cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.30790557.v1
title: Mapping evolutionary paradigm of oropouche virus driven by dinucleotide bias and context-dependent codon bias

description: Arthropod-borne viruses (arboviruses) pose significant public health threats, and understanding their evolutionary mechanisms can inform molecular diagnostics and vaccine design. Oropouche virus (OROV), a relatively understudied arbovirus, exhibits unique evolutionary dynamics in nucleotide composition. We analyzed 45 OROV strains across genotypes to assess selective pressures shaping nucleoprotein, glycoprotein, and RNA-dependent RNA polymerase (RdRp) evolution. We utilized information entropy, dinucleotide odds ratios, relative synonymous codon usage values, and context-dependent codon bias (CDCB) to elucidate the genetic characteristics associated with mono-, di-, tri-, and tetranucleotide compositions. The extent of overall nucleotide usage bias, dinucleotide bias, and synonymous codon usage bias did not correlate with genotype-specific patterns, but rather exhibited a protein function-dependent pattern across the three proteins. Although dinucleotide bias and synonymous codon usage bias varied within a relatively broad range, the dinucleotide CpG, the over- and under-represented synonymous codons, and CDCB remained strongly influenced by natural selective pressures from both the host and the viral life cycle. Furthermore, the codon usage patterns, as indicated by the effective number of codons, suggest that the OROV nucleoprotein has been subject to stronger selective pressures in its evolutionary paradigm compared to the glycoprotein and RdRp, which appear to be primarily influenced by natural selection and mutation pressure. Additionally, analysis of relative codon deoptimization index (RCDI) and tRNA adaptation index (tAI) revealed suboptimal translational efficiency of OROV coding sequences in human hosts, suggesting limited codon usage adaptation.
DOI: 10.6084/m9.figshare.28449981
title: The Hog1-Nmd5 signaling pathway regulates asexual development, lipid metabolism, stress response, trap morphogenesis, and secondary metabolism of <i>Arthrobotrys oligospora</i>

description: The high-osmolarity glycerol (HOG) signalling pathway, comprising Ste11/Ssk2/Ssk22 (MAPKKK), Pbs2 (MAPKK), and Hog1 (MAPK), is an important and conserved pathway in fungi. However, the functions and downstream regulatory factors of Hog1 in nematode-trapping (NT) fungi remain poorly understood. Here, three proteins (AoNmd5, AoPyp1, and AoPtp) interacting with Hog1 were screened in a representative NT fungus <i>Arthrobotrys oligospora</i> using yeast screening library and verified using yeast two-hybrid (Y2H) assay. The function of AoNmd5 was furtherly characterized by phenotypic comparison, staining technique, and multi-omics analyses. AoNmd5 was essential for vegetative growth, conidial development, trap morphogenesis, and nematode predation ability. In addition, AoNmd5 played crucial roles in endocytosis, lipid metabolism, reactive oxygen species, stress response, autophagy, and other metabolic processes. Furthermore, we constructed an AoNmd5 interaction network based on transcriptomic analysis and Y2H, revealing its significant role in the respiratory chain and redox processes as well as its interaction with the small GTPase Ran1, which mediates Hog1 nucleocytoplasmic shuttling. These findings suggest that the Hog1-Nmd5 signalling pathway has pleiotropic roles in <i>A. oligospora</i>. This study deepens our understanding of the HOG pathway and its interaction with importins in NT fungi.
DOI: 10.6084/m9.figshare.28449981.v1
title: The Hog1-Nmd5 signaling pathway regulates asexual development, lipid metabolism, stress response, trap morphogenesis, and secondary metabolism of <i>Arthrobotrys oligospora</i>

description: The high-osmolarity glycerol (HOG) signalling pathway, comprising Ste11/Ssk2/Ssk22 (MAPKKK), Pbs2 (MAPKK), and Hog1 (MAPK), is an important and conserved pathway in fungi. However, the functions and downstream regulatory factors of Hog1 in nematode-trapping (NT) fungi remain poorly understood. Here, three proteins (AoNmd5, AoPyp1, and AoPtp) interacting with Hog1 were screened in a representative NT fungus <i>Arthrobotrys oligospora</i> using yeast screening library and verified using yeast two-hybrid (Y2H) assay. The function of AoNmd5 was furtherly characterized by phenotypic comparison, staining technique, and multi-omics analyses. AoNmd5 was essential for vegetative growth, conidial development, trap morphogenesis, and nematode predation ability. In addition, AoNmd5 played crucial roles in endocytosis, lipid metabolism, reactive oxygen species, stress response, autophagy, and other metabolic processes. Furthermore, we constructed an AoNmd5 interaction network based on transcriptomic analysis and Y2H, revealing its significant role in the respiratory chain and redox processes as well as its interaction with the small GTPase Ran1, which mediates Hog1 nucleocytoplasmic shuttling. These findings suggest that the Hog1-Nmd5 signalling pathway has pleiotropic roles in <i>A. oligospora</i>. This study deepens our understanding of the HOG pathway and its interaction with importins in NT fungi.
DOI: 10.15468/dl.nsudqc
title: Occurrence Download

description: A dataset containing 28090 species occurrences available in GBIF matching the query:
{
 "and" : [
 "OccurrenceStatus is Present",
 "TaxonKey is Tsuga heterophylla",
 "Year 1986-2026"
 ]
}

 The dataset includes 28090 records from 247 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003552-260120142942310/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.6084/m9.figshare.30460253
title: Conserved and acquired: Decoding YbjX and VirK in the pathogenicity of <i>Shigella flexneri</i>

description: The pathogenicity of <i>Shigella</i> spp. human pathogens responsible for bacillary dysentery, results from the combination of factors encoded both on the chromosome and on the virulence plasmid acquired during pathoadaptation. While many key elements have been extensively investigated, several remain poorly characterized. Among these, YbjX and VirK exhibit high structural similarity and are encoded by genes located on the chromosome and the virulence plasmid, respectively. We provide a molecular and functional characterization of <i>Shigella flexneri</i> YbjX and VirK. We defined the <i>ybjX</i> and <i>virK</i> promoter regions and confirmed that their expression is regulated by the PhoPQ two-component system. Localization studies demonstrated that both proteins are cytoplasmic. <i>In silico</i> analysis predicted a similar structure for the two proteins, resembling members of the Gcn5-related N-acetyltransferase superfamily. Functionally, lack of VirK resulted in increased permeability of the OM, sensitivity to cationic antimicrobial peptides, and an intensified release of proinflammatory cytokines by infected macrophages (THP-1-derived) and epithelial cells (Caco-2). The deletion of <i>ybjX</i> alone didn’t confer detectable phenotypes. When both genes were deleted at the same time a complementary function of YbjX was revealed, as all the phenotypes described above were reinforced. Our findings underscore a synergistic role for YbjX and VirK in OM integrity and the modulation of the host response, suggesting a prominent role of VirK and a supporting role of YbjX. From an evolutionary perspective, our work suggests that the retention of <i>ybjX</i> and the acquisition of <i>virK</i> reinforced bacterial survival and fitness during the infection of the host.
DOI: 10.6084/m9.figshare.30460253.v1
title: Conserved and acquired: Decoding YbjX and VirK in the pathogenicity of <i>Shigella flexneri</i>

description: The pathogenicity of <i>Shigella</i> spp. human pathogens responsible for bacillary dysentery, results from the combination of factors encoded both on the chromosome and on the virulence plasmid acquired during pathoadaptation. While many key elements have been extensively investigated, several remain poorly characterized. Among these, YbjX and VirK exhibit high structural similarity and are encoded by genes located on the chromosome and the virulence plasmid, respectively. We provide a molecular and functional characterization of <i>Shigella flexneri</i> YbjX and VirK. We defined the <i>ybjX</i> and <i>virK</i> promoter regions and confirmed that their expression is regulated by the PhoPQ two-component system. Localization studies demonstrated that both proteins are cytoplasmic. <i>In silico</i> analysis predicted a similar structure for the two proteins, resembling members of the Gcn5-related N-acetyltransferase superfamily. Functionally, lack of VirK resulted in increased permeability of the OM, sensitivity to cationic antimicrobial peptides, and an intensified release of proinflammatory cytokines by infected macrophages (THP-1-derived) and epithelial cells (Caco-2). The deletion of <i>ybjX</i> alone didn’t confer detectable phenotypes. When both genes were deleted at the same time a complementary function of YbjX was revealed, as all the phenotypes described above were reinforced. Our findings underscore a synergistic role for YbjX and VirK in OM integrity and the modulation of the host response, suggesting a prominent role of VirK and a supporting role of YbjX. From an evolutionary perspective, our work suggests that the retention of <i>ybjX</i> and the acquisition of <i>virK</i> reinforced bacterial survival and fitness during the infection of the host.
DOI: 10.6084/m9.figshare.29041350
title: Exploring the biological mechanisms of severe COVID-19 in the elderly: Insights from an aged mouse model

description: The elderly population, who have increased susceptibility to severe outcomes, have been particularly impacted by the coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), leading to a global health crisis. However, definitive parameters or mechanisms underlying the severity of COVID-19 in elderly people remain unclear. Thus, this study seeks to elucidate the mechanism behind the increased vulnerability of elderly individuals to severe COVID-19. We employed an aged mouse model with a mouse-adapted SARS-CoV-2 strain to mimic the severe symptoms observed in elderly patients with COVID-19. Comprehensive analyses of the whole lung were performed using transcriptome and proteome sequencing, comparing data from aged and young mice. For transcriptome analysis, bulk RNA sequencing was conducted using an Illumina sequencing platform. Proteomic analysis was performed using mass spectrometry following protein extraction, digestion, and peptide labelling. We analysed the transcriptome and proteome profiles of young and aged mice and discovered that aged mice exhibited elevated baseline levels of inflammation and tissue damage repair. After SARS-CoV-2 infection, aged mice showed increased antiviral and inflammatory responses; however, these responses were weaker than those in young mice, with significant complement and coagulation cascade responses. In summary, our study demonstrates that the increased vulnerability of the elderly to severe COVID-19 may be attributed to an attenuated antiviral response and the overactivation of complement and coagulation cascades. Future research on antiviral and inflammatory responses is likely to yield treatments that reduce the severity of viral respiratory diseases in the elderly.
DOI: 10.6084/m9.figshare.29041350.v1
title: Exploring the biological mechanisms of severe COVID-19 in the elderly: Insights from an aged mouse model

description: The elderly population, who have increased susceptibility to severe outcomes, have been particularly impacted by the coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), leading to a global health crisis. However, definitive parameters or mechanisms underlying the severity of COVID-19 in elderly people remain unclear. Thus, this study seeks to elucidate the mechanism behind the increased vulnerability of elderly individuals to severe COVID-19. We employed an aged mouse model with a mouse-adapted SARS-CoV-2 strain to mimic the severe symptoms observed in elderly patients with COVID-19. Comprehensive analyses of the whole lung were performed using transcriptome and proteome sequencing, comparing data from aged and young mice. For transcriptome analysis, bulk RNA sequencing was conducted using an Illumina sequencing platform. Proteomic analysis was performed using mass spectrometry following protein extraction, digestion, and peptide labelling. We analysed the transcriptome and proteome profiles of young and aged mice and discovered that aged mice exhibited elevated baseline levels of inflammation and tissue damage repair. After SARS-CoV-2 infection, aged mice showed increased antiviral and inflammatory responses; however, these responses were weaker than those in young mice, with significant complement and coagulation cascade responses. In summary, our study demonstrates that the increased vulnerability of the elderly to severe COVID-19 may be attributed to an attenuated antiviral response and the overactivation of complement and coagulation cascades. Future research on antiviral and inflammatory responses is likely to yield treatments that reduce the severity of viral respiratory diseases in the elderly.
DOI: 10.6084/m9.figshare.29815114
title: MaMsb2, a signaling mucin, is involved in conidiation, stress tolerances, and virulence in the entomopathogenic fungus <i>Metarhizium acridum</i>

description: Entomopathogenic fungi are pivotal microbial resources for crop protection in agriculture, offering a natural and environmentally friendly alternative to chemical pesticides. The signalling mucin gene <i>Msb2</i> contributes to the modulation of fungal development and virulence, yet its functions have remained unexplored in entomopathogenic fungi. In this study, we aimed to characterize the functions of <i>Msb2</i> in the model entomopathogenic fungus <i>Metarhizium acridum</i> using gene knockout and complementation strategies. The absence of <i>MaMsb2</i> led to a delay in conidial germination and an increase in conidial yield due to a shift in the conidiation pattern. Additionally, the <i>MaMsb2</i>-disruption bring about the significantly reduced tolerances to various adversities in <i>M. acridum</i>. Moreover, inactivation of <i>MaMsb2</i> resulted in the decreased virulence of <i>M. acridum</i> owing to the decrease in conidial hydrophobicity and adhesion, the impairment of appressorium formation, and the reduction of <i>M. acridum</i> growth in the locust haemolymph. To elucidate the molecular mechanisms by which <i>MaMsb2</i> exerts its influence, we conducted an RNA-seq analysis during appressorium formation. As a result, 880 differentially expressed genes (DEGs) regulated by MaMsb2 were identified. Our data indicated that MaMsb2 governs the appressorium formation of <i>M. acridum</i> by mediating the expression of genes associated with conidia adhesion, appressorium formation, and host cuticle penetration. These findings not only shed light on the multifaceted role of <i>MaMsb2</i> in the biology of entomopathogenic fungi but also lay the groundwork for future research aimed at unravelling the intricate mechanisms by which MaMsb2 regulates conidiation and pathogenesis.
DOI: 10.6084/m9.figshare.29815114.v1
title: MaMsb2, a signaling mucin, is involved in conidiation, stress tolerances, and virulence in the entomopathogenic fungus <i>Metarhizium acridum</i>

description: Entomopathogenic fungi are pivotal microbial resources for crop protection in agriculture, offering a natural and environmentally friendly alternative to chemical pesticides. The signalling mucin gene <i>Msb2</i> contributes to the modulation of fungal development and virulence, yet its functions have remained unexplored in entomopathogenic fungi. In this study, we aimed to characterize the functions of <i>Msb2</i> in the model entomopathogenic fungus <i>Metarhizium acridum</i> using gene knockout and complementation strategies. The absence of <i>MaMsb2</i> led to a delay in conidial germination and an increase in conidial yield due to a shift in the conidiation pattern. Additionally, the <i>MaMsb2</i>-disruption bring about the significantly reduced tolerances to various adversities in <i>M. acridum</i>. Moreover, inactivation of <i>MaMsb2</i> resulted in the decreased virulence of <i>M. acridum</i> owing to the decrease in conidial hydrophobicity and adhesion, the impairment of appressorium formation, and the reduction of <i>M. acridum</i> growth in the locust haemolymph. To elucidate the molecular mechanisms by which <i>MaMsb2</i> exerts its influence, we conducted an RNA-seq analysis during appressorium formation. As a result, 880 differentially expressed genes (DEGs) regulated by MaMsb2 were identified. Our data indicated that MaMsb2 governs the appressorium formation of <i>M. acridum</i> by mediating the expression of genes associated with conidia adhesion, appressorium formation, and host cuticle penetration. These findings not only shed light on the multifaceted role of <i>MaMsb2</i> in the biology of entomopathogenic fungi but also lay the groundwork for future research aimed at unravelling the intricate mechanisms by which MaMsb2 regulates conidiation and pathogenesis.
DOI: 10.6084/m9.figshare.28104610
title: The PA-X host shutoff site 100 V exerts a contrary effect on viral fitness of the highly pathogenic H7N9 influenza A virus in mice and chickens

description: Several viruses, including influenza A virus (IAV), encode viral factors to hijack cellular RNA biogenesis processes to direct the degradation of host mRNAs, termed “host shutoff.” Host shutoff enables viruses to simultaneously reduce antiviral responses and provides preferential access for viral mRNAs to cellular translation machinery. IAV PA-X is one of these factors that selectively shuts off the global host genes. However, the specific role of PA-X host shutoff activity in viral fitness of IAV remains poorly understood. Herein, we successfully mapped PA-X 100 V as a novel site important for host shutoff of the H7N9 and H5N1 viruses. By analysing the polymorphism of this residue in various subtype viruses, we found that PA-X 100 was highly variable in H7N9 viruses. Structural analysis revealed that 100 V was generally close to the PA-X endonuclease active site, which may account for its host shutoff activity. By generating the corresponding mutant viruses derived from the parental H7N9 virus and the PA-X-deficient H7N9 virus, we determined that PA-X 100 V significantly enhanced viral fitness in mice while diminishing viral virulence in chickens. Mechanistically, PA-X 100 V significantly increased viral polymerase activity and viral replication in mammalian cells. Furthermore, PA-X 100 V highly blunted the global host response in 293T cells, particularly restraining genes involved in energy metabolism and inflammatory response. Collectively, our data provided information about the intricate role of the PA-X host shutoff site in regulating the viral fitness of the H7N9 influenza virus, which furthers our understanding of the complicated pathogenesis of the influenza A virus.
DOI: 10.6084/m9.figshare.28104610.v1
title: The PA-X host shutoff site 100 V exerts a contrary effect on viral fitness of the highly pathogenic H7N9 influenza A virus in mice and chickens

description: Several viruses, including influenza A virus (IAV), encode viral factors to hijack cellular RNA biogenesis processes to direct the degradation of host mRNAs, termed “host shutoff.” Host shutoff enables viruses to simultaneously reduce antiviral responses and provides preferential access for viral mRNAs to cellular translation machinery. IAV PA-X is one of these factors that selectively shuts off the global host genes. However, the specific role of PA-X host shutoff activity in viral fitness of IAV remains poorly understood. Herein, we successfully mapped PA-X 100 V as a novel site important for host shutoff of the H7N9 and H5N1 viruses. By analysing the polymorphism of this residue in various subtype viruses, we found that PA-X 100 was highly variable in H7N9 viruses. Structural analysis revealed that 100 V was generally close to the PA-X endonuclease active site, which may account for its host shutoff activity. By generating the corresponding mutant viruses derived from the parental H7N9 virus and the PA-X-deficient H7N9 virus, we determined that PA-X 100 V significantly enhanced viral fitness in mice while diminishing viral virulence in chickens. Mechanistically, PA-X 100 V significantly increased viral polymerase activity and viral replication in mammalian cells. Furthermore, PA-X 100 V highly blunted the global host response in 293T cells, particularly restraining genes involved in energy metabolism and inflammatory response. Collectively, our data provided information about the intricate role of the PA-X host shutoff site in regulating the viral fitness of the H7N9 influenza virus, which furthers our understanding of the complicated pathogenesis of the influenza A virus.
DOI: 10.6084/m9.figshare.29041356
title: Mannan is a context-dependent shield that modifies virulence in <i>Nakaseomyces glabratus</i>

description: Fungal-host interaction outcomes are influenced by how the host recognizes fungal cell wall components. Mannan is a major cell wall carbohydrate and can be a glycoshield that blocks the inner cell wall β-1,3-glucan from activating pro-inflammatory immune responses. Disturbing this glycoshield in <i>Candida albicans</i> results in enhanced antifungal host responses and reduced fungal virulence. However, deletions affecting mannan synthesis can lead to systemic hypervirulence for <i>Nakaseomyces glabratus</i> (formerly <i>Candida glabrata</i>) suggesting that proper mannan architecture dampens virulence for this organism. <i>N. glabratus</i> is the second leading cause of invasive and superficial candidiasis, but little is known about how the cell wall affects <i>N. glabratus</i> pathogenesis. In order to better understand the importance of these species-specific cell wall adaptations in infection, we set out to investigate how the mannan polymerase II complex gene, <i>MNN10</i>, contributes to <i>N. glabratus</i> cell wall architecture, immune recognition, and virulence in reference strains BG2 and CBS138. <i>mnn10</i>Δ cells had thinner inner and outer cell wall layers and elevated mannan, chitin, and β-1,3-glucan exposure compared to wild-type cells. Consistent with these observations, <i>mnn10</i>Δ cells activated the β-1,3-glucan receptor in oral epithelial cells (OECs), EphA2, and caused less OEC damage than wild-type. <i>mnn10</i>Δ replication was also restricted in macrophages compared to wild-type controls. Yet, during systemic infection in <i>Galleria mellonella</i> larvae, <i>mnn10</i>Δ cells induced rapid larval melanization and BG2 <i>mnn10</i>Δ cells killed larvae significantly faster than wild-type. Thus, our data suggest that mannan plays context-dependent roles in <i>N. glabratus</i> pathogenesis, acting as a glycoshield in superficial disease models and modulating virulence during systemic infection.