cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.21600484.v2
title: Spleen-based proteogenomics reveals that <i>Escherichia coli</i> infection induces activation of phagosome maturation pathway in chicken

description: Avian pathogenic <i>Escherichia coli</i> (APEC) leads to economic losses in poultry industry and is also a threat to human health. Various strategies were used for searching virulence factors, while little is known about the mechanism by which APEC survives in host or is eliminated by host. Thus, chicken colibacillosis model was constructed by intraperitoneally injecting <i>E. coli</i> O78 in this study, then the protein dynamic expression of spleen was characterized at different post-infection times by quantitative proteome. Comparative analysis showed that <i>E. coli</i> induced significant dysregulation at 72 h post infection in spleen tissue. Transcriptomic method was further used to assess the changes of dysregulated proteins at 72 h post infection at the mRNA level. Total 278 protein groups (5.7%) and 2,443 genes (24.4%) were dysregulated, respectively. The upregulated proteins and genes were consistently enriched in phagosome and lysosome pathways, indicating <i>E. coli</i> infection activates phagosome maturation pathway. The matured phagolysosome might kill the invasive <i>E. coli</i>. This study illuminated the genetic dysregulation in chicken spleen at the protein and mRNA levels after <i>E. coli</i> infecting and identified candidate genes for host response to APEC infection.
DOI: 10.6084/m9.figshare.21600484.v1
title: Spleen-based proteogenomics reveals that <i>Escherichia coli</i> infection induces activation of phagosome maturation pathway in chicken

description: Avian pathogenic <i>Escherichia coli</i> (APEC) leads to economic losses in poultry industry and is also a threat to human health. Various strategies were used for searching virulence factors, while little is known about the mechanism by which APEC survives in host or is eliminated by host. Thus, chicken colibacillosis model was constructed by intraperitoneally injecting <i>E. coli</i> O78 in this study, then the protein dynamic expression of spleen was characterized at different post-infection times by quantitative proteome. Comparative analysis showed that <i>E. coli</i> induced significant dysregulation at 72 h post infection in spleen tissue. Transcriptomic method was further used to assess the changes of dysregulated proteins at 72 h post infection at the mRNA level. Total 278 protein groups (5.7%) and 2,443 genes (24.4%) were dysregulated, respectively. The upregulated proteins and genes were consistently enriched in phagosome and lysosome pathways, indicating <i>E. coli</i> infection activates phagosome maturation pathway. The matured phagolysosome might kill the invasive <i>E. coli</i>. This study illuminated the genetic dysregulation in chicken spleen at the protein and mRNA levels after <i>E. coli</i> infecting and identified candidate genes for host response to APEC infection.
DOI: 10.6084/m9.figshare.23616677
title: Identification of miRnas with possible prognostic roles for HAM/TSP

description: Human T-cell lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropic spastic paraparesis (HAM/TSP) is an insidiously progressive spinal cord disease for which there is no effective treatment. There is great interest in developing potential biomarkers to predict the pathogenesis of HAM/TSP disease. In this study, Illumina Massive Parallel Sequencing (MPS) technology was used to investigate the cellular global noncoding RNAome expression profile in HAM/TSP patients (<i>n</i> = 10), asymptomatic HTLV-1-infected carriers (ASP, <i>n</i> = 8), and a second group of healthy controls (<i>n</i> = 5). Various bioinformatics tools were used to align, annotate, and profile the sRNA-MPS reads. Among the 402 sRNAs detected, 251 were known and 50 were potentially novel sRNAs in the HAM and ASP groups compared with the HC group. Sixty-eight known sRNAs were significantly different between the ASP and HAM groups. Eighty-eight mature miRNAs were downregulated in subjects from HAM compared with ASP. Three of these miRs (hsa-miR-185-5p, 32-5p, and 192-5p) have the potential to be used as biomarkers for predicting the pathogenesis of HAM/TSP. The seven most deregulated miRs target genes have been associated with a variety of biological processes and molecular functions. The reactome pathways relevant to our findings provide a rich source of data and offer the opportunity to better understand sRNA regulation and function in HTLV-1 pathophysiology. To the best of our knowledge, this study is the first to demonstrate evaluates sRNAs in HTLV-1 patients with HAM/TSP.
DOI: 10.6084/m9.figshare.23616677.v1
title: Identification of miRnas with possible prognostic roles for HAM/TSP

description: Human T-cell lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropic spastic paraparesis (HAM/TSP) is an insidiously progressive spinal cord disease for which there is no effective treatment. There is great interest in developing potential biomarkers to predict the pathogenesis of HAM/TSP disease. In this study, Illumina Massive Parallel Sequencing (MPS) technology was used to investigate the cellular global noncoding RNAome expression profile in HAM/TSP patients (<i>n</i> = 10), asymptomatic HTLV-1-infected carriers (ASP, <i>n</i> = 8), and a second group of healthy controls (<i>n</i> = 5). Various bioinformatics tools were used to align, annotate, and profile the sRNA-MPS reads. Among the 402 sRNAs detected, 251 were known and 50 were potentially novel sRNAs in the HAM and ASP groups compared with the HC group. Sixty-eight known sRNAs were significantly different between the ASP and HAM groups. Eighty-eight mature miRNAs were downregulated in subjects from HAM compared with ASP. Three of these miRs (hsa-miR-185-5p, 32-5p, and 192-5p) have the potential to be used as biomarkers for predicting the pathogenesis of HAM/TSP. The seven most deregulated miRs target genes have been associated with a variety of biological processes and molecular functions. The reactome pathways relevant to our findings provide a rich source of data and offer the opportunity to better understand sRNA regulation and function in HTLV-1 pathophysiology. To the best of our knowledge, this study is the first to demonstrate evaluates sRNAs in HTLV-1 patients with HAM/TSP.
DOI: 10.6084/m9.figshare.21755892
title: Genome-wide identification of genes critical for <i>in vivo</i> fitness of multi-drug resistant porcine extraintestinal pathogenic <i>Escherichia coli</i> by transposon-directed insertion site sequencing using a mouse infection model

description: Extraintestinal pathogenic <i>Escherichia coli</i> (ExPEC) is an important zoonotic pathogen. Recently, ExPEC has been reported to be an emerging problem in pig farming. However, the mechanism of pathogenicity of porcine ExPEC remains to be revealed. In this study, we constructed a transposon (Tn) mutagenesis library covering Tn insertion in over 72% of the chromosome-encoded genes of a virulent and multi-drug resistant porcine ExPEC strain PCN033. By using a mouse infection model, a transposon-directed insertion site sequencing (TraDIS) assay was performed to identify <i>in vivo</i> fitness factors. By comparing the Tn insertion frequencies between the input Tn library and the recovered library from different organs, 64 genes were identified to be involved in fitness during systemic infection. 15 genes were selected and individual gene deletion mutants were constructed. The <i>in vivo</i> fitness was evaluated by using a competitive infection assay. Among them, Δ<i>fimG</i> was significantly outcompeted by the WT strain <i>in vivo</i> and showed defective adhesion to host cells. <i>rfa</i> which was involved in lipopolysaccharide biosynthesis was shown to be critical for <i>in vivo</i> fitness which may have resulted from its role in the resistance to serum killing. In addition, several metabolic genes including <i>fepB</i>, <i>sdhC</i>, <i>fepG</i>, <i>gltS</i>, <i>dcuA</i>, <i>ccmH</i>, <i>ddpD</i>, <i>narU</i>, <i>glpD</i>, <i>malM</i>, and <i>yabL</i> and two regulatory genes <i>metJ</i> and <i>baeS</i> were shown as important determinants of <i>in vivo</i> fitness of porcine ExPEC. Collectively, this study performed a genome-wide screening for <i>in vivo</i> fitness factors which will be important for understanding the pathogenicity of porcine ExPEC.
DOI: 10.6084/m9.figshare.21755892.v1
title: Genome-wide identification of genes critical for <i>in vivo</i> fitness of multi-drug resistant porcine extraintestinal pathogenic <i>Escherichia coli</i> by transposon-directed insertion site sequencing using a mouse infection model

description: Extraintestinal pathogenic <i>Escherichia coli</i> (ExPEC) is an important zoonotic pathogen. Recently, ExPEC has been reported to be an emerging problem in pig farming. However, the mechanism of pathogenicity of porcine ExPEC remains to be revealed. In this study, we constructed a transposon (Tn) mutagenesis library covering Tn insertion in over 72% of the chromosome-encoded genes of a virulent and multi-drug resistant porcine ExPEC strain PCN033. By using a mouse infection model, a transposon-directed insertion site sequencing (TraDIS) assay was performed to identify <i>in vivo</i> fitness factors. By comparing the Tn insertion frequencies between the input Tn library and the recovered library from different organs, 64 genes were identified to be involved in fitness during systemic infection. 15 genes were selected and individual gene deletion mutants were constructed. The <i>in vivo</i> fitness was evaluated by using a competitive infection assay. Among them, Δ<i>fimG</i> was significantly outcompeted by the WT strain <i>in vivo</i> and showed defective adhesion to host cells. <i>rfa</i> which was involved in lipopolysaccharide biosynthesis was shown to be critical for <i>in vivo</i> fitness which may have resulted from its role in the resistance to serum killing. In addition, several metabolic genes including <i>fepB</i>, <i>sdhC</i>, <i>fepG</i>, <i>gltS</i>, <i>dcuA</i>, <i>ccmH</i>, <i>ddpD</i>, <i>narU</i>, <i>glpD</i>, <i>malM</i>, and <i>yabL</i> and two regulatory genes <i>metJ</i> and <i>baeS</i> were shown as important determinants of <i>in vivo</i> fitness of porcine ExPEC. Collectively, this study performed a genome-wide screening for <i>in vivo</i> fitness factors which will be important for understanding the pathogenicity of porcine ExPEC.
DOI: 10.6084/m9.figshare.21818969
title: Epithelial cell invasion by <i>salmonella</i> typhimurium induces modulation of genes controlled by aryl hydrocarbon receptor signaling and involved in extracellular matrix biogenesis

description: <i>Salmonella</i> is the only bacterium able to enter a host cell by the two known mechanisms: trigger and zipper. The trigger mechanism relies on the injection of bacterial effectors into the host cell through the <i>Salmonella</i> type III secretion system 1. In the zipper mechanism, mediated by the invasins Rck and PagN, the bacterium takes advantage of a cellular receptor for invasion. This study describes the transcriptomic reprogramming of the IEC-6 intestinal epithelial cell line to <i>Salmonella</i> Typhimurium strains that invaded cells by a trigger, a zipper, or both mechanisms. Using <i>S</i>. Typhimurium strains invalidated for one or other entry mechanism, we have shown that IEC-6 cells could support both entries. Comparison of the gene expression profiles of exposed cells showed that irrespective of the mechanism used for entry, the transcriptomic reprogramming of the cell was nearly the same. On the other hand, when gene expression was compared between cells unexposed or exposed to the bacterium, the transcriptomic reprogramming of exposed cells was significantly different. It is particularly interesting to note the modulation of expression of numerous target genes of the aryl hydrocarbon receptor showing that this transcription factor was activated by <i>S</i>. Typhimurium infection. Numerous genes associated with the extracellular matrix were also modified. This was confirmed at the protein level by western-blotting showing a dramatic modification in some extracellular matrix proteins. Analysis of a selected set of modulated genes showed that the expression of the majority of these genes was modulated during the intracellular life of <i>S</i>. Typhimurium.
DOI: 10.6084/m9.figshare.21818969.v1
title: Epithelial cell invasion by <i>salmonella</i> typhimurium induces modulation of genes controlled by aryl hydrocarbon receptor signaling and involved in extracellular matrix biogenesis

description: <i>Salmonella</i> is the only bacterium able to enter a host cell by the two known mechanisms: trigger and zipper. The trigger mechanism relies on the injection of bacterial effectors into the host cell through the <i>Salmonella</i> type III secretion system 1. In the zipper mechanism, mediated by the invasins Rck and PagN, the bacterium takes advantage of a cellular receptor for invasion. This study describes the transcriptomic reprogramming of the IEC-6 intestinal epithelial cell line to <i>Salmonella</i> Typhimurium strains that invaded cells by a trigger, a zipper, or both mechanisms. Using <i>S</i>. Typhimurium strains invalidated for one or other entry mechanism, we have shown that IEC-6 cells could support both entries. Comparison of the gene expression profiles of exposed cells showed that irrespective of the mechanism used for entry, the transcriptomic reprogramming of the cell was nearly the same. On the other hand, when gene expression was compared between cells unexposed or exposed to the bacterium, the transcriptomic reprogramming of exposed cells was significantly different. It is particularly interesting to note the modulation of expression of numerous target genes of the aryl hydrocarbon receptor showing that this transcription factor was activated by <i>S</i>. Typhimurium infection. Numerous genes associated with the extracellular matrix were also modified. This was confirmed at the protein level by western-blotting showing a dramatic modification in some extracellular matrix proteins. Analysis of a selected set of modulated genes showed that the expression of the majority of these genes was modulated during the intracellular life of <i>S</i>. Typhimurium.
DOI: 10.6084/m9.figshare.23688668
title: Sucrose non-fermenting protein kinase gene <i>UvSnf1</i> is required for virulence in <i>Ustilaginoidea virens</i>

description: Rice false smut caused by <i>Ustilaginoidea virens</i> is becoming one of the most devastating diseases in rice production areas in the world. Revealing <i>U. virens</i> potential pathogenic mechanisms provides ideas for formulating more effective prevention and control strategies. Sucrose non-fermenting 1 (Snf1) protein kinase plays a critical role in activating transcription and suppressing gene expression, as well as in cellular response to various stresses, such as nutrient limitation. In our study, we identified the Snf1 homolog UvSnf1 and analyzed its biological functions in <i>U. virens</i>. The expression level of <i>UvSnf1</i> was dramatically up-regulated during invasion, indicating that <i>UvSnf1</i> may participate in infection. Phenotypic analyses of <i>UvSnf1</i> deletion mutants revealed that <i>UvSnf1</i> is necessary for hyphae growth, spore production, and virulence in <i>U. virens</i>. Moreover, UvSnf1 promotes <i>U. virens</i> to use unfavorable carbon sources when the sucrose is insufficient. In addition, deletion of <i>UvSnf1</i> down-regulates the expression of the <i>cell wall-degrading enzymes</i> (<i>CWDE</i>s) genes under sucrose limitation conditions in <i>U. virens</i>. Further analyses showed that <i>CWDEs</i> (<i>UvCut1</i> and <i>UvXyp1</i>) are not only involved in growth, spore production, and virulence but are also required for the utilization of carbon sources. In conclusion, this study demonstrates that UvSnf1 plays vital roles in virulence and carbon source utilization in <i>U. virens</i>, and one of the possible mechanisms is playing a role in regulating the expression of <i>CWDE</i> genes.
DOI: 10.6084/m9.figshare.23660547
title: Overexpression of chitinase <i>PbChia1</i> from <i>Plasmodiophora brassicae</i> improves broad-spectrum disease resistance of Arabidopsis

description: Chitinase plays an important role in plant resistance against chitin-containing pathogens through hydrolysis of chitin. Clubroot caused by <i>Plasmodiophora brassicae</i> is a major disease for cruciferous crops and vegetables worldwide. The cell wall of <i>P. brassicae</i> resting spores contains chitin. Chitinase is regarded as capable of improving plant resistance to fungal diseases. However, there has been no report about the function of chitinase in <i>P. brassicae</i>. Here, wheat germ agglutinin staining and commercial chitinase treatment demonstrated that chitin is a functional component in <i>P. brassicae</i>. In addition, Chitinase PbChia1 was identified by chitin pull-down assay combined with LC-MS/MS. PbChia1 was found to be a typical secreted chitinase, which could bind chitin with chitinase activity <i>in vitro</i>. PbChia1 could significantly decrease the resting spores of <i>P. brassicae</i> and therefore relieve the severity of clubroot symptom, with a biocontrol effect of 61.29%. Overexpression of <i>PbChia1</i> in <i>Arabidopsis thaliana</i> improved its resistance to <i>P. brassicae</i>, increased host survival rate and seed yield, enhanced PAMPs-triggered reactive oxygen species burst, MAPK activation and expression of immune-related genes. <i>PbChia1</i> transgenic plants also showed resistance to other pathogens, such as biotrophic bacterium <i>Pst</i> DC3000, necrotrophic fungi <i>Sclerotinia sclerotiorum</i> and <i>Rhizoctonia solani</i>. These findings indicate that chitinase <i>PbChia1</i> is a candidate gene that can confer broad-spectrum disease resistance in breeding.
DOI: 10.6084/m9.figshare.23660547.v1
title: Overexpression of chitinase <i>PbChia1</i> from <i>Plasmodiophora brassicae</i> improves broad-spectrum disease resistance of Arabidopsis

description: Chitinase plays an important role in plant resistance against chitin-containing pathogens through hydrolysis of chitin. Clubroot caused by <i>Plasmodiophora brassicae</i> is a major disease for cruciferous crops and vegetables worldwide. The cell wall of <i>P. brassicae</i> resting spores contains chitin. Chitinase is regarded as capable of improving plant resistance to fungal diseases. However, there has been no report about the function of chitinase in <i>P. brassicae</i>. Here, wheat germ agglutinin staining and commercial chitinase treatment demonstrated that chitin is a functional component in <i>P. brassicae</i>. In addition, Chitinase PbChia1 was identified by chitin pull-down assay combined with LC-MS/MS. PbChia1 was found to be a typical secreted chitinase, which could bind chitin with chitinase activity <i>in vitro</i>. PbChia1 could significantly decrease the resting spores of <i>P. brassicae</i> and therefore relieve the severity of clubroot symptom, with a biocontrol effect of 61.29%. Overexpression of <i>PbChia1</i> in <i>Arabidopsis thaliana</i> improved its resistance to <i>P. brassicae</i>, increased host survival rate and seed yield, enhanced PAMPs-triggered reactive oxygen species burst, MAPK activation and expression of immune-related genes. <i>PbChia1</i> transgenic plants also showed resistance to other pathogens, such as biotrophic bacterium <i>Pst</i> DC3000, necrotrophic fungi <i>Sclerotinia sclerotiorum</i> and <i>Rhizoctonia solani</i>. These findings indicate that chitinase <i>PbChia1</i> is a candidate gene that can confer broad-spectrum disease resistance in breeding.
DOI: 10.6084/m9.figshare.23688668.v1
title: Sucrose non-fermenting protein kinase gene <i>UvSnf1</i> is required for virulence in <i>Ustilaginoidea virens</i>

description: Rice false smut caused by <i>Ustilaginoidea virens</i> is becoming one of the most devastating diseases in rice production areas in the world. Revealing <i>U. virens</i> potential pathogenic mechanisms provides ideas for formulating more effective prevention and control strategies. Sucrose non-fermenting 1 (Snf1) protein kinase plays a critical role in activating transcription and suppressing gene expression, as well as in cellular response to various stresses, such as nutrient limitation. In our study, we identified the Snf1 homolog UvSnf1 and analyzed its biological functions in <i>U. virens</i>. The expression level of <i>UvSnf1</i> was dramatically up-regulated during invasion, indicating that <i>UvSnf1</i> may participate in infection. Phenotypic analyses of <i>UvSnf1</i> deletion mutants revealed that <i>UvSnf1</i> is necessary for hyphae growth, spore production, and virulence in <i>U. virens</i>. Moreover, UvSnf1 promotes <i>U. virens</i> to use unfavorable carbon sources when the sucrose is insufficient. In addition, deletion of <i>UvSnf1</i> down-regulates the expression of the <i>cell wall-degrading enzymes</i> (<i>CWDE</i>s) genes under sucrose limitation conditions in <i>U. virens</i>. Further analyses showed that <i>CWDEs</i> (<i>UvCut1</i> and <i>UvXyp1</i>) are not only involved in growth, spore production, and virulence but are also required for the utilization of carbon sources. In conclusion, this study demonstrates that UvSnf1 plays vital roles in virulence and carbon source utilization in <i>U. virens</i>, and one of the possible mechanisms is playing a role in regulating the expression of <i>CWDE</i> genes.
DOI: 10.6084/m9.figshare.24329709
title: Uncovering the hidden threat: The widespread presence of chromosome-borne accessory genetic elements and novel antibiotic resistance genetic environments in <i>Aeromonas</i>

description: The emergence of antibiotic-resistant <i>Aeromonas</i> strains in clinical settings has presented an escalating burden on human and public health. The dissemination of antibiotic resistance in <i>Aeromonas</i> is predominantly facilitated by chromosome-borne accessory genetic elements, although the existing literature on this subject remains limited. Hence, the primary objective of this study is to comprehensively investigate the genomic characteristics of chromosome-borne accessory genetic elements in <i>Aeromonas</i>. Moreover, the study aims to uncover novel genetic environments associated with antibiotic resistance on these elements. <i>Aeromonas</i> were screened from nonduplicated strains collected from two tertiary hospitals in China. Complete sequencing and population genetics analysis were performed. BLAST analysis was employed to identify related elements. All newly identified elements were subjected to detailed sequence annotation, dissection, and comparison. We identified and newly designated 19 chromosomal elements, including 18 integrative and mobilizable elements (IMEs) that could be classified into four categories: Tn<i>6737</i>-related, Tn<i>6836</i>-related, Tn<i>6840</i>-related, and Tn<i>6844a</i>-related IMEs. Each class exhibited a distinct pattern in the types of resistance genes carried by the IMEs. Several novel antibiotic resistance genetic environments were uncovered in these elements. Notably, we report the first identification of the <i>bla</i><sub>OXA-10</sub> gene and <i>bla</i><sub>VEB-1</sub> gene in clinical <i>A. veronii</i> genome, the first presence of a <i>tetA</i>(E)–<i>tetR</i>(E) resistance gene environment within the backbone region in IMEs, and a new <i>mcr-3.15</i> resistance gene environment. The implications of these findings are substantial, as they provide new insights into the evolution, structure, and dissemination of chromosomal-borne accessory elements.