cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.12852033.v1
title: New insights into the evolution of host specificity of three <i>Penicillium</i> species and the pathogenicity of <i>P. Italicum</i> involving the infection of Valencia orange (<i>Citrus sinensis</i>)

description: Blue and green molds, the common phenotypes of post-harvest diseases in fruits, are mainly caused by<i> Penicillium </i>fungal species, including<i> P. italicum, P. digitatum,</i> and <i>P. expansum</i>. We sequenced and assembled the genome of a <i>P. italicum </i>strain, which contains 31,034,623 bp with 361 scaffolds and 627 contigs. The mechanisms underlying the evolution of host specificity among the analyzed <i>Penicillium </i>species were associated with the expansion of protein families, genome restructuring, horizontal gene transfer, and positive selection pressure. A dual-transcriptome analysis following the infection of Valencia orange <i>(Citrus sinensis)</i> by <i>P. italicum </i>resulted in the annotation of 9,307 <i>P. italicum</i> genes and 24,591 Valencia orange genes. The pathogenicity of<i> P. italicum </i>may be due to the activation of effectors, including 51 small secreted cysteine-rich proteins, 110 carbohydrate-active enzymes, and 12 G protein-coupled receptors. Additionally, 211 metabolites related to the interactions between<i> P. italicum </i>and Valencia orange were identified by gas chromatography-time of flight mass spectrography, three of which were further confirmed by ultra-high performance liquid chromatography triple quadrupole mass spectrometry. A metabolomics analysis indicated that <i>P. italicum </i>pathogenicity is associated with the sphingolipid and salicylic acid signaling pathways. Moreover, a correlation analysis between the metabolite contents and gene expression levels suggested that<i> P. italicum </i>induces carbohydrate metabolism in Valencia orange fruits as part of its infection strategy. This study provides useful information regarding the genomic determinants that drive the evolution of host specificity in<i> Penicillium </i>species and clarifies the host-plant specificity during the infection of Valencia orange by <i>P. italicum</i>. P. italicum GL_Gan1, a local strain in Guangzhou, China, was sequenced. Comparison of the genome of <i>P. italicum</i> GL_Gan1 with other pathogenic <i>Penicillium</i> species, <i>P. digitatum</i> and <i>P. expansum</i>, revealed that the expansion of protein families, genome restructuring, HGT, and positive selection pressure were related to the host range expansion of the analyzed <i>Penicillium</i> species. Moreover, gene gains or losses might be associated with the speciation of these <i>Penicillium</i> species. In addition, the molecular basis of host-plant specificity during the infection of Valencia orange (<i>Citrus sinensis</i>) by <i>P. italicum</i> was also elucidated by transcriptomic and metabolomics analysis. The data presented herein may be useful for further elucidating the molecular basis of the evolution of host specificity of <i>Penicillium</i> species and for illustrating the host-plant specificity during the infection of Valencia orange by <i>P. italicum</i>.
DOI: 10.6084/m9.figshare.12852033.v3
title: New insights into the evolution of host specificity of three <i>Penicillium</i> species and the pathogenicity of <i>P. Italicum</i> involving the infection of Valencia orange (<i>Citrus sinensis</i>)

description: Blue and green molds, the common phenotypes of post-harvest diseases in fruits, are mainly caused by<i> Penicillium </i>fungal species, including<i> P. italicum, P. digitatum,</i> and <i>P. expansum</i>. We sequenced and assembled the genome of a <i>P. italicum </i>strain, which contains 31,034,623 bp with 361 scaffolds and 627 contigs. The mechanisms underlying the evolution of host specificity among the analyzed <i>Penicillium </i>species were associated with the expansion of protein families, genome restructuring, horizontal gene transfer, and positive selection pressure. A dual-transcriptome analysis following the infection of Valencia orange <i>(Citrus sinensis)</i> by <i>P. italicum </i>resulted in the annotation of 9,307 <i>P. italicum</i> genes and 24,591 Valencia orange genes. The pathogenicity of<i> P. italicum </i>may be due to the activation of effectors, including 51 small secreted cysteine-rich proteins, 110 carbohydrate-active enzymes, and 12 G protein-coupled receptors. Additionally, 211 metabolites related to the interactions between<i> P. italicum </i>and Valencia orange were identified by gas chromatography-time of flight mass spectrography, three of which were further confirmed by ultra-high performance liquid chromatography triple quadrupole mass spectrometry. A metabolomics analysis indicated that <i>P. italicum </i>pathogenicity is associated with the sphingolipid and salicylic acid signaling pathways. Moreover, a correlation analysis between the metabolite contents and gene expression levels suggested that<i> P. italicum </i>induces carbohydrate metabolism in Valencia orange fruits as part of its infection strategy. This study provides useful information regarding the genomic determinants that drive the evolution of host specificity in<i> Penicillium </i>species and clarifies the host-plant specificity during the infection of Valencia orange by <i>P. italicum</i>. P. italicum GL_Gan1, a local strain in Guangzhou, China, was sequenced. Comparison of the genome of <i>P. italicum</i> GL_Gan1 with other pathogenic <i>Penicillium</i> species, <i>P. digitatum</i> and <i>P. expansum</i>, revealed that the expansion of protein families, genome restructuring, HGT, and positive selection pressure were related to the host range expansion of the analyzed <i>Penicillium</i> species. Moreover, gene gains or losses might be associated with the speciation of these <i>Penicillium</i> species. In addition, the molecular basis of host-plant specificity during the infection of Valencia orange (<i>Citrus sinensis</i>) by <i>P. italicum</i> was also elucidated by transcriptomic and metabolomics analysis. The data presented herein may be useful for further elucidating the molecular basis of the evolution of host specificity of <i>Penicillium</i> species and for illustrating the host-plant specificity during the infection of Valencia orange by <i>P. italicum</i>.
DOI: 10.6084/m9.figshare.12852033.v2
title: New insights into the evolution of host specificity of three <i>Penicillium</i> species and the pathogenicity of <i>P. Italicum</i> involving the infection of Valencia orange (<i>Citrus sinensis</i>)

description: Blue and green molds, the common phenotypes of post-harvest diseases in fruits, are mainly caused by<i> Penicillium </i>fungal species, including<i> P. italicum, P. digitatum,</i> and <i>P. expansum</i>. We sequenced and assembled the genome of a <i>P. italicum </i>strain, which contains 31,034,623 bp with 361 scaffolds and 627 contigs. The mechanisms underlying the evolution of host specificity among the analyzed <i>Penicillium </i>species were associated with the expansion of protein families, genome restructuring, horizontal gene transfer, and positive selection pressure. A dual-transcriptome analysis following the infection of Valencia orange <i>(Citrus sinensis)</i> by <i>P. italicum </i>resulted in the annotation of 9,307 <i>P. italicum</i> genes and 24,591 Valencia orange genes. The pathogenicity of<i> P. italicum </i>may be due to the activation of effectors, including 51 small secreted cysteine-rich proteins, 110 carbohydrate-active enzymes, and 12 G protein-coupled receptors. Additionally, 211 metabolites related to the interactions between<i> P. italicum </i>and Valencia orange were identified by gas chromatography-time of flight mass spectrography, three of which were further confirmed by ultra-high performance liquid chromatography triple quadrupole mass spectrometry. A metabolomics analysis indicated that <i>P. italicum </i>pathogenicity is associated with the sphingolipid and salicylic acid signaling pathways. Moreover, a correlation analysis between the metabolite contents and gene expression levels suggested that<i> P. italicum </i>induces carbohydrate metabolism in Valencia orange fruits as part of its infection strategy. This study provides useful information regarding the genomic determinants that drive the evolution of host specificity in<i> Penicillium </i>species and clarifies the host-plant specificity during the infection of Valencia orange by <i>P. italicum</i>. P. italicum GL_Gan1, a local strain in Guangzhou, China, was sequenced. Comparison of the genome of <i>P. italicum</i> GL_Gan1 with other pathogenic <i>Penicillium</i> species, <i>P. digitatum</i> and <i>P. expansum</i>, revealed that the expansion of protein families, genome restructuring, HGT, and positive selection pressure were related to the host range expansion of the analyzed <i>Penicillium</i> species. Moreover, gene gains or losses might be associated with the speciation of these <i>Penicillium</i> species. In addition, the molecular basis of host-plant specificity during the infection of Valencia orange (<i>Citrus sinensis</i>) by <i>P. italicum</i> was also elucidated by transcriptomic and metabolomics analysis. The data presented herein may be useful for further elucidating the molecular basis of the evolution of host specificity of <i>Penicillium</i> species and for illustrating the host-plant specificity during the infection of Valencia orange by <i>P. italicum</i>.
DOI: 10.6084/m9.figshare.12852048
title: Exoproteomic profiling uncovers critical determinants for virulence of livestock-associated and human-originated <i>Staphylococcus aureus</i> ST398 strains

description: Staphylococcus aureus: with the sequence type (ST) 398 was previously associated with livestock carriage. However, in recent years livestock-independent <i>S. aureus</i> ST398 has emerged, representing a potential health risk for humans especially in nosocomial settings. Judged by whole-genome sequencing analyses, the livestock- and human originated strains belong to two different <i>S. aureus</i> ST398 clades but, to date, it was not known to what extent these clades differ in terms of actual virulence. Therefore, the objective of this study was to profile the exoproteomes of 30 representative <i>S. aureus</i> ST398 strains by mass spectrometry, to assess clade-specific differences in virulence factor secretion, and to correlate the identified proteins and their relative abundance to the strains’ actual virulence. Although the human-originated strains are more heterogeneous at the genome level, our observations show that they are more homogeneous in terms of virulence factor production than the livestock-associated strains. To assess differences in virulence, infection models based on larvae of the wax moth <i>Galleria mellonella</i> and the human HeLa cell line were applied. Correlation of the exoproteome data to larval killing and toxicity toward HeLa cells uncovered critical roles of the staphylococcal Sbi, SpA, SCIN and CHIPS proteins in virulence. These findings were validated by showing that <i>sbi</i> or <i>spa</i> mutant bacteria are attenuated in <i>G. mellonella</i> and that the purified SCIN and CHIPS proteins are toxic for HeLa cells. Altogether, we show that exoproteome profiling allows the identification of critical determinants for virulence of livestock-associated and human-originated <i>S. aureus</i> ST398 strains.
DOI: 10.6084/m9.figshare.12852048.v1
title: Exoproteomic profiling uncovers critical determinants for virulence of livestock-associated and human-originated <i>Staphylococcus aureus</i> ST398 strains

description: Staphylococcus aureus: with the sequence type (ST) 398 was previously associated with livestock carriage. However, in recent years livestock-independent <i>S. aureus</i> ST398 has emerged, representing a potential health risk for humans especially in nosocomial settings. Judged by whole-genome sequencing analyses, the livestock- and human originated strains belong to two different <i>S. aureus</i> ST398 clades but, to date, it was not known to what extent these clades differ in terms of actual virulence. Therefore, the objective of this study was to profile the exoproteomes of 30 representative <i>S. aureus</i> ST398 strains by mass spectrometry, to assess clade-specific differences in virulence factor secretion, and to correlate the identified proteins and their relative abundance to the strains’ actual virulence. Although the human-originated strains are more heterogeneous at the genome level, our observations show that they are more homogeneous in terms of virulence factor production than the livestock-associated strains. To assess differences in virulence, infection models based on larvae of the wax moth <i>Galleria mellonella</i> and the human HeLa cell line were applied. Correlation of the exoproteome data to larval killing and toxicity toward HeLa cells uncovered critical roles of the staphylococcal Sbi, SpA, SCIN and CHIPS proteins in virulence. These findings were validated by showing that <i>sbi</i> or <i>spa</i> mutant bacteria are attenuated in <i>G. mellonella</i> and that the purified SCIN and CHIPS proteins are toxic for HeLa cells. Altogether, we show that exoproteome profiling allows the identification of critical determinants for virulence of livestock-associated and human-originated <i>S. aureus</i> ST398 strains.
DOI: 10.6084/m9.figshare.12852054
title: Bacteria elevate extracellular adenosine to exploit host signaling for blood-brain barrier disruption

description: Bacterial meningitis remains a substantial cause of mortality worldwide and survivors may have severe lifelong disability. Although we know that meningeal bacterial pathogens must cross blood-central nervous system (CNS) barriers, the mechanisms which facilitate the virulence of these pathogens are poorly understood. Here, we show that adenosine from a surface enzyme (Ssads) of <i>Streptococcus suis</i> facilitates this pathogen’s entry into mouse brains. Monolayer translocation assays (from the human cerebrovascular endothelium) and experiments using diverse inhibitors and agonists together demonstrate that activation of the A1 adenosine receptor signaling cascade in hosts, as well as attendant cytoskeleton remodeling, promote <i>S. suis</i> penetration across blood-CNS barriers. Importantly, our additional findings showing that Ssads orthologs from other bacterial species also promote their translocation across barriers suggest that exploitation of A1 AR signaling may be a general mechanism of bacterial virulence.
DOI: 10.6084/m9.figshare.12852054.v1
title: Bacteria elevate extracellular adenosine to exploit host signaling for blood-brain barrier disruption

description: Bacterial meningitis remains a substantial cause of mortality worldwide and survivors may have severe lifelong disability. Although we know that meningeal bacterial pathogens must cross blood-central nervous system (CNS) barriers, the mechanisms which facilitate the virulence of these pathogens are poorly understood. Here, we show that adenosine from a surface enzyme (Ssads) of <i>Streptococcus suis</i> facilitates this pathogen’s entry into mouse brains. Monolayer translocation assays (from the human cerebrovascular endothelium) and experiments using diverse inhibitors and agonists together demonstrate that activation of the A1 adenosine receptor signaling cascade in hosts, as well as attendant cytoskeleton remodeling, promote <i>S. suis</i> penetration across blood-CNS barriers. Importantly, our additional findings showing that Ssads orthologs from other bacterial species also promote their translocation across barriers suggest that exploitation of A1 AR signaling may be a general mechanism of bacterial virulence.
DOI: 10.6084/m9.figshare.12852054.v3
title: Bacteria elevate extracellular adenosine to exploit host signaling for blood-brain barrier disruption

description: Bacterial meningitis remains a substantial cause of mortality worldwide and survivors may have severe lifelong disability. Although we know that meningeal bacterial pathogens must cross blood-central nervous system (CNS) barriers, the mechanisms which facilitate the virulence of these pathogens are poorly understood. Here, we show that adenosine from a surface enzyme (Ssads) of <i>Streptococcus suis</i> facilitates this pathogen’s entry into mouse brains. Monolayer translocation assays (from the human cerebrovascular endothelium) and experiments using diverse inhibitors and agonists together demonstrate that activation of the A1 adenosine receptor signaling cascade in hosts, as well as attendant cytoskeleton remodeling, promote <i>S. suis</i> penetration across blood-CNS barriers. Importantly, our additional findings showing that Ssads orthologs from other bacterial species also promote their translocation across barriers suggest that exploitation of A1 AR signaling may be a general mechanism of bacterial virulence.
DOI: 10.6084/m9.figshare.12852054.v2
title: Bacteria elevate extracellular adenosine to exploit host signaling for blood-brain barrier disruption

description: Bacterial meningitis remains a substantial cause of mortality worldwide and survivors may have severe lifelong disability. Although we know that meningeal bacterial pathogens must cross blood-central nervous system (CNS) barriers, the mechanisms which facilitate the virulence of these pathogens are poorly understood. Here, we show that adenosine from a surface enzyme (Ssads) of <i>Streptococcus suis</i> facilitates this pathogen’s entry into mouse brains. Monolayer translocation assays (from the human cerebrovascular endothelium) and experiments using diverse inhibitors and agonists together demonstrate that activation of the A1 adenosine receptor signaling cascade in hosts, as well as attendant cytoskeleton remodeling, promote <i>S. suis</i> penetration across blood-CNS barriers. Importantly, our additional findings showing that Ssads orthologs from other bacterial species also promote their translocation across barriers suggest that exploitation of A1 AR signaling may be a general mechanism of bacterial virulence.
DOI: 10.6084/m9.figshare.12852060
title: Inactivation of the <i>htps</i>A gene affects capsule development and pathogenicity of <i>Streptococcus suis</i>

description: <b>Streptococcus suis</b> serotype 2 (<i>S. suis</i> 2) is an important swine pathogen and also an emerging zoonotic agent. HtpsA has been reported as an immunogenic cell surface protein on the bacterium. In the present study, we constructed an isogenic mutant strain of <i>htps</i>A, namely Δ<i>htps</i>A, to study its role in the development and virulence of <i>S. suis</i> 2. Our results showed that the mutant strain lost its typical encapsulated structure with decreased concentrations of sialic acid. Furthermore, the survival rate in whole blood, the anti-phagocytosis by RAW264.7 murine macrophage, and the adherence ability to HEp-2 cells were all significantly affected in the Δ<i>htps</i>A. In addition, the deletion of <i>htps</i>A sharply attenuated the virulence of <i>S. suis</i> 2 in an infection model of mouse. RNA-seq analysis revealed that 126 genes were differentially expressed between the Δ<i>htps</i>A and the wild-type strains, including 28 upregulated and 98 downregulated genes. Among the downregulated genes, many were involved in carbohydrate metabolism and synthesis of virulence-associated factors. Taken together, <i>htps</i>A was demonstrated to play a role in the morphological development and pathogenesis of the highly virulent <i>S. suis</i> 2 05ZYH33 strain.
DOI: 10.6084/m9.figshare.12852060.v1
title: Inactivation of the <i>htps</i>A gene affects capsule development and pathogenicity of <i>Streptococcus suis</i>

description: <b>Streptococcus suis</b> serotype 2 (<i>S. suis</i> 2) is an important swine pathogen and also an emerging zoonotic agent. HtpsA has been reported as an immunogenic cell surface protein on the bacterium. In the present study, we constructed an isogenic mutant strain of <i>htps</i>A, namely Δ<i>htps</i>A, to study its role in the development and virulence of <i>S. suis</i> 2. Our results showed that the mutant strain lost its typical encapsulated structure with decreased concentrations of sialic acid. Furthermore, the survival rate in whole blood, the anti-phagocytosis by RAW264.7 murine macrophage, and the adherence ability to HEp-2 cells were all significantly affected in the Δ<i>htps</i>A. In addition, the deletion of <i>htps</i>A sharply attenuated the virulence of <i>S. suis</i> 2 in an infection model of mouse. RNA-seq analysis revealed that 126 genes were differentially expressed between the Δ<i>htps</i>A and the wild-type strains, including 28 upregulated and 98 downregulated genes. Among the downregulated genes, many were involved in carbohydrate metabolism and synthesis of virulence-associated factors. Taken together, <i>htps</i>A was demonstrated to play a role in the morphological development and pathogenesis of the highly virulent <i>S. suis</i> 2 05ZYH33 strain.
DOI: 10.6084/m9.figshare.13900673
title: Genetic polymorphisms of 44 Y chromosomal genetic markers in the Inner Mongolia Han population and its genetic relationship analysis with other reference populations

description: Y chromosomal genetic markers in the non-recombining region are commonly used for human evolution research, familial searching, and forensic male differentiation since they strictly follow paternal inheritance. Y chromosomal short tandem repeats (Y-STRs) possess extraordinarily advantages in forensic applications because of their high polymorphisms and special genetic pattern. Here, we assessed the genetic diversities of 41 Y-STRs and three Y chromosomal insertion/deletion (Y-InDels) loci in the Chinese Inner Mongolia Han population; besides, genetic differentiation analyses among the studied Han population and other previously reported populations were conducted based on 27 same Y-STRs. Totally, 425 alleles were observed in 324 Inner Mongolia Han individuals for these Y-markers. Gene diversities of these Y-markers distributed from 0.0306 to 0.9634. The haplotype diversity and discriminatory capacity of these Y-markers in the Inner Mongolia Han population were 0.9999 and 0.98457, respectively. Haplotype resolution comparisons of different Y-marker groups in the studied Han population revealed that higher haplotype resolution could be achieved for these 44 Y-markers. Population genetic analyses of the Inner Mongolia Han population and other reference populations demonstrated that the studied Han population had relatively closer genetic affinities with Northern Han Chinese populations than Southern Han and other minority groups. To sum up, these 44 Y-markers can be utilized as a valuable tool for male differentiation in the Inner Mongolia Han population.