}/LXR pathway. Conclusions(P)RR activated by prorenin inhibited the expression of ABCA1/ABCG1 through the PPAR{gamma}/LXR pathway and the functions of ABCA1- and ABCG1-mediated cholesterol efflux, resulting in dyslipidemia and eventually atherosclerosis. HighlightsWith RPA increases in hypertension, plasma TC, TG, LDL-c, and apoB were higher, while HDL-c and apoA were lower. Prorenin binding to (P)RR accelerated atherosclerosis by inhibiting ABCA1/G1 expression and function. Prorenin reduced ABCA1/G1 expression of THP-1 cells through PPAR{gamma}/LXR pathway.

pathology↗

Regulation of fatty acid delivery to metastases by tumor endothelium

Tumor metastasis, the main cause of death in cancer patients, requires outgrowth of tumor cells after their dissemination and residence in microscopic niches. Nutrient sufficiency is a determinant of such outgrowth1. Fatty acids (FA) can be metabolized by cancer cells for their energetic and anabolic needs but impair the cytotoxicity of T cells in the tumor microenvironment (TME)2, 3, thereby supporting metastatic progression. However, despite the important role of FA in metastatic outgrowth, the regulation of intratumoral FA is poorly understood. In this report, we show that tumor endothelium actively promotes tumor growth and restricts anti-tumor cytolysis by transferring FA into developing metastatic tumors. This process uses transendothelial fatty acid transport via endosome cargo trafficking in a mechanism that requires mTORC1 activity. Thus, tumor burden was significantly reduced upon endothelial-specific targeted deletion of Raptor, a unique component of the mTORC1 complex (RptorECKO). In vivo trafficking of a fluorescent palmitic acid analog to tumor cells and T cells was reduced in RptorECKO lung metastatic tumors, which correlated with improved markers of T cell cytotoxicity. Combination of anti-PD1 with RAD001/everolimus, at a low dose that selectively inhibits mTORC1 in endothelial cells4, impaired FA uptake in T cells and reduced metastatic disease, corresponding to improved anti-tumor immunity. These findings describe a novel mechanism of transendothelial fatty acid transfer into the TME during metastatic outgrowth and highlight a target for future development of therapeutic strategies.

cancer biology↗

SERBP1 interacts with PARP1 and is present in PARylation-dependent protein complexes regulating splicing, cell division, and ribosome biogenesis

RNA binding proteins (RBPs) containing intrinsically disordered regions (IDRs) are present in diverse molecular complexes where they function as dynamic regulators. Their characteristics promote liquid-liquid phase separation (LLPS) and the formation of membraneless organelles such as stress granules and nucleoli. IDR-RBPs are particularly relevant in the nervous system and their dysfunction is associated with neurodegenerative diseases and brain tumor development. Serpine1 mRNA-binding protein 1 (SERBP1) is a unique member of this group, being mostly disordered and lacking canonical RNA-binding domains. We defined SERBP1s interactome, uncovered novel roles in splicing, cell division and ribosomal biogenesis, and showed its participation in pathological stress granules and Tau aggregates in Alzheimers brains. SERBP1 preferentially interacts with other G-quadruplex (G4) binders, implicated in different stages of gene expression, suggesting that G4 binding is a critical component of SERBP1 function in different settings. Similarly, we identified important associations between SERBP1 and PARP1/polyADP-ribosylation (PARylation). SERBP1 interacts with PARP1 and its associated factors and influences PARylation. Moreover, protein complexes in which SERBP1 participates contain mostly PARylated proteins and PAR binders. Based on these results, we propose a feedback regulatory model in which SERBP1 influences PARP1 function and PARylation, while PARylation modulates SERBP1 functions and participation in regulatory complexes.

genomics↗

CircRNA-Pro: A Novel Toolkit for High-Precision Detection of Differentially Expressed Circular RNAs and Translatable Circular RNAs

With the increasing discovery of circular RNAs (circRNAs) and their critical roles in gene regulation and disease progression, there is a growing need for more accurate and efficient tools for circRNAs research. In response, we have developed an integrated software suite specifically for circRNAs. This all-in-one tool specializes in detecting differentially expressed circRNAs, including those with the potential to be translated into proteins, and allows for comparing against relevant databases, thereby enabling comprehensive circRNA profiling and annotation. To enhance the accuracy in detecting differentially expressed circRNAs, we incorporated three different software algorithms and cross-validated their results through mutual verification. Additionally, this toolkit improves the effectiveness in identifying translatable circRNAs by optimizing Ribo-seq alignment and verifying against public circRNA databases. The performance of circRNA-pro has been evaluated through its application to public RNA-seq and Ribo-seq datasets on breast cancer and SARS-CoV-2 infected cells, and the results obtained have been validated against previous literature and databases. Overall, our integrated toolkit provides a reliable workflow for circRNA research, facilitating insights into their diverse roles across life sciences.

bioinformatics↗

Antigenicity assessment of SARS-CoV-2 saltation variant BA.2.87.1

The recent emergence of a SARS-CoV-2 saltation variant, BA.2.87.1, which features 65 spike mutations relative to BA.2, has attracted worldwide attention. In this study, we elucidate the antigenic characteristics and immune evasion capability of BA.2.87.1. Our findings reveal that BA.2.87.1 is more susceptible to XBB-induced humoral immunity compared to JN.1. Notably, BA.2.87.1 lacks critical escaping mutations in the receptor binding domain (RBD) thus allowing various classes of neutralizing antibodies (NAbs) that were escaped by XBB or BA.2.86 subvariants to neutralize BA.2.87.1, although the deletions in the N-terminal domain (NTD), specifically 15-23del and 136-146del, compensate for the resistance to humoral immunity. Interestingly, several neutralizing antibody drugs have been found to restore their efficacy against BA.2.87.1, including SA58, REGN-10933 and COV2-2196. Hence, our results suggest that BA.2.87.1 may not become widespread until it acquires multiple RBD mutations to achieve sufficient immune evasion comparable to that of JN.1.

immunology↗

Chrom-pro: A User-Friendly Toolkit for De-novo Chromosome Assembly and Genomic Analysis

Chromosome-level genome assembly is fundamental to current genomic and post-genomic research, however, the process remains complicated and challenging due to the lack of a standardized automatic workflow. The frequently-used method for high-quality genome assembly generally employs second-generation sequencing (SGS) low error reads, third-generation sequencing (TGS) long reads and Hi-C reads. In this study, we developed a multifunctional toolkit called Chrom-pro that integrated commonly-used algorithms for de novo chromosome-level genome assembly with above three data sets into a user-friendly, automatic workflow. Besides chromosome assembly, Chrom-pro also encompasses multiple functionalities for genome quality assessment, comparative genomic analysis, and structural variant detection, which offers substantial support for downstream research. To evaluate the performance of Chrom-pro software, we tested the software with publicly available sequencing data of mango, pufferfish, and plum, and the excellence was confirmed by achieving a BUSCO completeness score of over 95% as well as high collinearity with the reference genome. Furthermore, we applied Chrom-pro to investigating the impact of different internal algorithm options on the accuracy of chromosome assembly, providing guidance for advancing relevant research in the future. Overall, the development of Chrom-pro will significantly improve the efficiency and quality of chromosome assembly and contributing to the advancement of genomic research.

bioinformatics↗

Chlomito: a novel tool for precise elimination of organelle genome contamination in nuclear genome assemblies

Accurate genome assemblies are crucial for understanding biological evolution, mechanisms of disease, and biodiversity. However, contamination from organelle genomes in nuclear genome analyses often leads to inaccuracies and unreliability in results. To address this issue, we developed a tool named Chlomito, which employs innovative algorithms to precisely identify and eliminate organelle genome contamination sequences from nuclear genome assemblies. Compared to conventional approaches, Chlomito can not only detect and eliminate organelle sequences but also effectively distinguish true organelle sequences from those transferred into the nucleus via horizontal gene transfer. To evaluate the accuracy of Chlomito, we conducted tests using sequencing data from Plum and Mango. The results confirmed that Chlomito can accurately detect contigs originating from the organelle genome, and the identified contigs covered most regions of the organelle reference genomes, demonstrating its efficiency and precision in comprehensively recognizing organelle genome sequences. Additionally, for user convenience, we packaged this method into a Docker image, simplifying the data processing workflow. Overall, Chlomito provides a highly efficient and accurate method for identifying and removing contigs derived from organelle genomes in genomic assembly data, thereby contributing to the improvement of genome assembly quality and advancing research in genomics and evolutionary biology.

bioinformatics↗