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Chen, X.

Publications and source records attributed to Chen, X..

At least 1,009 records · Page 56Linked to original sources
bioRxiv2022

Inferring transcriptional bursting kinetics from single-cell snapshot data using a generalized telegraph model

MotivationGene expression has inherent stochasticity resulting from transcriptions burst manners. Single-cell snapshot data can be exploited to rigorously infer transcriptional burst kinetics, using mathematical models as blueprints. The classical telegraph model (CTM) has been widely used to explain transcriptional bursting with Markovian assumptions (i.e., exponentially distributed dwell time in ON and OFF states). However, growing evidence suggests that the gene-state dwell times are nonexponential, as gene-state switching is a multi-step process in organisms. Therefore, interpretable non-Markovian mathematical models and efficient statistical inference methods are urgently required in investigating transcriptional burst kinetics. ResultsWe develop an interpretable and tractable model, the generalized telegraph model (GTM), to carve transcriptional bursting that allows arbitrary dwell-time distributions, rather than exponential distributions, to be incorporated into the ON and OFF switching process. Based on the GTM, we propose an inference method for transcriptional bursting kinetics using an approximate Bayesian computation framework (BayesGTM). BayesGTM demonstrates efficient and scalable estimation of burst frequency and burst size on synthetic data. Further, the application of BayesGTM to genome-wide data from mouse embryonic fibroblasts reveals that CTM would overestimate burst frequency and underestimate burst size. In conclusion, the GTM and the corresponding BayesGTM are effective tools to infer dynamic transcriptional bursting from static single-cell snapshot data.

systems biology↗
bioRxiv2022

Porous microneedle patch with sustained exosomes delivery repairs severe spinal cord injury

1.Mesenchymal stem cell-derived exosome (MSC-EXO) transplantation has been suggested as an efficacious treatment to suppress spinal cord injury (SCI)-triggered neuroinflammation. However, an ethically acceptable method to continuously deliver MSC-EXOs to acute spinal lesions, without damaging nearby tissues/axons, has never been achieved. In this study, we fabricated a device comprising a patch containing MSCs and a microneedle array (MN-MSC patch) to treat severe SCI. When topically applied to an acute spinal lesion beneath the spinal dura, the soft microneedle (MN) array with reasonable mechanical strength avoided damaging the nearby spinal tissues, and the porous microstructure of MNs facilitated highly efficient MSC-EXO delivery. With the capacity for sustained delivery of MSC-EXOs, the MN-MSC patch was evaluated in a contusive rat SCI model. The MSCs encapsulated in the patch could survive for at least 7 days, encompassing the optimal time window for downregulating SCI-triggered neuroinflammation. As a result, MN-MSC patch treatment led to reduced cavity and scar tissue formation, greater angiogenesis, and improved survival of nearby tissues/axons. Remarkably, rats treated by this method achieved superior muscle control and exhibited robust hindlimb locomotion functional recovery. Conclusively, the MN-MSC patch device proposed here overcomes the current dilemma between treatment efficacy and ethical issues in treating acute SCI.

bioengineering↗
bioRxiv2022

Biphasic response of CD8 T cell to asparagine restriction maximizes its metabolic fitness and antitumoral functionality

Robust and effective T cell immune surveillance and cancer immunotherapy require properly allocating metabolic resources to sustain energetically costly processes, including growth and cytokine production. Amino acids are major cellular constituents that serve as protein building blocks, energy sources, and signaling molecules. Although T cells can synthesize all nonessential amino acids, including asparagine (Asn), activated CD8 T cells still consume considerable quantities of exogenous Asn. Unexpectedly, Asn restriction on CD8 T cells induced a biphasic response, consisting of sequential actions with opposing effects at two conceptually separated phases after activation. Asn restriction suppressed activation and cell cycle entry in the early phase by depleting the intracellular Asn pool while rapidly engaging an ATF4/NRF2-dependent stress response, conferring robust proliferation and effector function of CD8 T cells in the late phase. Mechanistically, ATF4 and NRF2 activation rendered CD8 T cells to utilize de novo biosynthesis of Asn, consuming less glucose and glutamine but producing more intracellular nucleotides for proliferation. Moreover, NRF2 activation promoted the expression of inflammatory and effector genes to enhance effector functions in CD8 T cells. Accordingly, Asn restriction or overexpression of ATF4 or NRF2 potentiated T cell-mediated antitumoral response in the metabolically restricted tumor microenvironment. Our studies revealed Asn as a critical metabolic node in directing the stress signaling to shape T cell metabolic fitness and effector functions. Asn restriction is a promising and clinically relevant strategy to enhance cancer immunotherapy.

immunology↗
bioRxiv2022

An updated nomenclature for plant ribosomal protein genes

Ban et al. (2014) proposed a nomenclature for ribosomal proteins (r-proteins) that reflects the current understanding of ribosomal protein evolution. In the past few years, this nomenclature has been widely adopted among biomedical researchers and microbiologists. This homology-based r-protein nomenclature has not been as widely adopted among plant biologists, however, presumably because r-protein nomenclature is much more complicated in plants due to gene duplication. Here, we propose compatible upgrades to the homology-guided nomenclature proposed by Ban et al. (2014) so that this naming system can be adopted for widespread use in the plant biology community. We note that Lan et al. (2022) recently proposed updated nomenclature for plant cytosolic ribosomal proteins, focused on Arabidopsis and rice. The nomenclature outlined here is an extension of that proposed by Lan et al. (2022), expanding to include organellar ribosomes and additional species, with the intent that this nomenclature can serve as a template to guide future plant genome annotations. A more detailed comparison highlighting how this naming system builds on the Ban et al. (2014) and Lan et al. (2022) nomenclatures is offered below. At this time, we request community feedback on this proposed nomenclature so that the naming system ultimately chosen represents a broad consensus. Feedback can be communicated to the this working group at plantribosome@gmail.com before July 25th, 2022. Coauthors of this letter and anyone in the scientific community expressing significant interest will then discuss this feedback as a group, reach a consensus agreement, and communicate the updated nomenclature rules through a letter to the editor (expected to be published at The Plant Cell) and the databases at TAIR and MaizeGDB.

plant biology↗
bioRxiv2022

Human iPSC-derived neuron of 16p11.2 deletion reveals haplotype-specific expression of MAPK3 and its contribution to variable NDD phenotypes

Recurrent proximal 16p11.2 deletion (16p11.2del) is risk factor of diverse neurodevelopmental disorders (NDDs) with variable penetrance. Although previous human induced pluripotent stem cell (hiPSC) models of 16p11.2del confirmed disrupted neuron development, it is not known which gene(s) at this interval are mainly responsible for the abnormal cellular phenotypes and how the NDD penetrance is regulated. After haplotype phasing of 16p11.2 region, we generated hiPSCs for two 16p11.2del families with distinct residual haplotypes and variable NDD phenotypes. We also differentiated the hiPSCs to cortical neural cells and demonstrated MAPK3 as a driver signal of 16p11.2 region contributing to the dysfunctions in multiple pathways related to neuron development, which leads to altered morphological or electrophysiological properties in neuron cells. Furthermore, residual haplotype-specific MAPK3 expression was identified in 16p11.2del neuron cells, associating MAPK3 down-expression with the minor allele of the residual haplotype. Ten SNPs of the residual haplotype are mapped as enhancer SNPs (enSNPs) of MAPK3, eight enSNPs were functionally validated by luciferase assays, implying enSNPs contribute to residual haplotype-specific MAPK3 expression via cis-regulation. Finally, the analyses of three different patient cohorts showed that the residual haplotype of 16p11.2del is associated with variable NDD phenotypes.

genetics↗
bioRxiv2022

Kynurenic acid promotes A1 to A2 astrocyte conversion against HIV-associated neurocognitive disorder

Although extensive astrocyte activation is present in the CNS of patients suffering from HIV-associated neurocognitive disorder (HAND), little is known about the contribution of reactive astrocytes to HAND neuropathology. Here, we report that the imbalance between neurotoxic (A1 astrocytes) and protective astrocytes (A2 astrocytes) occurring in HIV-1 gp120 transgenic mice impedes the resolution of inflammation in the CNS, perpetuating neuron damage and cognitive deficits. Kynurenic acid (KYNA), a tryptophan metabolite with 7 nicotinic acetylcholine receptors (7nAChR) inhibitory property, blunts gp120-induced A1 astrocyte activation while promoting A2 astrocyte formation through blockade of 7nAChR/JAK2/STAT3 signaling activation. Meanwhile, we provide evidence that 7nAChR deletion and tryptophan administration convert astrocyte phenotypes, ultimately facilitating neuronal and cognitive improvement in the gp120tg mice. These initial and determinant findings mark a turning point in our understanding of the role of 7nAChR in gp120-mediated astrocyte activation, which opens new opportunities to control reactive astrocyte generation through KYNA and tryptophan administration as a pharmacological approach for treating HAND.

microbiology↗
bioRxiv2022

Monoallelically-expressed Noncoding RNAs form nucleolar territories on NOR-containing chromosomes and regulate rRNA expression

Out of the several hundred copies of rRNA genes that are arranged in the nucleolar organizing regions (NOR) of the five human acrocentric chromosomes, [~]50% remain transcriptionally inactive. NOR-associated sequences and epigenetic modifications contribute to differential expression of rRNAs. However, the mechanism(s), controlling the dosage of active versus inactive rRNA genes in mammals is yet to be determined. We have discovered a family of ncRNAs, SNULs (Single NUcleolus Localized RNA), which form constrained sub-nucleolar territories on individual NORs and influences rRNA expression. Individual members of the SNULs monoallelically associate with specific NOR-containing chromosome. SNULs share sequence similarity to pre-rRNA and localize in the sub-nucleolar compartment with pre-rRNA. Finally, SNULs control rRNA expression by influencing pre-rRNA sorting to the DFC compartment and pre-rRNA processing. Our study discovered a novel class of ncRNAs that by forming constrained nucleolar territories on individual NORs contribute to rRNA expression.

cell biology↗
bioRxiv2022

Injectable hydrogel embedded with mesenchymal stem cells repairs severe spinal cord injury

Mesenchymal stem cell (MSC) transplantation was suggested as a promising approach to treat spinal cord injury (SCI). However, the heterogeneity of MSC and the lack of appropriate delivery methods impede its clinical application. To tackle these challenges, we first generated human MSCs derived from a single cell with a great homogeneity of batch quality and then developed a biocompatible injectable hydrogel to embed these cells to treat severe SCI. In a clinically relevant rat severe SCI model, we showed that the injection of MSCs with injectable hydrogel into the lesion site promoted robust functional recovery, while the intrathecal delivery of MSCs only resulted in limited therapeutic effects. Mechanistically, the hydrogel protected MSCs from the damage of harmful neuroinflammatory microenvironment in the spinal cord lesion. The hydrogel with the survived MSCs ameliorates the neuroinflammatory microenvironment of spinal cord lesion, preventing cavity formation and leads to the remnant of spared axons/tissues, which results in a better prognosis in the end.

bioengineering↗
bioRxiv2022

Identification of a Broadly Fibrogenic Macrophage Subset Induced by Type 3 Inflammation in Human and Murine Liver and Lung Fibrosis

Macrophages are central orchestrators of the tissue response to injury, with distinct macrophage activation states playing key roles in the progression and resolution of fibrosis. Identifying the unique fibrogenic macrophages that are found in human fibrotic tissues could lead to new and more effective treatments for fibrosis. Here we used human liver and lung single cell RNA sequencing datasets to identify a unique subset of CD9+ TREM2+ macrophages expressing SPP1, GPNMB, FABP5, and CD63 with strong pro-fibrotic activity. This population was validated across orthogonal techniques, species and tissues. These macrophages were enriched at the outside edges of scarring adjacent to activated mesenchymal cells, and in the fibrotic niche across species and organs. Neutrophils producing the type 3 cytokines GM-CSF and IL-17A, and expressing MMP9, which participates in the activation of TGF-{beta}1, clustered with these scar-associated macrophages. Using in vitro primary human cell assays, we determined that GM-CSF, IL-17A and TGF-{beta}1 drive the differentiation of these scar-associated macrophages, and that co-culture of monocyte-derived macrophages with hepatic stellate cells and TGF-{beta}1 augmented type 1 collagen deposition. In vivo blockade of GM-CSF, IL-17A or TGF-{beta}1 with small or large molecules reduced scar-associated macrophage expansion and fibrosis in multiple models of hepatic and pulmonary fibrosis. Our work demonstrates that a specific scar-associated macrophage population is linked with fibrosis across species and tissues. It further provides a strategy for unbiased discovery, triage and preclinical validation of therapeutic targets within this fibrogenic macrophage population.

immunology↗
bioRxiv2022

The LncRNA Carmn is a Critical Regulator for Gastrointestinal Smooth Muscle Contractile Function and Motility

Background & aimsVisceral smooth muscle cells (SMCs) are an integral component of the gastrointestinal (GI) tract and are critical for regulating motility. SMC contraction is regulated by changes in post-translational signaling and the state of differentiation. Impaired SMC contraction is associated with significant morbidity and mortality but the mechanisms regulating the expression levels of SMC-specific contractile proteins, including the role of long non-coding RNAs (lncRNAs), remains largely unexplored. Herein, we have uncovered an important role of Carmn (Cardiac mesoderm enhancer-associated noncoding RNA), a SMC-specific lncRNA, in regulating the phenotype of visceral SMCs of the GI tract. MethodsAnalysis of GTEx and publicly available single-cell RNA sequencing (scRNA-seq) datasets from embryonic, adult human and mouse GI tissues were used to identify SMC-specific lncRNAs. The functional role of Carmn was investigated using a novel GFP knock-in (KI) reporter/knockout (KO) mouse model. Bulk RNA sequencing (RNA-seq) and single nuclei RNA sequencing (snRNA-seq) of colonic muscularis were used to investigate underlying mechanisms. ResultsUnbiased in silico analyses and GFP expression patterns in Carmn GFP KI mice revealed that Carmn is specifically expressed in SMCs in human and mouse GI tract. Premature lethality was observed in global Carmn KO (gKO) and inducible SMC-specific KO (iKO) mice due to colonic pseudo-obstruction, severe distension of the GI tract with blockages in cecum and colon segments. Histology, whole-gut GI transit time and muscle myography analysis revealed severe dilation, significantly delayed GI transit and impaired GI contractility in Carmn KO mice versus control mice. Bulk RNA-seq of colonic muscularis revealed that Carmn deficiency promotes SMC de-differentiation as evidenced by up-regulation of extracellular matrix genes and down-regulation of SMC contractile genes including Mylk, a key regulator of SMC contraction. SnRNA-seq further revealed SMC Carmn deficiency not only compromised myogenic motility by reducing expression of contractile genes but also impaired neurogenic motility by disrupting cell-cell connectivity in the colonic muscularis. These findings may have translational significance as silencing CARMN in human colonic SMCs significantly attenuated contractile gene expression including MYLK and decreased SMC contractility. Luciferase reporter assays showed that CARMN enhances the transactivation activity of the master regulator of SMC contractile phenotype, myocardin, thereby maintaining the GI SMC myogenic program. ConclusionOur data suggest that Carmn is indispensable for maintaining GI SMC contractile function in mice, and that loss of function of CARMN may contribute to human visceral myopathy. To our knowledge this is the first study showing an essential role of lncRNA in the regulation of visceral SMC phenotype.

cell biology↗
bioRxiv2022

Small cytosolic dsDNAs repress cGAS activation and induce autophagy

Cyclic GMP-AMP (cGAMP) synthase (cGAS), a major cytosolic DNA sensor, activates innate immune responses by producing cGAMP, which activates stimulator of interferon genes (STING)1. Cytosolic DNA induces autophagy in a cGAS-dependent manner to avoid persistent immune stimulation. Although dsDNAs < 20 bp can bind to cGAS, robust cGAS activation requires dsDNAs > 45 bp 2-4. However, whether cytosolic dsDNAs < 45 bp exist in mammalian cells remains unclear. Here, we identified a class of small cytosolic DNAs (scDNAs) of [~]20-40 bp in human and mouse cell lines. scDNAs competed with herring testis DNA (HT-DNA, [~]200-1500 bp) for binding to cGAS, and repressing HT-DNA-induced cGAS activation and the associated interferon {beta} (IFN{beta}) production. Moreover, scDNAs promoted cGAS and Beclin-1 interaction, triggering the release of Rubicon, a negative regulator of phosphatidylinositol 3-kinase class III (PI3KC3)5,6, from the Beclin-1-PI3KC3 complex, activating PI3KC3 and inducing autophagy. DNA damage decreased and autophagy inducers increased scDNA levels. scDNA transfection or autophagy induction attenuated DNA damage-induced cGAS-STING activation and IFN{beta} expression. Thus, scDNAs acted as molecular brakes of cGAS activation, preventing excessive inflammatory cytokine production following DNA damage. Our findings lay foundations for understanding the physiological and pathological functions of scDNAs.

molecular biology↗
bioRxiv2022

Granger causality analysis for calcium transients in neuronal networks: challenges and improvements

One challenge in neuroscience is to understand how information flows between neurons in vivo to trigger specific behaviors. Granger causality (GC) has been proposed as a simple and effective measure for identifying dynamical interactions. At single-cell resolution however, GC analysis is rarely used compared to directionless correlation analysis. Here, we study the applicability of GC analysis for calcium imaging data in diverse contexts. We first show that despite underlying linearity assumptions, GC analysis successfully retrieves non-linear interactions in a synthetic network simulating intracellular calcium fluctuations of spiking neurons. We highlight the potential pitfalls of applying GC analysis on real in vivo calcium signals, and offer solutions regarding the choice of GC analysis parameters. We took advantage of calcium imaging datasets from motoneurons in embryonic zebrafish to show how the improved GC can retrieve true underlying information flow. Applied to the network of brainstem neurons of larval zebrafish, our pipeline reveals strong driver neurons in the locus of the mesencephalic locomotor region (MLR), driving target neurons matching expectations from anatomical and physiological studies. Altogether, this practical toolbox can be applied on in vivo population calcium signals to increase the selectivity of GC to infer flow of information across neurons.

neuroscience↗
bioRxiv2022

Neutrophils reprograms the bone marrow to impair T-cell immunity during tuberculosis

Mycobacterium tuberculosis (Mtb) infection induces persistent influx of neutrophils that associates with poor bacterial control and clinical outcome from tuberculosis (TB). Although implicated in TB pathology, the mechanism by which these cells contribute to pathogenesis is poorly understood. Using Cell-DIVE multiplexed immunofluorescence imaging and spatial analysis of inflammatory TB lesions, we demonstrated that persistent neutrophil infiltration affects the spatiotemporal organization of T-lymphocytes and impairs their function. Instead of directly suppressing T-cells, neutrophils produce granulocyte colony stimulating factor (CSF3/G-CSF) that collaborates with type I interferon (IFN-I) to promote a granulocyte-skewed hematopoiesis impacting T-lymphocyte production. Importantly, neutrophil-intrinsic IFN-I receptor 1 (IFNAR1) is both necessary and sufficient to promote pathologic granulopoiesis. Finally, inhibition of IFNAR1-signaling alone mitigates immunopathogenesis by restoring hematopoietic equilibrium. Collectively, our work uncovers a potential immunevasion strategy by which virulent Mtb strains induce IFN-I to generate pathogen-permissive neutrophils that produce G-CSF and sustain pathogenic hematopoiesis to impair T-cell immunity during TB.

immunology↗
bioRxiv2022

Yeast U6 snRNA made by RNA polymerase II is less stable but functional

U6 small nuclear (sn)RNA is the shortest and most conserved snRNA in the spliceosome and forms a substantial portion of its active site. Unlike the other four spliceosomal snRNAs, which are synthesized by RNA polymerase (RNAP) II, U6 is made by RNAP III. To determine if some aspect of U6 function is incompatible with synthesis by RNAP II, we created a U6 snRNA gene with RNAP II promoter and terminator sequences. This "U6-II" gene is functional as the sole source of U6 snRNA in yeast, but its transcript is much less stable than U6 snRNA made by RNAP III. Addition of the U4 snRNA Sm protein binding site to U6-II increased its stability and led to formation of U6-II*Sm complexes. We conclude that synthesis of U6 snRNA by RNAP III is not required for its function and that U6 snRNPs containing the Sm complex can form in vivo. The ability to synthesize U6 snRNA with RNAP II relaxes sequence restraints imposed by intragenic RNAP III promoter and terminator elements and allows facile control of U6 levels via regulators of RNAP II transcription.

molecular biology↗
bioRxiv2022

Arabidopsis AAR2, a conserved splicing factor in eukaryotes, acts in microRNA biogenesis

MicroRNAs (miRNAs) play an essential role in plant growth and development, and as such, their biogenesis is fine-tuned via regulation of the core microprocessor components. Here, we report that Arabidopsis AAR2, a homolog of a U5 snRNP assembly factor in yeast and humans, not only acts in splicing but also promotes miRNA biogenesis. AAR2 interacts with the microprocessor component HYPONASTIC LEAVES1 (HYL1) in the cytoplasm, nucleus and dicing bodies. In aar2 mutants, abundance of nonphosphorylated HYL1, the active form of HYL1, and the number of HYL1-labeled dicing bodies are reduced. Primary miRNA (pri-miRNA) accumulation is compromised despite normal promoter activities of MIR genes in aar2 mutants. RNA decay assays show that the aar2-1 mutation leads to faster degradation of pri-miRNAs in a HYL1-dependent manner, which reveals a previously unknown and negative role of HYL1 in miRNA biogenesis. Taken together, our findings reveal a dual role of AAR2 in miRNA biogenesis and pre-mRNA splicing. SignificanceIn yeast and humans, AAR2 is involved in pre-mRNA splicing through regulating U5 snRNP assembly. This study shows that Arabidopsis AAR2 promotes microRNA (miRNA) accumulation in addition to its conserved role in pre-mRNA splicing. AAR2 is associated with the microprocessor component HYL1 and promotes its dephosphorylation to produce the active form in miRNA biogenesis. The study also reveals a previously unknown role of HYL1 in causing the degradation of the primary precursors to miRNAs (pri-miRNAs) and a role of AAR2 in protecting pri-miRNAs from HYL1-depedent degradation. Taken together, our findings provide new insights into the role of a conserved splicing factor in miRNA biogenesis in plants.

plant biology↗
bioRxiv2022

Rab7/Retromer-based endolysosomal trafficking facilitates effector secretion and host invasion in rice blast

Secretion is a fundamental process in all living organisms. Using conventional secretion pathways, many plant pathogens release effectors into the host plants to downregulate immunity and promote infection. However, this does not always constitute the only way that effectors are sorted and tracked to their final destination such as the biotrophic interfacial complex-associated effectors produced by the blast fungus Magnaporthe oryzae. Here, we uncover a novel unconventional route originating from fungal vacuolar membrane to the host interface and plasma membrane. We found that a GFP-MoRab7 labeled vacuole is closely associated with the interface structure throughout M. oryzae invasive growth. Conditional inactivation of MoRab7 impaired the establishment of the biotrophy interface and secretion of Pwl2 effector. To perform the vacuolar trafficking pathway, MoRab7 first recruits the retromer complex to the vacuole membrane, enabling it recognizes a batch of SNARE proteins, including the v-SNARE MoSnc1. Live-cell imaging supports both retromer complex component and MoSnc1 protein labeled vesicles showing the trafficking dynamics toward the interface or plasma membrane, and then fusion with target membranes. Lastly, disruption of the MoRab7/Retromer/MoSnc1-based endolysosomal cascade affects effector secretion and fungal pathogenicity. Taken together, we discovered an unconventional protein and membrane trafficking route starting from the fungal endolysosomes to the M. oryzae-rice interaction interface, and dissect the role of MoRab7/Retromer/MoSnc1 constituent sorting machinery in effector secretion during invasive growth in M. oryzae.

plant biology↗
bioRxiv2022

A novel inovirus reprograms metabolism and motility of marine Alteromonas

Members from the Inoviridae family with striking features are widespread, highly diverse and ecologically pervasive across multiple hosts and environments; however, very small amount of inoviruses have been isolated and studied. Here, a filamentous phage infecting Alteromonas abrolhosensis, designated {phi}AFP1, was isolated from the South China Sea and represented as a novel genus of Inoviridae. {phi}AFP1 consisted of a single-stranded DNA genome (5986 bp), encoding eight putative ORFs. Comparative analyses revealed {phi}AFP1 could be regarded as genetic mosaics, which especially came from Ralstonia and Stenotrophomonas phages. The temporal transcriptome analysis of A. abrolhosensis to {phi}AFP1 infection reveals that 7.78% of the host genes were differentially expressed. The genes involved in translation processes, ribosome pathways and degradation of multiple amino acid pathways at plateau period were upregulated, while host material catabolic and bacterial motility-related genes were downregulated, indicating that {phi}AFP1 might hijack the energy of the host for the synthesis of phage proteins. {phi}AFP1 exerted the step-by-step control on host genes through the appropriate level of the utilizing host resources, affirming a new non-standard regulatory strategy of viral temperately control over the host transcriptional profile. Our study provides novel information for a better understanding of filamentous phage characteristics and phage-host interactions.

microbiology↗