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Biology subjects

Lei, C.

Publications and source records attributed to Lei, C..

At least 19 recordsLinked to original sources

DCAF: Unifying Data Validity, Evaluation Validity and Predictive Modeling for Single-cell Perturbation Simulation

Single-cell perturbation profiling is limited by cost and throughput, while computational methods remain constrained by inconsistent evaluation and underperformance relative to simple baselines. Here we present DCAF, a unified framework for single-cell perturbation simulation that that jointly addresses data validity, evaluation validity and predictive modeling. Among its three components, DCAF-data addresses the single-measurement limitation by reconstructing pre- and post-perturbation status using entropy-regularized optimal transport, and is demonstrated on both cell line and multi-cell type datasets. DCAF-criterion evaluates log fold changes in non-silenced genes to improve sensitivity to model error and robustness to zero inflation noise, validated on synthetic datasets. DCAF-model combines JEPA with explicit modeling for regulatory-dynamics modeling for interpretable prediction. Across benchmarks, DCAF outperforms state-of-the-art deep-learning methods, as well as mean and linear baselines in cross-gene, cross-cell-type and cross-region generalization. In adult Mouse brain, DCAF recapitulates known cell-type-specific regulatory heterogeneity of Dgcr8 knockdown at both cell type and gene levels. DCAF thus provides a rigorous and biologically grounded foundation for reliable perturbation simulation across development, disease and therapeutic discovery.

bioinformatics↗

Assessing and Optimizing Low-Frequency Somatic Mutation Detection: A Multi-Platform High-Throughput Sequencing Perspective

The availability of multiple commercial short-read sequencing platforms necessitates systematic cross-platform performance comparisons, particularly for challenging applications such as low-frequency somatic mutation detection. Here, a large-scale targeted sequencing dataset from five Genome in a Bottle (GIAB) human genomic DNA reference standards, HG001 to HG005, alongside Twist Biosciences cfDNA reference standards featuring 1% variant allele frequency (VAF), was generated by six platforms (NovaSeq 6000, NovaSeq X, FASTASeq 300, GenoLab M, SURFSeq 5000, and MGISEQ-T7). To build a realistic benchmark while keeping authentic sequencing backgrounds, we developed PosMix, a simulating tool that generates position-specific VAFs. To overcome the limitations of conventional variant callers (high recall with poor precision for VarScan2, higher precision with lower recall for Strelka2/Mutect2), we developed SomaticXGB, a machine learning-based caller. In this study, SURFSeq 5000 consistently exhibited the lowest error rates and achieved superior accuracy for VAFs as low as 0.5%, outperforming all other sequencing platforms. On the other hand, SomaticXGB attained F1 scores of approximately 0.92 on simulated datasets with VAFs ranging from 0.5% to 1.5% and 0.89 on Twist 1% standards, substantially outperforming conventional methods. This work delivers a valuable rich multi-platform data resource, offering a standardized pipeline for performance benchmarking and a machine learning-based strategy for optimized somatic mutation detection.

bioinformatics↗

ArchaicSeeker 3.0: A deep-learning framework for scalable, haplotype-resolved inference of archaic introgression

Archaic introgression has left a significant mark on human genetic diversity, but reliably identifying introgressed segments remains a major challenge, especially with complex demographic histories and limited sample sizes. Existing methods often rely on demographic assumptions or cohort-specific parameter fitting, which compromises robustness and scalability. We introduce ArchaicSeeker 3.0 (AS3), a deep-learning framework designed for haplotype-resolved detection of archaic introgression. AS3 integrates a tract-scale sequence model with an overlap-aware reassembly approach and boundary refinement, enabling accurate, boundary-coherent reconstruction of introgressed segments across diverse genomic contexts. By leveraging a simulation-trained model, AS3 avoids inference-time recalibration, offering stable performance across unrepresented demographic scenarios and small cohorts. In extensive simulations, AS3 outperforms existing methods in precision, recall, and F1 score, while providing more continuous segments with accurate boundary localization. It demonstrates robustness in small-target regimes and varying marker densities. Applied to 3,453 genomes from 209 populations, AS3 shows strong concordance with existing introgression callers and identifies additional introgressed regions, including high-frequency AS3-specific introgressed segments supported by locus-level haplotype and phylogenetic analyses. AS3 provides a scalable, robust solution for detecting archaic introgression from single individuals to large biobank datasets, marking a significant advancement in the field of local ancestry inference and opening new possibilities for the study of human evolutionary genetics. ArchaicSeeker 3.0 is available at https://github.com/Shuhua-Group/ArchaicSeeker3.0.

bioinformatics↗

Proteome profiling reveals HES1-driven mitotic catastrophe in ovarian serous carcinoma

Ovarian high-grade serous cancer (HGSC) is an aggressive subtype of epithelial ovarian cancer. Here, we identify BX-912, a phosphoinositide-dependent kinase 1 (PDPK1) inhibitor, as a promising therapeutic agent for HGSC. BX-912 suppressed HGSC growth as a single agent and synergized with olaparib independently of BRCA status. Unexpectedly, BX-912 treatment induced multinucleation, a phenotype not observed with other PDPK1 inhibitors. Proteome Integral Solubility Alteration (PISA) profiling revealed the transcription factor HES1 as a functional target of BX-912. Structural modeling showed that BX-912 binds the Orange domain of HES1, while its WRPW motif mediates interactions with protein partners, including the AP2 endocytic protein complex, coordinating their nuclear accumulation that leads to a mitotic catastrophe. Furthermore, cell cycle analyses showed that BX-912 combined with olaparib synergistically enhanced DNA damage and G2-M arrest. Our study demonstrates the value of proteomics for revealing hidden drug activities. It also identifies potential inhibition strategies for HES1, which is commonly overexpressed in HGSC. Additionally, this study proposes a novel strategy of targeting consecutive cell cycle phases to enhance treatment efficacy in HGSC.

cancer biology↗

Single-nucleus RNA sequencing reveals the cellular diversity of cerebrospinal fluid in the context of intraventricular hemorrhage

BackgroundIntraventricular hemorrhage (IVH) is a common and severe complication of hemorrhagic brain injury. Current treatments offer limited improvement in long-term neurological outcomes. Inflammatory responses in the cerebrospinal fluid (CSF) after IVH are thought to drive secondary injury, but the cellular mechanisms underlying this inflammation remain poorly defined. MethodsWe performed single-nucleus RNA sequencing of leukocytes isolated from CSF collected through external ventricular drains in subjects with intracerebral (n = 6) or subarachnoid (n = 1) hemorrhage. We characterized transcriptionally distinct subpopulations of neutrophils, monocytes, and lymphocytes by comparison to reference datasets. Cell-cell signaling networks were analyzed to infer cytokine-mediated communication, and a flow cytometry panel was developed to validate transcriptomic findings in independent CSF samples. ResultsWe obtained 11,191 high-quality nuclei comprising neutrophils (53.8%), monocytes (26.1%), lymphocytes (17.8%), and non-immune cells (2.4%). Neutrophils segregated into Nascent, Quiescent, and Interferon-Activated states. Monocytes exhibited classical phenotypes that include interferon-activated states (characterized by expression of VCAN or PROK2) and CXC-chemokine expressing states (characterized by expression of CXCL5 or CXCL8). Lymphocytes were mainly naive and central memory CD4 T cells. Cell-cell signaling analysis predicted strong CXC chemokine signaling from monocytes to neutrophil subsets and IL-1 family-driven inflammatory responses across multiple populations. Type I and III interferon signaling defined a neutrophil population not previously described in the central nervous system. ConclusionThis study delineates the diverse cellular immune landscape of CSF after IVH. Transcriptomic profiles reveal interferon, IL-1, and CXC chemokine signaling networks as potential therapeutic targets to mitigate secondary injury.

genomics↗

Bovine Formative Embryonic Stem Cell Plasticity in Embryonic and Extraembryonic Differentiation

Bovine embryonic stem cells (bESCs) can greatly enhance understanding of bovine embryonic development and applications for disease-resistance, biomedical and zoonotic pre-clinical models. However, formative bESCs with distinct morphology and complete differentiation capacity are still unreported. We document here the generation of bESCs which are pluripotent both in vitro and in vivo, and efficiently converted into neural progenitor cells (NPCs) and primordial germ cell-like cells (PGCLCs) by direct differentiation. These cells exhibited distinct metabolic features from human and mouse ESCs and early embryos. Formative bESCs contributed to a wide range of cell types within embryonic and extraembryonic tissues after aggregating with mouse and bovine embryos. The establishment of bovine formative ESCs with dual developmental plasticity represents a milestone for agricultural biotechnology and decoding the underlying mechanism of bona fide bovine pluripotency. Summary statementGenerating bovine ESCs would greatly enhance understanding of bovine embryonic development and bioengineering of cattle for disease-resistance, biomedical and zoonotic pre-clinical models.

developmental biology↗

Molecular epidemiology of carbapenem-resistant hypervirulent Klebsiella pneumoniae: Risk factors and resistance mechanism of ceftazidime/avibactam in China

The high morbidity and mortality rates associated with carbapenem-resistant hypervirulent Klebsiella pneumoniae have become a global public health problem. We analyzed the whole genome sequence and epidemiological data of 81 carbapenem-resistant Klebsiella pneumoniae strains and conducted sensitivity experiments to explore the optimal concentration of carbapenem-resistant Klebsiella pneumoniae. We verified the resistance and virulence genes of carbapenem-resistant Klebsiella pneumoniae using polymerase chain reaction and compared virulence between carbapenem-resistant hypervirulent Klebsiella pneumoniae a ndcarbapenem-resistant-non-hypervirulent Klebsiella pneumoniae through Galleria mellonella assays.The prevalent types of multilocus sequence typing in our carbapenem-resistant Klebsiella pneumoniae strains were ST11 (69.14%, 56/81). ST11-K64-O1/O2v1 has become an epidemic type in our hospital, with drug-resistance genes dominated by blaKPC-2 (90.12%, 73/81). Ceftazidime/avibactam has better antibacterial effects on carbapenem-resistant Klebsiella pneumoniae, and its resistance is mainly mediated by a resistance plasmid containing the blaKPC-2 gene. 52 carbapenem-resistant hypervirulent Klebsiella pneumoniae strains carry the blaKPC-2, with a high detection rate of siderophore. Further research has shown that the genetic environment of the blaKPC-2 contains TnpR_Tn3 and ISKpn27 upstream and ISKpn6 insertion sequences downstream. Galleria mellonella revealed that the survival rate of carbapenem-resistant hypervirulent Klebsiella pneumoniae was lower than that of carbapenem-resistant-non-hypervirulent Klebsiella pneumoniae, and the survival rate of carbapenem-resistant hypervirulent Klebsiella pneumoniae-K64 was lower than that of carbapenem-resistant hypervirulent Klebsiella pneumoniae-K47.The spread of carbapenem-resistant hypervirulent Klebsiella pneumoniae strains is alarming, necessitating molecular monitoring of hypervirulent strains and strengthening the nosocomial infection prevention and control measures. Antibiotics should be used reasonably based on patients infection status and local epidemiological data. ImportanceCarbapenem-resistant Klebsiella pneumonia is a global public health concern. We conducted a molecular epidemiological analysis of 81 carbapenem-resistant hypervirulent Klebsiella pneumoniae strains from our hospital and explored the resistance mechanism of ceftazidime/avibactam. We identified the blaKPC-2 gene to be primarily responsible for carbapenem resistance in our hospital, and ST11-K64 was the dominant clone. A high-risk clone, ST307-K102, was detected, necessitating strengthened surveillance to prevent its spread. This studys findings contribute to the optimization of antimicrobial management and indicate that genomic research can assist with the tracking of hospital infection outbreaks and the improvement of infection-control measures.

microbiology↗

Downregulation of astrocytic C3 production alleviates neuronal mitochondrial dysfunction in tauopathy models

Neuronal mitochondrial dysfunction is associated with cognitive decline in neurodegenerative disorders such as Alzheimers Disease (AD). In this study, multiple pieces of evidence proved that phosphorylated tau (p-Tau) caused mitochondrial swelling and dysfunction in neurons. In a novel in vitro newborn neurons culture system, we discovered mitochondrial swelling and dysfunction were associated with increased p-Tau, leading to necroptosis activation, which was induced by Complement C3 (C3) produced from activated astrocytes. In the in vivo tauopathy mouse models, the effects of astrocytic C3 on tau-associated mitochondrial dysfunction and necroptosis were also discovered in hippocampal newborn neurons, and we directly showed that p-Tau aggregation was associated with mitochondria swelling in the hippocampal neurons by electron microscopy analysis. In addition, we proved the ability of compound anserine, which can block Tak1-Ikk dependent NF-{kappa}B activation, to further down-regulate astrocytic C3 production and alleviate neuronal mitochondrial dysfunction in vitro and in vivo, respectively. Down-regulation of astrocyte C3-production by anserine could also rescue mortality as well as cognitive and motor functions. Our findings first reported the contribution of p-Tau on neuronal mitochondrial dysfunction and proposed the therapies that down-regulate astrocytic C3 production have a potential role in alleviating this neurotoxic effect.

neuroscience↗

Circular DNA vcDNA-S7 derived from segmented-dsRNA virus BmCPV attenuated viral infection through RNase H1

Viral circDNA derived from insect positive-sense single-stranded RNA viruses plays a crucial role in regulating viral infections depending on the RNAi pathway. Our previous research has revealed that Bombyx mori cypovirus (BmCPV), a segmented-dsRNA virus, can generate viral circDNA vcDNA-S7, which can be transcribed to form RNA and further processed into small RNAs to defend against the virus through RNAi. However, whether vcDNA-S7 employs other mechanisms to resist the viruses. Presently, vcDNA-S7 has been found to resist BmCPV infection via a novel mechanism that depends on ribonuclease RNase H1 activity. It was found that the expression level of RNase H1 increased upon BmCPV infection (RNA virus) but not upon B. mori nucleopolyhedrovirus (BmNPV) (DNA virus) infection. RNase H1 has been shown to negatively regulate BmCPV infections. In addition, vcDNA-S7 was found to form a heteroduplex with the viral RNA and subsequently recruit RNase H1 to degrade the viral RNA within the heteroduplex, ultimately leading to the suppression of viral replication. Furthermore, the resistance of vcDNA-S7 to viruses was significantly reduced when cellular RNase H1 gene was silenced. These findings not only reveal a new antiviral mechanism involving circular DNA formed by reovirus but also offer intriguing insights into the antiviral function of RNase H1 in cells.

immunology↗

AncestryPainter 2.0: Visualizing ancestry composition and admixture history graph

To effectively depict the results of population genetics studies, it is essential to present ancestry composition and genetic distance. The growing amount of genomic data prompted us to design AncestryPainter 1.0, a Perl program to display the ancestry composition of numerous individuals using a rounded graph. Motivated by the requests of users in practical applications, we updated AncestryPainter to version 2.0 by coding in an R package and improving the layout, providing more options and compatible statistical functions for graphing. In particular, AncestryPainter 2.0 implements a method admixture history graph (AHG) to infer the admixture sequence of multiple ancestry populations, and allows for multiple pie charts at the center of the graph to display the ancestry composition of more than one target population. We also introduced an additional graphing module to visualize genetic distance through radial bars of varying lengths surrounding a core. Visualization functions per se have been enhanced in this update as well. Furthermore, AncestryPainter 2.0 includes two statistical modules to 1) merge ancestry proportion matrices and 2) infer admixture sequences through correlation analyses. AncestryPainter 2.0 is publicly available at https://github.com/Shuhua-Group/AncestryPainterV2 and https://pog.fudan.edu.cn/#/Software.

genetics↗

Geographic Distribution of a Missense Mutation in the KRT38 Gene and Its Association with Heat Tolerance in Chinese Indigenous Cattle Breeds

ContextChina has a vast area across many temperature zones and a variety of cattle breeds. These cattle resources are ideal models to research their adaptability to the environment. The KRT38 gene is an acidic protein, and its coding product can be used as a component of hair production. AimsThe objective of this study was to investigate the diversity of the KRT38 gene in Chinese local cattle and the association of different genotypes with mean temperature (T), relative humidity (RH) and temperature humidity index (THI). MethodsA missense mutation g.41650738 A > G in the KRT38 gene was screened from the database of bovine genomic variation (BGVD), was genotyped in a total of 246 samples from 15 local cattle breeds in China by PCR amplification and sequencing. Finally, the correlation between the locus and the three climatic factors was analysed. Key resultsWe successfully obtained the frequency of this SNP in three groups of cattle in northern, central and southern China. The frequency of allele A gradually declined from north to south, while the frequency of allele G showed the opposite trend with a clear geographic distribution. ConclusionsOur results indicate that KRT38 variation in Chinese indigenous cattle might be linked to heat tolerance. ImplicationsOur analysis may support in finding out its importance as a genetic signal for heat tolerance in cattle reproduction and genetics.

genomics↗

Structural basis of nucleosomal H4K20 recognition and methylation by SUV420H1 methyltransferase

Histone lysine methyltransferase of SUV420H1, which is responsible for site-specific di-/tri-methylation of histone H4 lysine 20 (H4K20), has crucial roles in DNA-templated processes, including DNA replication, DNA damage repair and chromatin compaction. Its mutations frequently occur in human cancers. Nucleosomes containing the histone variant H2A.Z enhance the catalytic activities of SUV420H1 in H4K20 di-methylation deposition, regulating early replication origins. However, the molecular mechanism of how H4K20 methyl marks are deposited on nucleosomes by SUV420H1 remains poorly understood. Here we report the cryo-electron microscopy (cryo-EM) structures of SUV420H1 associated with canonical nucleosome core particles (NCPs) or H2AZ containing NCPs. We find that SUV420H1 make extensive site-specific contacts with histone and DNA regions. SUV420H1 C-terminal domain recognizes the H2A-H2B acidic pocket of NCPs through its two arginine anchors, thus enabling H4K20 insertion for catalysis specifically. We also identify important residues increasing the catalytic activities of SUV420H1 bound to H2A.Z NCPs. In vitro and in vivo functional analysis reveal that multiple disease associated mutations at the interfaces are essential for its catalytic activity and chromatin states regulation. Together, our study provides molecular insights into the nucleosome-based recognition and methylation mechanisms of SUV420H1, and a structural basis for understanding SUV420H1-related human disease.

molecular biology↗

Ecological dynamics of the gut microbiome in response to dietary fiber

Dietary fibers are generally thought to benefit intestinal health. Their impacts on the composition and metabolic function of the gut microbiome, however, vary greatly across individuals. Previous research showed that each individuals response to fibers depends on their baseline gut microbiome, but the ecology driving microbiota remodeling during fiber intake remained unclear. Here, we studied the long-term dynamics of gut microbiome and short-chain fatty acids (SCFAs) in isogenic mice with distinct microbiota baselines fed with the fermentable fiber inulin compared to the non-fermentable fiber cellulose. We found that inulin produced generally rapid response followed by gradual stabilization to new equilibria, and those dynamics were baseline-dependent. We parameterized an ecology model from the timeseries data, which revealed a group of bacteria whose growth significantly increases in response to inulin. and whose baseline abundance and interspecies competition explains the baseline-dependence of microbiome density and community composition dynamics. Fecal levels of of SCFAs, such as propionate, is associated with the abundance of inulin responders, yet inter-individual variation of gut microbiome impedes the prediction of SCFAs by machine learning models. Finally, we showed that our methods and major findings are generalizable to dietary resistant starch. This study emphasizes the importance of ecological modeling to understand microbiome responses to dietary changes and the need for personalized interventions.

ecology↗

T-cell Repertoire Characteristics of Asymptomatic and Re-detectable Positive COVID-19 Patients

BackgroundThe prevention of COVID-19 pandemic is highly complicated by the prevalence of asymptomatic and recurrent infection. Many previous immunological studies have focused on symptomatic and convalescent patients, while the immune responses in asymptomatic patients and re-detectable positive cases remain unclear. MethodsHere we comprehensively analyzed the peripheral T-cell receptor (TCR) repertoire of 54 COVID-19 patients in different phases, including asymptomatic, symptomatic, convalescent and re-detectable positive cases. ResultsWe found progressed immune responses from asymptomatic to symptomatic phase. Furthermore, the TCR profiles of re-detectable positive cases were highly similar to those of asymptomatic patients, which could predict the risk of recurrent infection. ConclusionTherefore, TCR repertoire surveillance has the potential to strengthen the clinical management and the immunotherapy development for COVID-19. FundingThe Science and Technology Innovation Project of Foshan Municipality (2020001000431) and the National Key Research and Development Project (2020YFA0708001).

immunology↗

Characterization of a novel Fgf10CreERT2 knock-in mouse line targeting postnatal lung Fgf10 lineages

Fgf10 is a key gene during development, homeostasis and repair after injury. We previously reported a Fgf10CreERT2 line (with the CreERT2 cassette inserted in frame with the start codon of exon 1), called thereafter Fgf10Ki-v1, to target Fgf10Pos cells. While this line allowed fairly efficient and specific labeling of Fgf10Pos cells during the embryonic stage, it failed to target these cells after birth, particularly in the postnatal lung, which has been the focus on our research. We report here the generation and validation of a new Fgf10CreERT2 (called thereafter Fgf10Ki-v2) with the insertion of the expression cassette in frame with the stop codon of exon 3. This new Fgf10Ki-v2 line exhibited comparable Fgf10 expression level to their wild type counterpart. However, a disconnection between the Fgf10 and the Cre expression was observed in Fgf10Ki-v2/+ lungs. In addition, lung and limb agenesis were observed in homozygous embryos suggesting a loss of Fgf10 functional allele in Fgf10Ki-v2 mice. Bio-informatics analysis shows that the 3UTR, where the CreERT2 cassette is inserted, contains numerous putative transcription factor binding sites. By crossing this line with tdTomato reporter line, we demonstrated that tdTomato expression faithfully recapitulated Fgf10 expression during development. Significantly, Fgf10Ki-v2 mouse is capable of significantly targeting Fgf10Pos cells in the adult lung. Therefore, despite the aforementioned limitations, this new Fgf10Ki-v2 line opens the way for future mechanistic experiments involving the postnatal lung.

developmental biology↗

TIGIT-Fc Promotes Antitumour Immunity

T cell immunoreceptor with Ig and ITIM domains (TIGIT) is a checkpoint receptor that mediates both T cell and natural killer (NK) cell exhaustion in tumours. An Fc-TIGIT fusion protein was shown to induce an immune-tolerance effect in a previous report, but the relevance of the TIGIT-Fc protein to tumour immunity is unknown. Here, we unexpectedly found that TIGIT-Fc promotes rather than suppresses tumour immunity. TIGIT-Fc treatment promoted the effector function of CD8+ T and NK cells in several tumour-bearing mouse models. Additionally, TIGIT-Fc treatment resulted in potent T cell and NK-cell-mediated tumour reactivity, sustained memory-induced immunity in tumour re-challenge models, enhanced therapeutic effects via an antibody against PD-L1, and induction of Th1 development in CD4+ T cells. TIGIT-Fc showed a potent antibody-dependent cell-mediated cytotoxicity (ADCC) effect but no intrinsic effect on tumour cell development. Our findings elucidate the unexpected role of TIGIT-Fc in tumour immune reprogramming, suggesting that TIGIT-Fc treatment alone or in combination with other checkpoint receptor blockers is a promising anticancer therapeutic strategy.

bioengineering↗

CAR Macrophages for SARS-CoV-2 Immunotherapy

Targeted therapeutics for the treatment of coronavirus disease 2019 (COVID-19), especially severe cases, are currently lacking. As macrophages have unique effector functions as a first-line defense against invading pathogens, we genetically armed human macrophages with chimeric antigen receptors (CARs) to reprogram their phagocytic activity against SARS-CoV-2. After investigation of CAR constructs with different intracellular receptor domains, we found that although cytosolic domains from MERTK (CARMERTK) did not trigger antigen-specific cellular phagocytosis or killing effects, unlike those from MEGF10, FcR{gamma} and CD3{zeta} did, these CARs all mediated similar SARS-CoV-2 clearance in vitro. Notably, we showed that CARMERTK macrophages reduced the virion load without upregulation of proinflammatory cytokine expression. These results suggest that CARMERTK drives an immunologically silent scavenger effect in macrophages and pave the way for further investigation of CARs for the treatment of individuals with COVID-19, particularly those with severe cases at a high risk of hyperinflammation.

bioengineering↗

Autographa californica Multiple Nucleopolyhedrovirus orf13 is Required for Efficient Nuclear Egress of Nucleocapsids

Autographa californica multiple nucleopolyhedrovirus (AcMNPV) orf13 (ac13) is a conserved gene in all sequenced alphabaculoviruses. However, its function in the viral life cycle remains unknown. In this study we found that ac13 was a late gene and that the encoded protein, bearing a putative nuclear localization signal motif in the DUF3627 domain, colocalized with the nuclear membrane. Deletion of ac13 did not affect viral DNA replication, gene transcription, nucleocapsid assembly or occlusion body (OB) formation, but reduced virion budding from infected cells by approximately 400-fold compared with the wild-type virus. Deletion of ac13 substantially impaired the egress of nucleocapsids from the nucleus to the cytoplasm, while the number of occlusion-derived viruses embedded within OBs was unaffected. Taken together, our results indicated that ac13 was required for efficient nuclear egress of nucleocapsids during virion budding, but was dispensable for OB formation. IMPORTANCEEgress of baculovirus nucleocapsids from the nucleus is an essential process for morphogenesis of mature budded viruses, which is required to spread infection within susceptible cells and tissues. Although many viral and host proteins are required for nucleocapsid egress, the specific mechanisms underlying this process in baculoviruses remain somewhat enigmatic. In the present study, we found that the ac13 gene, in addition to ac11, ac51, ac66, ac75, ac78, gp41, ac93, p48, exon0 and ac142, was required for efficient nuclear egress of nucleocapsids. Our results contribute to a better understanding of nucleocapsid egress in baculoviruses.

microbiology↗