cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.26068078.v1
title: A shared mechanism of multidrug resistance in laboratory-evolved uropathogenic <i>Escherichia coli</i>

description: The emergence of multidrug-resistant bacteria poses a significant threat to human health, necessitating a comprehensive understanding of their underlying mechanisms. Uropathogenic <i>Escherichia coli</i> (UPEC), the primary causative agent of urinary tract infections, is frequently associated with multidrug resistance and recurrent infections. To elucidate the mechanism of resistance of UPEC to beta-lactam antibiotics, we generated ampicillin-resistant UPEC strains through continuous exposure to low and high levels of ampicillin in the laboratory, referred to as Low Amp<sup>R</sup> and High Amp<sup>R</sup>, respectively. Whole-genome sequencing revealed that both Low and High Amp<sup>R</sup> strains contained mutations in the <i>marR</i>, <i>acrR</i>, and <i>envZ</i> genes. The High Amp<sup>R</sup> strain exhibited a single additional mutation in the <i>nlpD</i> gene. Using protein modeling and qRT-PCR analyses, we validated the contributions of each mutation in the identified genes to antibiotic resistance in the Amp<sup>R</sup> strains, including a decrease in membrane permeability, increased expression of multidrug efflux pump, and inhibition of cell lysis. Furthermore, the Amp<sup>R</sup> strain does not decrease the bacterial burden in the mouse bladder even after continuous antibiotic treatment <i>in vivo</i>, implicating the increasing difficulty in treating host infections caused by the Amp<sup>R</sup> strain. Interestingly, ampicillin-induced mutations also result in multidrug resistance in UPEC, suggesting a common mechanism by which bacteria acquire cross-resistance to other classes of antibiotics.
DOI: 10.6084/m9.figshare.26412087
title: Functional characterization of BbEaf6 in <i>Beauveria bassiana</i>: Implications for fungal virulence and stress response

description: The Eaf6 protein, a conserved component of the NuA4 and NuA3 complexes in yeast and MOZ/MORF complexes in humans, plays crucial roles in transcriptional activation, gene regulation, and cell cycle control. Despite its significance in other organisms, the functional role of Eaf6 in entomopathogenic fungi (EPF) remained unexplored. Here, we investigate the function of BbEaf6, the Eaf6 homolog in the entomopathogenic fungus <i>Beauveria bassiana</i>. We demonstrate that BbEaf6 is predominantly localized in nuclei, similar to its counterpart in other fungi. Deletion of <i>BbEaf6</i> resulted in delayed conidiation, reduced conidial yield, and altered conidial properties. Transcriptomic analysis revealed dysregulation of the genes involved in asexual development and cell cycle progression in the Δ<i>BbEaf6</i> mutant. Furthermore, the Δ<i>BbEaf6</i> mutant exhibited decreased tolerance to various stresses, including ionic stress, cell wall perturbation, and DNA damage stress. Notably, the Δ<i>BbEaf6</i> mutant displayed attenuated virulence in insect bioassays, accompanied by dysregulation of genes associated with cuticle penetration and haemocoel infection. Overall, our study elucidates the multifaceted role of BbEaf6 in stress response, development, and virulence in <i>B. bassiana</i>, providing valuable insights into the molecular mechanisms governing fungal pathogenesis and potential targets for pest management strategies.
DOI: 10.6084/m9.figshare.26412087.v2
title: Functional characterization of BbEaf6 in <i>Beauveria bassiana</i>: Implications for fungal virulence and stress response

description: The Eaf6 protein, a conserved component of the NuA4 and NuA3 complexes in yeast and MOZ/MORF complexes in humans, plays crucial roles in transcriptional activation, gene regulation, and cell cycle control. Despite its significance in other organisms, the functional role of Eaf6 in entomopathogenic fungi (EPF) remained unexplored. Here, we investigate the function of BbEaf6, the Eaf6 homolog in the entomopathogenic fungus <i>Beauveria bassiana</i>. We demonstrate that BbEaf6 is predominantly localized in nuclei, similar to its counterpart in other fungi. Deletion of <i>BbEaf6</i> resulted in delayed conidiation, reduced conidial yield, and altered conidial properties. Transcriptomic analysis revealed dysregulation of the genes involved in asexual development and cell cycle progression in the Δ<i>BbEaf6</i> mutant. Furthermore, the Δ<i>BbEaf6</i> mutant exhibited decreased tolerance to various stresses, including ionic stress, cell wall perturbation, and DNA damage stress. Notably, the Δ<i>BbEaf6</i> mutant displayed attenuated virulence in insect bioassays, accompanied by dysregulation of genes associated with cuticle penetration and haemocoel infection. Overall, our study elucidates the multifaceted role of BbEaf6 in stress response, development, and virulence in <i>B. bassiana</i>, providing valuable insights into the molecular mechanisms governing fungal pathogenesis and potential targets for pest management strategies.
DOI: 10.6084/m9.figshare.26954706.v1
title: acetylcysteine promotes doxycycline resistance in the bacterial pathogen <i>edwardsiella tarda</i>

description: Bacterial resistance poses a significant threat to both human and animal health. N-acetylcysteine (NAC), which is used as an anti-inflammatory, has been shown to have distinct and contrasting impacts on bacterial resistance. However, the precise mechanism underlying the relationship between NAC and bacterial resistance remains unclear and requires further investigation. In this study, we study the effect of NAC on bacterial resistance and the underlying mechanisms. Specifically, we examine the effects of NAC on Edwardsiella tarda ATCC15947, a pathogen that exhibits resistance to many antibiotics. We find that NAC can promote resistance of E. tarda to many antibiotics, such as doxycycline, resulting in an increase in the bacterial survival rate. Through proteomic analysis, we demonstrate that NAC activates the amino acid metabolism pathway in E. tarda, leading to elevated intracellular glutathione (GSH) levels and reduced reactive oxygen species (ROS). Additionally, NAC reduces antibiotic influx while enhancing efflux, thus maintaining low intracellular antibiotic concentrations. We also propose that NAC promotes protein aggregation, thus contributing to antibiotic resistance. Our study describes the mechanism underlying E. tarda resistance to doxycycline and cautions against the indiscriminate use of metabolite adjuvants.
DOI: 10.6084/m9.figshare.27266916
title: Synergy of bacteriophage depolymerase with host immunity rescues sepsis mice infected with hypervirulent <i>Klebsiella pneumoniae</i> of capsule type K2

description: The hypervirulent <i>Klebsiella pneumoniae</i> (hvKp) with K1 and K2 capsular types causes liver abscess, pneumonia, sepsis, and invasive infections with high lethality. The presence of capsular polysaccharide (CPS) resists phagocytic engulfment and contributes to excessive inflammatory responses. Bacteriophage depolymerases can specifically target bacterial CPS, neutralizing its defense. Based on our previous research, we expressed and purified a bacteriophage depolymerase (Dep1979) targeting hvKp with capsule type K2. Interestingly, although Dep1979 lacked direct bactericidal activity <i>in vitro</i>, it exhibited potent antibacterial activity <i>in vivo</i>. Low-dose Dep1979 (0.1 mg/kg) improved the 7-day survival of immunocompetent mice to 100%. Even at 0.01 mg/kg, mice achieved 100% survival at 5 days, although efficacy sharply declined at doses as low as 0.001 mg/kg. Following Dep1979 treatment, reduced expression of inflammatory factors and no apparent tissue damage were observed. However, therapeutic efficacy significantly diminished in immunosuppressed mice. These findings underscore the critical role of Dep1979 in disarming CPS, which synergizes with host immunity to enhance antibacterial activity against hvKp.
DOI: 10.6084/m9.figshare.27266916.v1
title: Synergy of bacteriophage depolymerase with host immunity rescues sepsis mice infected with hypervirulent <i>Klebsiella pneumoniae</i> of capsule type K2

description: The hypervirulent <i>Klebsiella pneumoniae</i> (hvKp) with K1 and K2 capsular types causes liver abscess, pneumonia, sepsis, and invasive infections with high lethality. The presence of capsular polysaccharide (CPS) resists phagocytic engulfment and contributes to excessive inflammatory responses. Bacteriophage depolymerases can specifically target bacterial CPS, neutralizing its defense. Based on our previous research, we expressed and purified a bacteriophage depolymerase (Dep1979) targeting hvKp with capsule type K2. Interestingly, although Dep1979 lacked direct bactericidal activity <i>in vitro</i>, it exhibited potent antibacterial activity <i>in vivo</i>. Low-dose Dep1979 (0.1 mg/kg) improved the 7-day survival of immunocompetent mice to 100%. Even at 0.01 mg/kg, mice achieved 100% survival at 5 days, although efficacy sharply declined at doses as low as 0.001 mg/kg. Following Dep1979 treatment, reduced expression of inflammatory factors and no apparent tissue damage were observed. However, therapeutic efficacy significantly diminished in immunosuppressed mice. These findings underscore the critical role of Dep1979 in disarming CPS, which synergizes with host immunity to enhance antibacterial activity against hvKp.
DOI: 10.6084/m9.figshare.25028315
title: UvVelC is important for conidiation and pathogenicity in the rice false smut pathogen <i>Ustilaginoidea virens</i>

description: Rice false smut disease is one of the most significant rice diseases worldwide. <i>Ustilaginoidea virens</i> is the causative agent of this disease. Although several developmental and pathogenic genes have been identified and functionally analyzed, the pathogenic molecular mechanisms of <i>U. virens</i> remain elusive. The velvet family regulatory proteins are involved in fungal development, conidiation, and pathogenicity. In this study, we demonstrated the function of the VelC homolog UvVELC in <i>U. virens</i>. We identified the velvet family protein UvVELC and characterized its functions using a target gene deletion-strategy. Deletion of <i>UvVELC</i> resulted in conidiation failure and pathogenicity. The <i>UvVELC</i> expression levels during infection suggested that this gene might be involved in the early infection process. <i>UvVELC</i> is also important in resistance to abiotic stresses, the utilization efficiency of glucose, stachyose, raffinose, and other sugars, and the expression of transport-related genes. Moreover, UvVELC could physically interact with UvVEA in yeast, and <i>UvVELC</i>/<i>UvVEA</i> double-knockout mutants also failed in conidiation and pathogenicity. These results indicate that <i>UvVELC</i> play a critical role in the conidiation and pathogenicity in <i>U. virens</i>. Functional analysis indicated that UvVELC-mediated conidiation and nutrient acquisition from rice regulates the pathogenicity of <i>U. virens</i>. Understanding the function of the UvVELC homolog could provide a potential molecular target for controlling rice false smut disease.
DOI: 10.6084/m9.figshare.25028315.v1
title: UvVelC is important for conidiation and pathogenicity in the rice false smut pathogen <i>Ustilaginoidea virens</i>

description: Rice false smut disease is one of the most significant rice diseases worldwide. <i>Ustilaginoidea virens</i> is the causative agent of this disease. Although several developmental and pathogenic genes have been identified and functionally analyzed, the pathogenic molecular mechanisms of <i>U. virens</i> remain elusive. The velvet family regulatory proteins are involved in fungal development, conidiation, and pathogenicity. In this study, we demonstrated the function of the VelC homolog UvVELC in <i>U. virens</i>. We identified the velvet family protein UvVELC and characterized its functions using a target gene deletion-strategy. Deletion of <i>UvVELC</i> resulted in conidiation failure and pathogenicity. The <i>UvVELC</i> expression levels during infection suggested that this gene might be involved in the early infection process. <i>UvVELC</i> is also important in resistance to abiotic stresses, the utilization efficiency of glucose, stachyose, raffinose, and other sugars, and the expression of transport-related genes. Moreover, UvVELC could physically interact with UvVEA in yeast, and <i>UvVELC</i>/<i>UvVEA</i> double-knockout mutants also failed in conidiation and pathogenicity. These results indicate that <i>UvVELC</i> play a critical role in the conidiation and pathogenicity in <i>U. virens</i>. Functional analysis indicated that UvVELC-mediated conidiation and nutrient acquisition from rice regulates the pathogenicity of <i>U. virens</i>. Understanding the function of the UvVELC homolog could provide a potential molecular target for controlling rice false smut disease.
DOI: 10.6084/m9.figshare.26412087.v1
title: Functional characterization of BbEaf6, a homolog of Eaf6 in <i>Beauveria bassiana</i>: Implications for fungal virulence and stress response

description: The Eaf6 protein, a conserved component of the NuA4 and NuA3 complexes in yeast and MOZ/MORF complexes in humans, plays crucial roles in transcriptional activation, gene regulation, and cell cycle control. Despite its significance in other organisms, the functional role of Eaf6 in entomopathogenic fungi (EPF) remained unexplored. Here, we investigate the function of BbEaf6, the Eaf6 homolog in the entomopathogenic fungus <i>Beauveria bassiana</i>. We demonstrate that BbEaf6 is predominantly localized in nuclei, similar to its counterpart in other fungi. Deletion of <i>BbEaf6</i> resulted in delayed conidiation, reduced conidial yield, and altered conidial properties. Transcriptomic analysis revealed dysregulation of genes involved in asexual development and cell cycle progression in the Δ<i>BbEaf6</i> mutant. Furthermore, the Δ<i>BbEaf6</i> mutant exhibited decreased tolerance to various stresses, including ionic stress, cell wall perturbation, and DNA damage stress. Notably, the Δ<i>BbEaf6</i> mutant displayed attenuated virulence in insect bioassays, accompanied by dysregulation of genes associated with cuticle penetration and haemocoel infection. Overall, our study elucidates the multifaceted role of BbEaf6 in stress response, development, and virulence in <i>B. bassiana</i>, providing valuable insights into the molecular mechanisms governing fungal pathogenesis and potential targets for pest management strategies.
DOI: 10.6084/m9.figshare.25255185
title: Microbiome analysis reveals the inducing effect of <i>Pseudomonas</i> on prostatic hyperplasia via activating NF-κB signalling

description: Benign prostatic hyperplasia (BPH) is a prevalent disease among middle-aged and elderly males, but its pathogenesis remains unclear. Dysbiosis of the microbiome is increasingly recognized as a significant factor in various human diseases. Prostate tissue also contains a unique microbiome, and its dysbiosis has been proposed to contribute to prostate diseases. Here, we obtained prostate tissues and preoperative catheterized urine from 24 BPH individuals, and 8 normal prostate samples as controls, which followed strict aseptic measures. Using metagenomic next-generation sequencing (mNGS), we found the disparities in the microbiome composition between normal and BPH tissues, with <i>Pseudomonas</i> significantly enriched in BPH tissues, as confirmed by fluorescence in situ hybridization (FISH). Additionally, we showed that the prostate microbiome differed from the urine microbiome. In vitro experiments revealed that lipopolysaccharide (LPS) of <i>Pseudomonas</i> activated NF-κB signalling, leading to inflammation, proliferation, and EMT processes, while inhibiting apoptosis in prostatic cells. Overall, our research determines the presence of microbiome dysbiosis in BPH, and suggests that <i>Pseudomonas</i>, as the dominant microflora, may promote the progression of BPH through LPS activation of NF-κB signalling.
DOI: 10.6084/m9.figshare.25255185.v1
title: Microbiome analysis reveals the inducing effect of <i>Pseudomonas</i> on prostatic hyperplasia via activating NF-κB signalling

description: Benign prostatic hyperplasia (BPH) is a prevalent disease among middle-aged and elderly males, but its pathogenesis remains unclear. Dysbiosis of the microbiome is increasingly recognized as a significant factor in various human diseases. Prostate tissue also contains a unique microbiome, and its dysbiosis has been proposed to contribute to prostate diseases. Here, we obtained prostate tissues and preoperative catheterized urine from 24 BPH individuals, and 8 normal prostate samples as controls, which followed strict aseptic measures. Using metagenomic next-generation sequencing (mNGS), we found the disparities in the microbiome composition between normal and BPH tissues, with <i>Pseudomonas</i> significantly enriched in BPH tissues, as confirmed by fluorescence in situ hybridization (FISH). Additionally, we showed that the prostate microbiome differed from the urine microbiome. In vitro experiments revealed that lipopolysaccharide (LPS) of <i>Pseudomonas</i> activated NF-κB signalling, leading to inflammation, proliferation, and EMT processes, while inhibiting apoptosis in prostatic cells. Overall, our research determines the presence of microbiome dysbiosis in BPH, and suggests that <i>Pseudomonas</i>, as the dominant microflora, may promote the progression of BPH through LPS activation of NF-κB signalling.
DOI: 10.6084/m9.figshare.25913139
title: The <i>Salmonella</i> virulence protein PagN contributes to the advent of a hyper-replicating cytosolic bacterial population

description: <i>Salmonella enterica</i> subspecies <i>enterica</i> serovar Typhimurium is an intracellular pathogen that invades and colonizes the intestinal epithelium. Following bacterial invasion, <i>Salmonella</i> is enclosed within a membrane-bound vacuole known as a <i>Salmonella</i>-containing vacuole (SCV). However, a subset of <i>Salmonella</i> has the capability to prematurely rupture the SCV and escape, resulting in <i>Salmonella</i> hyper-replication within the cytosol of epithelial cells. A recently published RNA-seq study provides an overview of cytosolic and vacuolar upregulated genes and highlights <i>pagN</i> vacuolar upregulation. Here, using transcription kinetics, protein production profile, and immunofluorescence microscopy, we showed that PagN is exclusively produced by <i>Salmonella</i> in SCV. Gentamicin protection and chloroquine resistance assays were performed to demonstrate that deletion of <i>pagN</i> affects <i>Salmonella</i> replication by affecting the cytosolic bacterial population. This study presents the first example of a <i>Salmonella</i> virulence factor expressed within the endocytic compartment, which has a significant impact on the dynamics of <i>Salmonella</i> cytosolic hyper-replication.
DOI: 10.6084/m9.figshare.25913139.v1
title: The <i>Salmonella</i> virulence protein PagN contributes to the advent of a hyper-replicating cytosolic bacterial population

description: <i>Salmonella enterica</i> subspecies <i>enterica</i> serovar Typhimurium is an intracellular pathogen that invades and colonizes the intestinal epithelium. Following bacterial invasion, <i>Salmonella</i> is enclosed within a membrane-bound vacuole known as a <i>Salmonella</i>-containing vacuole (SCV). However, a subset of <i>Salmonella</i> has the capability to prematurely rupture the SCV and escape, resulting in <i>Salmonella</i> hyper-replication within the cytosol of epithelial cells. A recently published RNA-seq study provides an overview of cytosolic and vacuolar upregulated genes and highlights <i>pagN</i> vacuolar upregulation. Here, using transcription kinetics, protein production profile, and immunofluorescence microscopy, we showed that PagN is exclusively produced by <i>Salmonella</i> in SCV. Gentamicin protection and chloroquine resistance assays were performed to demonstrate that deletion of <i>pagN</i> affects <i>Salmonella</i> replication by affecting the cytosolic bacterial population. This study presents the first example of a <i>Salmonella</i> virulence factor expressed within the endocytic compartment, which has a significant impact on the dynamics of <i>Salmonella</i> cytosolic hyper-replication.
DOI: 10.6084/m9.figshare.27737420
title: <i>Chlamydia psittaci</i>: A zoonotic pathogen causing avian chlamydiosis and psittacosis

description: <i>Chlamydia psittaci</i> is an obligate intracellular gram-negative bacterium with a unique biphasic developmental cycle. It is a zoonotic pathogen with a wide range of hosts and can cause avian chlamydiosis in birds and psittacosis in humans. The pathogen is transmitted mainly through horizontal transmission between birds. Cross-species transmission sometimes occurs and human-to-human transmission has recently been confirmed. This review provides an updated overview of <i>C. psittaci</i> from the perspective of both avian chlamydiosis and psittacosis. We include the aspects of genotype, host–pathogen interaction, transmission, epidemiology, detection and diagnosis, clinical manifestation, management, and prevention, aiming to provide a basic understanding of <i>C. psittaci</i> and offer fresh insights focused on zoonosis and cross-species transmission.
DOI: 10.6084/m9.figshare.27737420.v1
title: <i>Chlamydia psittaci</i>: A zoonotic pathogen causing avian chlamydiosis and psittacosis

description: <i>Chlamydia psittaci</i> is an obligate intracellular gram-negative bacterium with a unique biphasic developmental cycle. It is a zoonotic pathogen with a wide range of hosts and can cause avian chlamydiosis in birds and psittacosis in humans. The pathogen is transmitted mainly through horizontal transmission between birds. Cross-species transmission sometimes occurs and human-to-human transmission has recently been confirmed. This review provides an updated overview of <i>C. psittaci</i> from the perspective of both avian chlamydiosis and psittacosis. We include the aspects of genotype, host–pathogen interaction, transmission, epidemiology, detection and diagnosis, clinical manifestation, management, and prevention, aiming to provide a basic understanding of <i>C. psittaci</i> and offer fresh insights focused on zoonosis and cross-species transmission.
DOI: 10.6084/m9.figshare.25040369
title: RNA-Seq and miRNA-Seq data from Epstein-Barr virus-infected tree shrews reveal a ceRNA network contributing to immune microenvironment regulation

description: Epstein-Barr virus (EBV) infection in humans is ubiquitous and associated with various diseases. Remodeling of the immune microenvironment is the primary cause of EBV infection and pathogenesis; however, the underlying mechanism has not been fully elucidated. In this study, we used whole-transcriptome RNA-Seq to detect mRNAs, long non-coding RNAs (lncRNA), and microRNA (miRNA) profiles in the control group, 3 days, and 28 days after EBV infection, based on the tree shrew model that we reported previously. First, we estimated the proportion of 22 cell types in each sample using CIBERSORT software and identified 18 high-confidence DElncRNAs related to immune microenvironment regulation after EBV infection. Functional enrichment analysis of these differentially expressed lncRNAs primarily focused on the autophagy, endocytosis, and ferroptosis signalling pathways. Moreover, EBV infection affects miRNA expression patterns, and many miRNAs are silenced. Finally, three competing endogenous RNA regulatory networks were built using lncRNAs that significantly correlated with immune cell types, miRNAs that responded to EBV infection, and potentially targeted the mRNA of the miRNAs. Among them, MRPL42-AS-5 might act as an hsa-miR-296-5p “sponge” and compete with target mRNAs, thus increasing mRNA expression level, which could induce immune cell infiltration through the cellular senescence signalling pathway against EBV infection. Overall, we conducted a complete transcriptomic analysis of EBV infection in vivo for the first time and provided a novel perspective for further investigation of EBV-host interactions.