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Biology subjects

Ji, Q.

Publications and source records attributed to Ji, Q..

At least 19 recordsLinked to original sources

Critical reassessment of lipophilic dye labeling reveals negligible incorporation into small extracellular vesicles derived form serum-free cultured cells

Lipophilic dyes are widely used to track extracellular vesicles (EVs), yet their labeling efficiency toward bona fide small EVs (sEVs) remains poorly defined. Using a serum-free HEK293F system that produces endogenously fluorescent protein-tagged sEVs (sEVs-FPT) as an unambiguous reference while minimizing interference from dye-binding non-vesicular particles, we reassessed this efficiency with two orthogonal methods: nanoflow cytometry and fluorescence microscopy. PKH26, PKH67, and DiD labeled less than 0.5% of sEVs-FPT, regardless of vesicle heterogeneity. In vivo, dye-derived signals were far less abundant than tag-derived signals and failed to colocalize with them. Mechanistic evidence indicates that this failure stems from the inability of sEVs, as acellular structures, to actively internalize dye aggregates. These findings reveal a fundamental limitation of lipophilic dye-based EV tracking and underscore the need for orthogonally validated labeling strategies. One Sentence SummaryLipophilic dyes fail to label bona fide small extracellular vesicles, calling dye-based vesicle tracking into question.

bioengineering↗

Eleven deep-sea coral genome assemblies unveil insights into evolution, adaptation, and coral biodiversity

Deep-sea corals are vital in maintaining coral ecosystem biodiversity, yet their genetic characteristics remain largely unexplored. Here, we present 11 deep-sea coral genome assemblies, including four Hexacorallia and seven Octocorallia species, significantly contributing new genomic information across two orders. Our analysis reveals the historical dynamics of coral speciation and the influence of environmental factors on the evolution of coral reef ecosystems.Total of 126 horizontal gene transfer (HGT) events were detected, among which genes from the ancestor of symbiodiniaceae indicate that the ancestors of deep-sea corals may have inhabited shallow-sea environments. Notably, several of these HGTs are involved in phosphorus (PhnX/PhnW) and cholesterol (DHCR7) metabolisms within corals, indicating that HGTs may serve as an adaptive survival strategy for the coral holobionts. Deep-sea corals also rely on symbiotic bacteria to synthesize 10 essential amino acids (such as valine and tyrosine), retaining only partial amino acid synthesis capacity. In addition, we investigated the evolution of key biological rhythm genes and temperature adaptation in corals. The loss of key rhythm genes (e.g., clock and cry) in deep-sea corals and copy number difference of genes related to heat stress (e.g., Cbl-b and Rchy) revealed genetic difference between deep-sea and shallow-sea corals. Our new genome assemblies enhance the understanding of deep-sea coral evolution, biodiversity, and adaptation, providing a genetic foundation for coral conservation.

genomics↗

The genetic repertoire of the deep sea: from sequence to structure and function

The deep sea as the largest and maybe most hostile environment on Earth is still underexplored especially regarding its genetic repertoire. Yet, previous work has revealed significant habitat-specific deep-sea biodiversity. Here, we present an integrated deep-sea genetic dataset comprising 502 million nonredundant genes from 2,138 samples and 2.4 million predicted structures, and used it to link specific protein structures with genetic variants associated with life in the deep sea and to assess their biotechnology potential. Combining global sequence analysis with biophysical and biochemical measurements revealed unprecedented sequence diversity, yet substantial structural conservation of proteins. Especially proteins involved in replication, recombination, and repair were identified to be under rapid evolution and with specialized properties. Among these, a structurally divergent helicase exhibited advantages in controlling nanopore sequencing speed. Thus, our work positions the deep sea as a unique evolutionary engine that generates and hosts genetic diversity and bridges genetic knowledge with biotechnology.

bioinformatics↗

AI-driven discovery of host thioredoxin as a CRISPR enhancer of phage-encoded miniature Cas12 hacker nuclease

The evolutionary arms race between bacteriophages and their bacterial hosts has driven the evolution of sophisticated adaptive immune systems, such as CRISPR-Cas, as a crucial defense mechanism. While bacteriophages have developed various anti-CRISPR strategies to counteract these immune systems, the role of bacterial host factors in enhancing CRISPR-Cas functions has been relatively unexplored. In this study, we employ an artificial intelligence (AI)-driven approach to systematically analyze potential interactions between Escherichia coli (E. coli) proteins and fifteen previously uncharacterized Cas12 proteins, generating 65,715 predicted binary complex structures. Our findings reveal a previously unknown dimension of CRISPR immunity, demonstrating that the hosts ubiquitous redox enzyme, thioredoxin (TrxA), significantly enhances the DNA cleavage efficiency of a phage-encoded, miniature Cas12 nuclease (termed Cas12 hacker). This synergistic relationship represents a strategic inversion, where a bacteriophage hijacks a host protein to reinforce its own genome degradation machinery, possibly targeting rival nucleic acids. Through comprehensive biochemical characterizations, structural analyses of the Cas12 hacker-TrxA-sgRNA-dsDNA quaternary complex, and in vivo bacterial defense assays, we uncover an intricate association in which thioredoxin binds to and activates the Cas12 hacker nuclease, intensifying its DNA cleavage capacity and bolstering CRISPR immunity. Our findings expand the understanding of the molecular interactions underlying host-phage conflicts and highlight the potential for harnessing endogenous host factors to enhance the capabilities of CRISPR-based genetic engineering tools.

microbiology↗

Structure and engineering of miniature Acidibacillus sulfuroxidans Cas12f1

The miniature CRISPR-Cas12f nucleases allow for efficient delivery via cargo-size-limited adeno-associated virus delivery vehicles, thereby showing promising potential for in vivo therapeutic applications. Acidibacillus sulfuroxidans Cas12f1 (AsCas12f1, 422 amino acids) is the most compact Cas12f nuclease identified to date, showing a moderate level of genome-editing activity in human cells compared to Cas9 and Cas12a. Understanding the mechanisms of why such a compact nuclease is active for genome editing would facilitate its rational engineering. Here, we report the cryo-EM structure of the AsCas12f1-sgRNA-dsDNA ternary complex, and reveal that AsCas12f1 functions as an asymmetric dimer for single-guide RNA (sgRNA) binding and DNA targeting. The detailed mechanisms for dimer formation, PAM recognition, and sgRNA accommodation are elucidated. Leading by the structural knowledge, we extensively engineer the AsCas12f1 nuclease and its corresponding sgRNA, resulting in an evolved AsCas12f1-sgRNA combination with drastically enhanced genome editing activity in human cells. These results provide further understanding of compact CRISPR systems and expand the mini CRISPR toolbox for therapeutic applications.

molecular biology↗

TERT accelerates BRAF mutant-induced thyroid cancer dedifferentiation and progression by regulating ribosome biogenesis

TERT reactivation occurs frequently in human malignancies. While BRAF activating mutation widely existed in cancers at various stages, TERT reactivation mainly occurs in advanced tumors. However, in vivo evidence for TERT role in cancer progression and the underlying mechanism is currently lacking. In this study, we induced TERT and/or BRAF V600E expression in mouse thyroid epithelium. TERT overexpression alone had no evident effect on tumor initiation. BRAFVE expression itself induced mediocre papillary thyroid cancer (PTC). Notably, the co-expression of BRAFVE and TERT resulted in aggressive poorly differentiated thyroid carcinoma (PDTC). Spatial transcriptome revealed that tumors from co-mutant mice were highly heterogeneous and dedifferentiation process significantly correlated with ribosomal pathways. Mechanistically, TERT boosted ribosomal RNA expression and protein synthesis. CX-5461, a rRNA transcription inhibitor, effectively blocked proliferation and induced redifferentiation. Thus, TERT promotes thyroid cancer progression by inducing dedifferentiation, and ribosome biogenesis inhibition represents a potential treatment strategy for TERT-reactivated cancers. Highlights[tpltrtarr] TERT accelerated thyroid cancer dedifferentiation and metastasis in vivo [tpltrtarr]TERT regulated rRNA metabolism and MTORC1/ S6K/RPS6 activities [tpltrtarr]CX-5461 inhibited the progression of TERT-reactivated melanoma and thyroid cancer [tpltrtarr]Inhibition of rRNA induced redifferentiation of advanced thyroid cancer with TERT activation

cancer biology↗

Therapeutic immunization against Helicobacter pylori infection in BALB/c mice induced by a multi-epitope vaccine based on computer-aided design

BackgroundCombined antibiotic regimens have caused problems such as increasing antimicrobial resistance to H. pylori and intestinal flora disturbance. Vaccination is a great alternative approach, but also faces the limited immune response induced by monovalent vaccines. Therefore, the development of multi-epitope vaccines is promising immunotherapy to control H. pylori infection. ObjectiveTo develop a multi-epitope vaccine and evaluate its therapeutic efficacy against H. pylori infection. Materials and MethodsThe B and T cell epitopes from UreB, FlaA, AlpB, SabA, and HpaA were linked for producing 2 multi-epitope vaccines (CTB-S3 and CTB-S5) by a structural evaluation based on computer-aided design. The abilities to produce antigen-specific antibodies and neutralizing antibodies of CTB-S3 and CTB-S5 were evaluated in BALB/c mice. After that, their therapeutic efficacy was explored in H. pylori-infected mice. ResultsCTB-S3 or CTB-S5 could induce high levels of specific antibodies against UreB, FlaA, AlpB, SabA, HpaA, and neutralizing antibodies against H. pylori urease and adhesion. Also, oral therapeutic immunization with CTB-S3 or CTB-S5 could decrease H. pylori colonization and reduce stomach damage; the protection was correlated with H. pylori-specific IgG, SIgA antibodies, and CD4+ T cell immune response. ConclusionsOur study developed a multi-epitope vaccine based on a computer-aided design. The CTB-S3 and CTB-S5 vaccines may be promising therapeutic candidate vaccines against H. pylori infection and provide a reference for vaccine design of other pathogens.

immunology↗

Resurrection of human endogenous retroviruses during aging reinforces senescence

Whether and how certain transposable elements with viral origins, such as endogenous retroviruses (ERVs) dormant in our genomes, can become awakened and contribute to the aging process are largely unknown. In human senescent cells, we found that HERVK (HML-2), the most recently integrated human ERVs, are unlocked to transcribe viral genes and produce retrovirus-like particles (RVLPs). These HERVK RVLPs constitute a transmissible message to elicit senescence phenotypes in young cells, which can be blocked by neutralizing antibodies. Activation of ERVs was also observed in organs of aged primates and mice, as well as in human tissues and serum from the elderly. Their repression alleviates cellular senescence and tissue degeneration and, to some extent, organismal aging. These findings indicate that the resurrection of ERVs is a hallmark and driving force of cellular senescence and tissue aging. In briefLiu and colleagues uncover the ways in which de-repression of human endogenous retrovirus triggers cellular senescence and tissue aging; the findings provide fresh insights into therapeutic strategies for alleviating aging. HighlightsO_LIDerepression of the endogenous retrovirus contributes to programmed aging C_LIO_LIUpregulation of HERVK triggers the innate immune response and cellular senescence C_LIO_LIExtracellular HERVK retrovirus-like particles induce senescence in young cells C_LIO_LIEndogenous retrovirus serves as a potential target to alleviate agings C_LI Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=194 SRC="FIGDIR/small/432260v2_ufig1.gif" ALT="Figure 1"> View larger version (64K): org.highwire.dtl.DTLVardef@31d384org.highwire.dtl.DTLVardef@13594c0org.highwire.dtl.DTLVardef@b8e070org.highwire.dtl.DTLVardef@196e5be_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

Identification and Evaluation of a Panel of Strong Constitutive Promoters in Listeria monocytogenes for Improving the Expression of Foreign Antigens

Attenuated Listeria monocytogenes (L. monocytogenes) could be used as a vaccine vector for immunotherapy of tumors or pathogens. However, the lack of reliable promoters limits its ability to express foreign antigens. In this work, 21 promoters from L. monocytogenes were identified by RNA-seq analysis under two conditions of pH 7.4 and pH 5.5. Based on the constructed fluorescence report system, 7 constitutive promoters showed higher strength than that of Phelp, a previously reported strong promoter. Further, the selected 5 constitutive promoters also showed high activity in the production of UreB, a widely used antigen against Helicobacter pylori (H. pylori). In particular, a well-characterized constitutive promoter P18, which performed best in both fluorescence intensity and UreB production, was proved to be highly active in vitro and in vivo. In summary, we provide a useful promoter library for Listeria species and offer a reference for constitutive promoter mining in other organisms. Key pointsO_LI21 promoters from L. monocytogenes were identified by RNA-seq. C_LIO_LIFluorescent tracer of L. monocytogenes (P18) was performed in vitro and in vivo. C_LIO_LIA well-characterized constitutive promoter P18 could improve the expression level of a foreign antigen UreB in L. monocytogenes C_LI

microbiology↗

Embedding of exogenous B cell epitopes on the surface of UreB structure generates a broadly reactive antibody response against Helicobacter pylori

Since Helicobacter pylori (H. pylori) resistance to antibiotic regimens is increased, vaccination is becoming an increasingly important alternative therapy to control H. pylori infection. UreB, FlaA, AlpB, SabA, and HpaA proteins of H. pylori were previously proved to be used as candidate vaccine antigens. Here, we developed an engineered antigen based on a recombinant chimeric protein containing a structural scaffold from UreB and B cell epitopes from FlaA, AlpB, SabA, and HpaA. The multi-epitope chimeric antigen, named MECU, could generate a broadly reactive antibody response including antigen-specific antibodies and neutralizing antibodies against H. pylori urease and adhesins. Moreover, therapeutic immunization with MECU could reduce H. pylori colonization in the stomach and protect the stomach in BALB/c mice. This study not only provides a promising immunotherapy to control H. pylori infection, but also offers a reference for antigen engineering against other pathogens.

immunology↗

Decoding the single-cell landscape and intercellular crosstalk in the transplanted liver: a 4-dimension mouse model

Graft remodeling after transplantation maintains graft functionality and determines graft survival. However, a comprehensive understanding of cellular diversity and interplay during graft remodeling remains to be fully characterized. In this study, we established a well tolerant C57BL/6 to C57BL/6 orthotopic liver transplantation (LT) mice model and observed two stages of graft recovery including an acute phase and a steady phase. We next performed single-cell RNA sequencing (scRNA-seq) and cytometry by time-of-flight (CyTOF) and recorded the cellular hierarchy in the transplanted liver during the two stages. Besides the dynamic change of cell proportion, it was notable that recipient-derived cells took over the transplanted liver in most cell types (e.g., B cells, T cells, dendritic cells, granulocytes and monocytes) except CD206+ MerTK+ macrophages and CD161+ CD49a+ CD49b-natural killer cells. We then focused on macrophages and captured 5 distinct transcriptional signatures to define novel subclusters. Using a ligand-receptor interaction strategy, we identified specific macrophage-hepatocyte interactions during the acute and stable phases, causing metabolic remodeling in the transplanted liver. Our results delineated a 4-dimension cell atlas (type-proportion-source-time) of the transplanted liver, which sheds light on the physiological process of liver graft maintenance and graft-recipient crosstalk.

immunology↗

Potent SARS-CoV-2 neutralizing antibodies selected from a human antibody library constructed decades ago

Combinatorial antibody libraries not only effectively reduce antibody discovery to a numbers game, but enable documentation of the history of antibody responses in an individual. The SARS-CoV-2 pandemic has prompted a wider application of this technology to meet the public health challenge of pandemic threats in the modern era. Herein, we used a combinatorial human antibody library constructed 20 years before the COVID-19 pandemic to discover three highly potent antibodies that selectively bind SARS-CoV-2 spike protein and neutralize authentic SARS-CoV-2 virus. Compared to neutralizing antibodies from COVID-19 patients with generally low somatic hypermutation (SHM), these antibodies contain over 13-22 SHMs, many of which are involved in specific interactions in crystal structures with SARS-CoV-2 spike RBD. The identification of these somatically mutated antibodies in a pre-pandemic library raises intriguing questions about the origin and evolution of human immune responses to SARS-CoV-2.

microbiology↗

iTRAQ-Based Proteomic Profiling of PLC-Mediated Expression of 20E-Induced Protein in Apolygus lucorum (Meyer-Dür)

The polyphagous pest Apolygus lucorum has become the dominant insect in Bacillus thuringiensis (Bt) cotton fields. The hormone 20-hydroxyecdysone (20E) regulates multiple events in insect development and physiology. 20E responses are controlled by pathways triggered by phospholipase C (PLC)-associated proteins. However, 20E-modulated genes whose expression is affected by PLC remain unknown. Here, isobaric tag for relative and absolute quantitation (iTRAQ) and immunoblot were carried out for comparing differentially expressed proteins (DEPs) in A. lucorum in response to 20E and the PLC inhibitor U73122, respectively. Totally 1624 DEPs were, respectively, found in the 20E/control, U73122/control, and 20E+U73122/control groups. Venn diagram analysis further revealed 8 DEPs that were shared among the three groups. Immunoblot validated these findings, which corroborated and highlighted the reliability of proteomics. KEGG enrichment analysis showed that the DEPs were included in diverse signaling pathways. The largest portion of DEPs among the three groups were categorized in metabolic pathways. In addition, DEPs among the three groups were also found to regulate the Ras-MAPK and PI3K-AKT pathways. This is the first time that iTRAQ was carried out to assess proteome alteration in A. lucorum nymphs in response to 20E and a PLC inhibitor. These findings provide novel insights into protein expression in A. lucorum in response to 20E, and a more comprehensive understanding of the function of PLC in 20E signal transduction.

biochemistry↗

A novel copper-sensing two-component system for activating Dsb genes in bacteria

Copper is an essential element for biological systems but becomes toxic when present in excess. In Pseudomonas aeruginosa, an important human pathogen, the resistance to copper requires the induction of dsbDEG operon encoding proteins involved in disulfide-bond formation (Dsb). However, it is unknown how the copper stress induces the transcription of the operon. Here, we report that the exogenous copper induces the transcription of the dsbDEG operon through a new copper-sensing two-component system named DsbRS. The dsbRS is divergently transcribed from the dsbDEG operon, and the response regulator DsbR binds to the intergenic region between the operons. In the absence of copper, the sensor kinase DsbS acts as a phosphatase toward DsbR and thus blocks the transcription of the operons. However, in the presence of copper, the metal ion directly binds to the sensor domain of DsbS, for which the Cys82 residue plays a critical role. The copper-binding appears to inhibit the phosphatase activity of DsbS, leading to activation of DsbR. The copper resistance of the dsbRS knock-out mutant was restored by ectopic expression of the dsbDEG operon, confirming the critical role of the operon in the resistance to copper. Strikingly, cognates of dsbRS-dsbDEG pair are widely distributed across eubacteria. Also, a DsbR-binding site, which contains the consensus sequence 5-TAA-N7-TTAAT-3, is detected in the promoter region of dsbDEG homologs in those species. Thus, regulation of Dsb genes by DsbRS represents a novel mechanism by which bacterial cells cope with copper stress. ImportanceCopper is an essential redox active cofactor that becomes highly cytotoxic when present in excess. Therefore, in order to evade copper toxicity, bacteria must perceive copper stress and tightly regulate genes expression. In the present study, we identify a new copper-sensing two-component system (designated DsbRS) in Pseudomonas aeruginosa, an important human pathogen. We provide multiple lines of evidence that upon copper binding to the periplasmic domain of DsbS, its phosphatase activity is blocked, and the phosphorylated DsbR directly activates the transcription of a number of copper-induced genes including those involved in protein disulfide-bond formation (Dsb). This study suggests that regulation of Dsb genes by DsbRS may be an underappreciated regulatory mechanism by which bacteria sense and respond to copper.

microbiology↗

Potentiating the anti-tumor response of tumor infiltrated T cells by NAD+ supplementation

Tumor immunotherapies have provided clinical benefits, yet great potential remains for optimizing therapeutic effects. Here, we show that low NAD+ levels restrict the function of tumor infiltrating T lymphocytes (TILs). TILs harvested from human ovarian tumor tissues showed decreased NAD+ levels compared with T cells from paired peripheral blood samples. The combination of whole-genome CRISPR and large-scale metabolic inhibitor screens implicated the NAD+ biosynthesis enzyme nicotinamide phosphoribosyltransferase (NAMPT) is required for T cell activation. Further isotopic labeling and LC-MS studies confirmed that NAD+ depletion suppressed mitochondrial energy biosynthesis in T cells. Excitingly, NAD+ supplementation significantly enhanced the tumor cell-killing efficacy of CAR-T cells ex vivo, and extended animal survive in both adoptive CAR-T model and immune checkpoint blockade treatment models in vivo. This study demonstrates an over-the-counter nutrient supplement NAD+ could robustly boost the efficacy of T cell-based immunotherapy and provides insights into the cellular basis of T cell metabolic reprogramming in treating cancers. One Sentence SummaryNAD+ supplementation during cancer immunotherapies significantly enhances T cell activation and tumor killing capacity.

immunology↗

Decoding mRNA translatability and stability from 5'UTR

Precise control of protein synthesis by engineering sequence elements in 5 untranslated region (5UTR) remains a fundamental challenge. To accelerate our understanding of cis-regulatory code embedded in 5UTR, we devised massively parallel reporter assays from a synthetic mRNA library composed of over one million 5UTR variants. A completely randomized 10-nucleotide sequence preceding an upstream open reading frame (uORF) and downstream GFP leads to a broad range of mRNA translatability and stability in mammalian cells. While efficient translation protects mRNA from degradation, uORF translation triggers mRNA decay in a UPF1-dependent manner. We also identified translational inhibitory elements in 5UTR with G-quadruplex as a mark for mRNA decay in the P-body. Unexpectedly, an unstructured A-rich element in 5UTR, while enabling cap-independent translation, destabilizes mRNAs in the absence of translation. Our results not only expose diverse sequence features of 5UTR in controlling mRNA translatability, but also reveal ribosome-dependent and -independent mRNA surveillance pathways.

biochemistry↗

Analysis of metagenome-assembled genomes from the mouse gut microbiota reveals distinctive strain-level characteristics

The laboratorial mouse harbors a unique gut microbiota with potential value for human microbiota-associated studies. Mouse gut microbiota has been explored at the genus and species levels, but features rarely been showed at the strain level. The identification of 833,051 and 658,438 nonredundant genes of faeces and gut content samples from the laboratorial C57/BL mice showed over half of these genes were newly found compared to the previous mouse gut microbial gene catalogue. Metagenome-assembled genomes (MAGs) was used to reconstruct 46 nonredundant MAGs belonging to uncultured specieses. These MAGs included members across all phyla in mouse gut (i.e. Firmicutes, Bacteroidetes, Proteobacteria, Deferribacteres, Verrucomicrobia, and Tenericutes) and allowed a strain-level delineating of the mouse gut microbiota. Comparison of MAGs with human gut colonies revealed distinctive genomic and functional characteristics of mouses Bacteroidetes and Firmicutes strains. Genomic characteristics of rare phyla in mouse gut microbiota were demonstrated by MAG approach, including strains of Mucispirillum schaedleri, Parasutterella excrementihominis, Helicobacter typhlonius, and Akkermansia muciniphila. ImportanceThe identification of nonredundant genes suggested the existence of unknown microbes in the mouse gut samples. The metagenome-assembled genomes (MAGs) instantiated the specificity of mouse gut species and revealed an intestinal microbial correlation between mouse and human. The cultivation of faeces and gut contents sample validated the existence of MAGs and estimate their accuracy. Full-length 16S ribosomal RNA gene sequencing enabled taxonomic characterization. This study highlighted a unique ecosystem in the gut of laboratorial mice that obviously differed with the human gut flora at the strain level. The outcomes may be beneficial to researches based on laboratorial mouse models.

microbiology↗

Highly efficient and specific genome editing in human cells with paired CRISPR-Cas9 nickase ribonucleoproteins

CRISPR technology has opened up many diverse genome editing possibilities in human somatic cells, but has been limited in the therapeutic realm by both potential off-target effects and low genome modification efficiencies. Recent advancements to combat these limitations include delivering Cas9 nucleases directly to cells as highly purified ribonucleoproteins (RNPs) instead of the conventional plasmid DNA and RNA-based approaches. Here, we extend RNP-based delivery in cell culture to a less characterized CRISPR format which implements paired Cas9 nickases. The use of paired nickase Cas9 RNP system, combined with a GMP-compliant non-viral delivery technology, enables editing in human cells with high specificity and high efficiency, a development that opens up the technology for further exploration into a more therapeutic role.

molecular biology↗