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《中国科学：生命科学英文版》是一本英文版的生命科学领域的综合性学术期刊，由中国科学院和国家自然科学基金委员会共同主办，以报道生物学、农学和基础医学领域等方面具有重要意义的创新性研究成果为主。是SCI核心期刊，并被CA，Medline等检索系统和数据库收录。
  • 发文量：3464
  • 被引量：1469
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  • 国内刊号/CN：CN 11-3752/N
    国际刊号/ISSN：1674-7305
  • 发行周期：月刊
    邮发代号：80-205
  • 主管单位：Chinese Academy of Sciences
    主办单位：Chinese Academy of Sciences(CAS);National Natural Science Foundating of China(NSFC)
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  • 主编：Jiayang Li
  • 电话：010-64015399 64016350
  • 邮箱：life@scichina.org
  • 地址：16 Donghuangchenggen North Street,Beijing
  • 邮编：100717
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中国科学 >2023年第12期

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  • 摘要：Goldfish comprise around 300 different strains with drastically altered and aesthetical morphologies making them suitable models for evolutionary developmental biology.The dragon-eye strain is characterized by protruding eyes(analogous to those of Chinese dragons).Although the strain has been selected for about 400 years,the mechanism of its eye development remains unclear.In this study,a stable dragon-eye goldfish strain with a clear genetic background was rapidly established and studied.We found that upregulation of the PPAR signaling pathway accompanied by an increase in lipid accumulation might trigger the morphological and structural transformation of the eye in dragon-eye goldfish.At the developmental stage of proptosis(eye protrusion),downregulation of the phototransduction pathway was consistent with the structural defects and myopia of the dragon-eye strain.With the impairment of retinal development,cytokine-induced inflammation was activated,especially after proptosis,similar to the pathologic symptoms of many human ocular diseases.In addition,differentially expressed transcription factors were significantly enriched in the PAX and homeobox families,two well-known transcription factor families involved in eye development.Therefore,our findings reveal the dynamic changes in key pathways during eye development in dragon-eye goldfish,and provide insights into the molecular mechanisms underlying drastically altered eyes in goldfish and human ocular disease.
  • 摘要：Alternative splicing of eukaryotic precursor(messenger)RNAs in the nucleus not only increases transcriptomic complexity,but also expands proteomic and functional diversity.In addition to basic types of alternative splicing,recent transcriptome-wide analyses have also suggested other new types of non-canonical splicing,such as back splicing and recursive splicing,and their widespread expression across species.Increasing lines of evidence have suggested mechanisms for back splicing,including insights from analyses of nascent RNA sequencing.In this review,we discuss our current understanding of back splicing regulation,and highlight its distinct characteristics in processing during nascent RNA synthesis by taking advantage of metabolic tagging nascent RNA sequencing.Features of recursive splicing are also discussed in the perspective of nascent RNA sequencing.
  • 摘要：Severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),the etiologic agent of the current coronavirus disease 2019(COVID-19)pandemic,has evolved to adapt to human host and transmission over the past 12 months.One prominent adaptive mutation is the asparagine-to-glycine substitution at amino acid position 614 in the viral spike protein(D614G),which has become dominant in the currently circulating virus strains.Since spike protein determines host ranges,tissue tropism,and pathogenesis through binding to the cellular receptor of angiotensin converting enzyme 2(ACE2),the D614G mutation is hypothesized to enhance viral fitness in human host,leading to increased transmission during the global pandemic.Here we summarize the recent progress on the role of the D614G mutation in viral replication,pathogenesis,transmission,and vaccine and therapeutic antibody development.These findings underscore the importance in closely monitoring viral evolution and defining their functions to ensure countermeasure efficacy against newly emerging variants.
  • 摘要：Non-steroidal anti-inflammatory drugs(NSAIDs)inhibit prostaglandin(PG)formation by targeting cyclooxygenase(COX)1 and 2.Long-term use of NSAIDs that selectively inhibit COX2 increases the risk for thrombotic events,cardiac failure,and hypertension.However,the underlying mechanisms remain unclear.In this study,COX1-and COX2-deficient rats were created via Cas9/RNA-mediated gene targeting.DNA genotyping and Western blot analysis confirmed successful generation of COX1^(-/-) and COX2^(-/-) rats.Adult COX1^(-/-) rats grew normally,while more than 70%of COX2^(-/-) rats after wean died within 2 months.Echocardiography showed markedly reduced left ventricular ejection fraction and fractional shortening in adult COX2^(-/-) rats compared to those in wildtype(WT)controls.Histological analysis revealed accumulation of inflammatory cells and severe interstitial and perivascular fibrosis in COX2^(-/-)cardiac tissues.Moreover,cardiac ATP and acetyl-Co A production was dramatically decreased in COX2^(-/-) rats.Consistently,the expression of genes related to mitochondrial oxidation,such as those that encode for subunits of pyruvate dehydrogenase complex and acyl Co A dehydrogenases,were downregulated,while glycolytic hexokinase 1(HK1)was upregulated in COX2^(-/-) heart tissues.These observations indicate that COX2-deficient rats developed spontaneously heart failure,likely as a result of dysregulated cardiac energy metabolism.
  • 摘要：Mural cells(MCs)wrap around the endothelium,and participate in the development and homeostasis of vasculature.MCs have been reported as heterogeneous population morphologically and functionally.However,the transcriptional heterogeneity of MCs was rarely studied.In this study,we illustrated the transcriptional heterogeneity of MCs with different perspectives by using publicly available single-cell dataset GSE109774.Specifically,MCs are transcriptionally different from other cell types,and ligand-receptor interactions of different cells with MCs vary.Re-clustering of MCs identified five distinct subclusters.The heterogeneity of MCs in tissues was reflected by MC coverage,various distribution of MC subclusters,and ligand-receptor interactions of MCs and parenchymal cells.The transcriptomic diversity of MCs revealed in this article will help facilitate further research into MCs.
  • 摘要：Acute graft-versus-host disease(a GVHD)is caused by allo-activated donor T cells infiltrating target organs.As a regulator of immune function,granulocyte colony-stimulating factor(G-CSF)has been demonstrated to relieve the a GVHD reaction.However,the role of G-CSF-primed donor Tcells in specific target organs is still unknown.In this study,we employed a classical MHC-mismatched transplantation mouse model(C57BL/6 into BALB/c)and found that recipient mice transplanted with GCSF-primed T cells exhibited prolonged survival compared with that of the PBS-treated group.This protective function against GVHD mediated by G-CSF-primed donor T cells was further confirmed by decreased clinical and pathological scores in this a GVHD mouse model,especially in the lung and gut.Moreover,we found that Tcells polarized towards Th2 cells and regulatory T cells were increased in specific target organs.In addition,G-CSF treatment inhibited inducible co-stimulator(ICOS)expression and increased the expression of tolerance-related genes in recipient mice.Our study provides new insight into the immune regulatory effects of G-CSF on T cell-mediated a GVHD,especially for its precise regulation in GVHD target organs.
  • 摘要：Neutrophils are crucial for immunity and play important roles in inflammatory diseases;however,mouse models selectively deficient in neutrophils are limited,and neutrophil-specific diphtheria toxin(DT)-based depletion system has not yet been established.In this study,we generated a novel knock-in mouse model expressing diphtheria toxin receptor(DTR)under control of the endogenous Ly6G promoter.We showed that DTR expression was restricted to Ly6G+neutrophils and complete depletion of neutrophils could be achieved by DT treatment at 24-48 h intervals.We characterized the effects of specific neutrophil depletion in mice at steady-state,with acute inflammation and during tumor growth.Our study presents a valuable new tool to study the roles of neutrophils in the immune system and during tumor progression.
  • 摘要：Evolutionary developmental biology,or Evo-Devo for short,has become an established field that,broadly speaking,seeks to understand how changes in development drive major transitions and innovation in organismal evolution.It does so via integrating the principles and methods of many subdisciplines of biology.Although we have gained unprecedented knowledge from the studies on model organisms in the past decades,many fundamental and crucially essential processes remain a mystery.Considering the tremendous biodiversity of our planet,the current model organisms seem insufficient for us to understand the evolutionary and physiological processes of life and its adaptation to exterior environments.The currently increasing genomic data and the recently available gene-editing tools make it possible to extend our studies to non-model organisms.In this review,we review the recent work on the regulatory signaling of developmental and regeneration processes,environmental adaptation,and evolutionary mechanisms using both the existing model animals such as zebrafish and Drosophila,and the emerging nonstandard model organisms including amphioxus,ascidian,ciliates,single-celled phytoplankton,and marine nematode.In addition,the challenging questions and new directions in these systems are outlined as well.
  • 摘要：Liver cancer is one of the most common causes of cancer-related death worldwide and mainly includes hepatocellular carcinoma(HCC)and cholangiocarcinoma(CCA).Extracellular vesicles(EVs)are membrane-derived nanometer-sized vesicles that can be released by different cell types under normal and pathological conditions and thus play important roles in the transmission of biological information between cells.Increasing evidence suggests that liver cancer cell-derived EVs may help establish a favorable microenvironment to support the proliferation,invasion and metastasis of cancer cells.In this review,we summarized the role of EVs in the tumor microenvironment(TME)during the development and progression of liver cancer.As messenger carriers,EVs are loaded by various biomolecules,such as proteins,RNA,DNA,lipids and metabolites,making them potential liquid biopsy biomarkers for the diagnosis and prognosis of liver cancer.We also highlighted the progress of EVs as antigen carriers and EV-based therapeutics in preclinical studies of liver cancer.
  • 摘要：Despite the use of many types of chemotherapies for pancreatic cancer, optimal efficacy has not been obtained so far. Pancreatic cancer shows a high incidence of TP53 mutations, inactivating its tumor suppressor activity. In this study, we identified sodium cantharidinate as a novel, potential anti-pancreatic cancer agent that activates p53 function. Sodium cantharidinate reduced the viability of pancreatic cancer cells, including the human primary pancreatic cancer cells, PANC-1, As PC-1, SW1990 and BXPC-3, in a dose-dependent manner. Sodium cantharidinate induced apoptosis and DNA damage of pancreatic cancer cells. Furthermore, proteome-wide sequencing analysis detected a marked perturbation in p53 signaling pathway on PANC-1 cells upon sodium cantharidinate. Consistent with the previous results, sodium cantharidinate treatment decreased Bcl-2 and mitochondrial cytochrome-c protein expression, as well as phosphorylation of MDM2;meanwhile, it increased the levels of cleaved-caspase-3,cleaved-caspase-9, cleaved-PARP, Bax, and phosphorylated p53, thus inducing the apoptosis of pancreatic cancer cells. The p53-activating effect of sodium cantharidinate was strongly abrogated by treatment with TP53-targeting sh RNA. Moreover, sodium cantharidinate inhibited neoplasm growth via the JAK2-STAT3 pathway, which was inhibited by sh RNA-TP53 and triggered by combination with gemcitabine. Combination therapy indicated that sodium cantharidinate and gemcitabine synergistically reduced ex vivo and in vivo growth of pancreatic neoplasm. Further docking studies revealed the different binding fates of sodium cantharidinate to activate wild-type p53 function. Thus, sodium cantharidinate could be a potential agent with promising anti-pancreatic cancer efficacy.
  • 摘要：Cell cycle is a fundamental process underlying growth and development in evolutionarily diverse organisms, including fungi. In human fungal pathogens, cell cycle control generally determines their life cycles, either in the environment or during infections.Thus, cell cycle components can potentially serve as important targets for the development of antifungal strategy against fungal infections. Here, in Cryptococcus neoformans, the most common cause of fatal fungal meningitis, we show that a previously uncharacterized B-type cyclin named Cbc1 is essential for both its infectious and sexual cycles. We reveal that Cbc1 coordinates various sexual differentiation and molecular processes, including meiosis. Especially, the absence of Cbc1 abolishes formation of sexual spores in C. neoformans, which are presumed infectious particles. Cbc1 is also required for the major Cryptococcus pathogenic attributes. Virulence assessment using the murine model of cryptococcosis revealed that the cbc1 mutant is avirulent.Together, our results provide an important insight into how C. neoformans employs shared cell cycle regulation to coordinate its infectious and sexual cycles, which are considered crucial for virulence evolution and the production of infectious spores.
  • 摘要：Chemosensation is indispensable for the survival of Caenorhabditis elegans to discriminate food and pathogenic bacteria in their living environment. Food-like odors emitted by the pathogen Bacillus nematocida B16 for trapping its hosts and an olfactory signaling pathway responsible to sense the attractant 2-heptanone were identified in our previous study. Here, we further explore how the worms recognize the attractive molecules indole and 2-ethyl hexanol, which have different chemical properties and modest nematode-luring ability. We show that the chemotaxis toward indole and 2-ethyl hexanol requires the G protein-coupled receptors encoded by str-193 on AWC and str-7 on AWA. In a further genetic screen for downstream effectors in olfactory signaling cascades, the Gα subunit GSA-1, guanylyl cyclase ODR-1 and DAF-11 and the c GMP-gated channel TAX-2/TAX-4 were found to be necessary for indole sensation, whereas the TRPV channels OSM-9/OCR-2 and the PLC pathway activated by GPA-6 are responsible for the detection of 2-ethyl hexanol. Altogether, our current work further clarifies the distinct olfactory signaling pathways through which C. elegans senses different chemicals and is lured by B. nematocida B16, improving our comprehensive understanding of the mechanisms by which bacterial pathogens effectively infect their hosts.
  • 摘要：Cytidine base editor(CBE),which is composed of a cytidine deaminase fused to Cas9 nickase,has been widely used to induce C-to-T conversions in a wide range of organisms.However,the targeting scope of current CBEs is largely restricted to protospacer adjacent motif(PAM)sequences containing G,T,or A bases.In this study,we developed a new base editor termed“nNme2-CBE”with excellent PAM compatibility for cytidine dinucleotide,significantly expanding the genome-targeting scope of CBEs.Using nNme2-CBE,targeted editing efficiencies of 29.0%-55.0%and 17.3%—52.5%were generated in human cells and rabbit embryos,respectively.In contrast to conventional nSp-CBE,the nNme2-CBE is a natural high-fidelity base editing platform with minimal DNA off-targeting detected in vivo.Significantly increased efficiency in GC context and precision were determined by combining nNme2Cas9 with rationally engineered cytidine deaminases.In addition,the Founder rabbits with accurate single-base substitutions at Fgf5 gene loci were successfully generated by using the nNme2-CBE system.These novel nNme2-CBEs with expanded PAM compatibility and high fidelity will expand the base editing toolset for efficient gene modification and therapeutic applications.
  • 摘要：Nanozymes,the functional nanomaterials with enzyme-like activities,have been widely explored for both in vitro and in vivo applications(Wei and Wang,2013;Wu et al.,2019;Huang et al.,2019;Liang and Yan,2019).Particularly,by modulating the levels of reactive oxygen species(ROS)in vivo,numerous therapeutic nanozymes have been developed to treat diseases,ranging from cancer to neurodegenerative diseases(Fan et al.,2018;Kwon et al.,2018).
  • 摘要：Nanozymes are nanomaterials exhibiting intrinsic enzymatic properties,which suggests that inorganic nanoparticles could be bioactive.It’s in 2007,when we introduced the biological methodologies for natural enzymes to systematically study the enzymatic properties of iron oxide nanoparticles,we discovered nanozymes.We found that nanozymes,just as natural enzymes,are able to catalyze biochemical reactions under the physiological conditions,following the similar enzymatic kinetics and catalytic mechanisms(Gao et al.,2007).Since then,the developments of nanozymes bloomed,and lots of nanomaterials were found exhibiting various enzymatic activities(Huang et ah,2019).
  • 摘要：While precision medicine driven by genome sequencing has revolutionized cancer care,such as lung cancer,its impact on gastric cancer(GC)has been minimal.GC patients are routinely treated with chemotherapy,but only a fraction of them receive the clinical benefit.There is an urgent need to develop biomarkers or algorithms to select chemo-sensitive patients or apply targeted therapy.Here,we carried out retrospective analyses of 1,020 formalin-fixed,paraffin-embedded GC surgical resection samples from 5 hospitals and developed a mass spectrometry-based workflow for proteomic subtyping of GC.We identified two proteomic subtypes:the chemo-sensitive group(CSG)and the chemo-insensitive group(CIG)in the discovery set.The 5-year overall survival of CSG was significantly improved in patients who had received adjuvant chemotherapy after surgery compared with those who received surgery only(64.2%vs.49.6%;Cox P-value=0.002),whereas no such improvement was observed in CIG(50.0%vs.58.6%;Cox P-value=0.495).We validated these results in an independent validation set.Further,differential proteome analysis uncovered 9 FDA-approved drugs that may be applicable for targeted therapy of GC.A prospective study is warranted to test these findings for future GC patient care.
  • 摘要：Dr.Daoxin Xie received Bachelor degree(Plant Protection)in 1983 from Hunan Agricultural College,Master degree(Plant Pathology)in 1987 and Ph.D.(Crop Genetic Breeding)in 1990 from Chinese Academy of Agricultural Sciences.He worked as Research Assistant in Hunan Cotton Research Institute during 1983-1984,Post-Doctoral Fellow and Senior Research Associate in John Innes Institute,Leicester University and University of East Anglia(UK)during 1990-1999.
  • 摘要：Seed size, an important agronomic trait determining crop yield, is regulated by multiple plant hormones. Jasmonate(JA) is a key phytohormone required for various plant defenses and diverse developmental processes. Here, we defined an essential role for JA in control of seed size. Through comprehensive analysis of genetic mutants in JA pathway, we showed that seed size was repressed by positive components in JA pathway including COI1, MYC2(and its homologues), MED25 and JAR1, but promoted by JA signaling repressor JAZ proteins such as JAZ6. We further demonstrated that exogenous application of JA suppressed seed size in a COI1-dependent manner. Our results reveal that JA signaling represses seed size and negatively regulates integument cell proliferation. Elucidation of jasmonate action in seed size control would advance our understanding of inner mechanism of seed size regulation.
  • 摘要：Colorectal cancer(CRC) progression is associated with cancer cell dedifferentiation and stemness acquisition. Several methods have been developed to identify stemness signatures in CRCs. However, studies that directly measured the degree of dedifferentiation in CRC tissues are limited. It is unclear how the differentiation states change during CRC progression. To address this, we develop a method to analyze the tissue differentiation spectrum in colorectal cancer using normal gastrointestinal singlecell transcriptome data. Applying this method on 281 tumor samples from The Cancer Genome Atlas Colon Adenocarcinoma dataset, we identified three major CRC subtypes with distinct tissue differentiation pattern. We observed that differentiation states are closely correlated with anti-tumor immune response and patient outcomes in CRC. Highly dedifferentiated CRC samples escaped the immune surveillance and exhibited poor outcomes;mildly dedifferentiated CRC samples showed resistance to anti-tumor immune responses and had a worse survival rate;well-differentiated CRC samples showed sustained anti-tumor immune responses and had a good prognosis. Overall, the spectrum of tissue differentiation observed in CRCs can be used for future clinical risk stratification and subtype-based therapy selection.
  • 摘要：Allergic asthma is a chronic inflammatory disease of the lung and the airway,which is characterized by aberrant type 2 immune responses to otherwise unharmful aeroallergens.While the central role of Th2 cells and type 2 cytokines in the pathogenesis of allergic asthma is well documented,the regulation and plasticity of Th2 cells remain incompletely understood.By using an animal model of allergic asthma in IL-4-reporter mice,we found that Th2 cells in the lung expressed higher levels of Rora than those in the lymph nodes,and that treatment with an RORa agonist SRI 078 resulted in diminished Th2 cell responses in vivo.To determine the T cell-intrinsic role of RORa in allergic asthma in vivo,we established T cell-specific RORa-deficient^(f/f)fyf(Cd4creRora^(f/f))mice.Upon intranasal allergen challenges,Cd4creRora^(f/f)mice exhibited a significantly increased Th2 cells in the lungs and the airway and showed an enhanced eosinophilic inflammation compared to littermate control mice.Studies with Foxp3^(YFP-cre)Rora^(f/f)mice and CD^(8+)T cell depletion showed that the increased Th2 cell responses in the Cd4creRora^(f/f)mice were independent of Treg cells and CD^(8+)T cells.Our findings demonstrate a critical regulatory role of RORa in Th2 cells,which suggest that RORa agonists could be effective for the treatment of allergic diseases.
  • 摘要：Dear Editor,The genetic mechanism of large-scale interspecies traits,including evolutionary novelties and the characteristics of high taxa,is a central issue in evolutionary biology.At present,genome-wide association studies(GWAS)are known as one of the most powerful and affordable tools for understanding the association between heritable variations and phenotypic changes in populations of single species.Therefore,it would be interesting to determine whether GWAS can be applied to study large-scale interspecies traits.
  • 摘要：Dear Editor,In recent years,CRISPR/Cas9-mediated genome editing has been successfully applied in various plants for functional analysis or crop improvement(Chen et al.,2019).We previously reported DNA-free genome-editing methods to generate transgene-free mutants(Liang et al.,2017;Zhang et al.,2016).
  • 摘要：Dear Editor,Lung disease is a serious concern in humans and domestic animals.Huge economic losses are caused by enzootic pneumonia in the swine industry worldwide(Maes et al.,2018).The lung can be easily invaded by environmental pathogens,resulting in lung diseases usually accompanied by lung lesions.
  • 摘要：Oral leukoplakia is the most common type of oral potentially malignant disorders and considered a precursor lesion to oral squamous cell carcinoma.However,a predictor of oral leukoplakia prognosis has not yet been identified.We investigated whether copy number alteration patterns may effectively predict the prognostic outcomes of oral leukoplakia using routinely processed paraffin sections.Comparison of copy number alteration patterns between oral leukoplakia with hyperplasia(HOL,n=22)and dysplasia(DOL,n=21)showed that oral leukoplakia with dysplasia had a higher copy number alteration rate(86%)than oral leukoplakia with hyperplasia(46%).Oral leukoplakia with dysplasia exhibited a wider range of genomic variations across all chromosomes compared with oral leukoplakia with hyperplasia.We also examined a retrospective cohort of 477 patients with oral leukoplakia with hyperplasia with detailed follow-up information.The malignant transformation(MT,n=19)and leukoplakia recurrence(LR,n=253)groups had higher frequencies of aneuploidy events and copy number loss rate than the free of disease(FD,n=205)group.Together,our results revealed the association between the degree of copy number alterations and the histological grade of oral leukoplakia and demonstrated that copy number alteration may be effective for prognosis prediction in oral leukoplakia patients with hyperplasia.
  • 摘要：In multicellular and even single-celled organisms,individual components are interconnected at multiscale levels to produce enormously complex biological networks that help these systems maintain homeostasis for development and environmental adaptation.Systems biology studies initially adopted network analysis to explore how relationships between individual components give rise to complex biological processes.Network analysis has been applied to dissect the complex connectivity of mammalian brains across different scales in time and space in The Human Brain Project.In plant science,network analysis has similarly been applied to study the connectivity of plant components at the molecular,subcellular,cellular,organic,and organism levels.Analysis of these multiscale networks contributes to our understanding of how genotype determines phenotype.In this review,we summarized the theoretical framework of plant multiscale networks and introduced studies investigating plant networks by various experimental and computational modalities.We next discussed the currently available analytic methodologies and multi-level imaging techniques used to map multiscale networks in plants.Finally,we highlighted some of the technical challenges and key questions remaining to be addressed in this emerging field.
  • 摘要：Chemical modifications expand the composition of RNA molecules from four standard nucleosides to over 160 modified nucleosides,which greatly increase the complexity and utility of RNAs.Transfer RNAs(tRNAs)are the most heavily modified cellular RNA molecules and contain the largest variety of modifications.Modification of tRNAs is pivotal for protein synthesis and also precisely regulates the noncanonical functions of tRNAs.Defects in tRNA modifications lead to numerous human diseases.Up to now,more than 100 types of modifications have been found in tRNAs.Intriguingly,some modifications occur widely on all tRNAs,while others only occur on a subgroup of tRNAs or even only a specific tRNA.The modification frequency of each tRNA is approximately 7% to 25%,with 5-20 modification sites present on each tRNA.The occurrence and modulation of tRNA modifications are specifically noticeable as plenty of interplays among different sites and modifications have been discovered.In particular,tRNA modifications are responsive to environmental changes,indicating their dynamic and highly organized nature.In this review,we summarized the known occurrence order,cross-talk,and cooperativity of tRNA modifications.
  • 摘要：Viral diseases cause serious economic loss in farmed animals industry.However,the efficacy of remedies for viral infection in farmed animals is limited,and treatment strategies are generally lacking for aquatic animals.Interactions of commensal microbiota and viral infection have been studied in recent years,demonstrating a third player in the interaction between hosts and viruses.Here,we discuss recent developments in the research of interactions between commensal bacteria and viral infection,including both promotion and inhibition effect of commensal bacteria on viral pathogenesis,as well as the impact of viral infection on commensal microbiota.The antiviral effect of commensal bacteria is mostly achieved through priming or regulation of the host immune responses,involving differential microbial components and host signaling pathways,and gives rise to various antiviral probiotics.Moreover,we summarize studies related to the interaction between commensal bacteria and viral infection in farmed animals,including pigs,chickens,fish and invertebrate species.Further studies in this area will deepen our understanding of antiviral immunity of farmed animals in the context of commensal microbiota,and promote the development of novel strategies for treatment of viral diseases in farmed animals.
  • 摘要：Genome-edited human induced pluripotent stem cells(iPSCs)hold great promise for therapeutic applications.However,low editing efficiency has hampered the applications of CRISPR-Cas9 technology in creating knockout and homology-directed repair(HDR)-edited iPSC lines,particularly for silent genes.This is partially due to chromatin compaction,inevitably limiting Cas9 access to the target DNA.Among the six HDAC inhibitors we examined,vorinostat,or suberoylanilide hydroxamic acid(SAHA),led to the highest HDR efficiency at both open and closed loci,with acceptable toxicity.HDAC inhibitors equally increased non-homologous end joining(NHEJ)editing efficiencies(~50%)at both open and closed loci,due to the considerable HDAC inhibitor-mediated increase in Cas9 and sgRNA expression.However,we observed more substantial HDR efficiency improvement at closed loci relative to open chromatin(2.8 vs.1.7-fold change).These studies provide a new strategy for HDRediting of silent genes in iPSCs.
  • 摘要：Genetic manipulation of mitochondrial DNA(mtDNA)could be harnessed for deciphering the gene function of mitochondria;it also acts as a promising approach for the therapeutic correction of pathogenic mutation in mtDNA.However,there is still a lack of direct evidence showing the edited mutagenesis within human mtDNA by clustered regularly interspaced short palindromic repeats-associated protein 9(CRISPR/Cas9).Here,using engineered CRISPR/Cas9,we observed numerous insertion/deletion(InDel)events at several mtDNA microhomologous regions,which were triggered specifically by double-strand break(DSB)lesions within mtDNA.InDel mutagenesis was significantly improved by sgRNA multiplexing and a DSB repair inhibitor,iniparib,demonstrating the evidence of rewiring DSB repair status to manipulate mtDNA using CRISPR/Cas9.These findings would provide novel insights into mtDNA mutagenesis and mitochondrial gene therapy for diseases involving pathogenic mtDNA.
  • 摘要：We aimed to assess the associations of large artery stenosis(LAS)and cerebral small vessel disease(CSVD)with the risk of ischemic stroke and to investigate their respective and combined contributions.In the prospective population-based Shunyi Study,1,082 stroke-free participants aged 55.9±9.1 years were included.Participants were followed for incident stroke throughout the study period(2013-2019).Total small vessel disease score was used to measure CSVD burden.Cervico-cerebral large artery stenosis was evaluated via brain magnetic resonance angiography and carotid ultrasound.We estimated the risk of ischemic stroke in relation to LAS and CSVD with Cox regression models.During a mean follow-up of 4.2 years,34 participants(3.1%)experienced at least one ischemic stroke.Severe LAS(≥50% stenosis versus no stenosis:HR=3.27(95%CI:1.31-8.18))and high CSVD burden(total small vessel disease score 2-4 versus 0 point:HR=12.73(4.83-33.53))were associated with increased stroke risk independently.In multivariate models,CSVD burden(7.72%)explained a larger portion of the variation in stroke risk than severity of LAS(3.49%).Our findings identified that both LAS and CSVD were associated with future ischemic stroke in asymptomatic subjects,while those with high CSVD burden deserve more attention in primary prevention of stroke.

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