cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.29041356.v1
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.
DOI: 10.6084/m9.figshare.29817972
title: Molecular epidemiology of <i>Nakaseomyces glabrata</i> associated with vulvovaginal candidiasis revealed high genetic variability and the presence of novel genotypes in China

description: <i>Nakaseomyces glabrata</i> (former name: <i>Candida glabrata</i>) is the second most common cause of vulvovaginal candidiasis (VVC), but its molecular epidemiology and antifungal resistance in China remain poorly understood. This study analysed 204 <i>N. glabrata</i> isolates from VVC patients in Suzhou, Eastern China, using multi-locus sequence typing (MLST) and microsatellite genotyping, alongside antifungal susceptibility testing. A total of 46 sequence types (STs) were identified by MLST, as well as 146 genotypes (GTs) revealed by microsatellite. According to MLST, ST7 was the predominant ST in vaginal <i>N. glabrata</i> isolates, along with a considerably high proportion (32/46, 69.6%) of novel STs. Notably, 27 STs were unique singletons, of which 25 unique STs were newly defined in this investigation. Microsatellite genotyping revealed a similar pattern as MLST with high variability. Population genetic analysis revealed evidence of recombination and ST7 could be the founding population of other related STs. However, there was no significant association between the genotypes and resistance phenotypes. Molecular epidemiology of <i>N. glabrata</i> associated with VVC revealed high genetic variability and the presence of novel genotypes in China. This study highlights the unique genetic profile of vaginal <i>N. glabrata</i> isolates in Suzhou, with the majority of resistant strains belonging to ST7.
DOI: 10.6084/m9.figshare.29817972.v2
title: Molecular epidemiology of <i>Nakaseomyces glabrata</i> associated with vulvovaginal candidiasis revealed high genetic variability and the presence of novel genotypes in China

description: <i>Nakaseomyces glabrata</i> (former name: <i>Candida glabrata</i>) is the second most common cause of vulvovaginal candidiasis (VVC), but its molecular epidemiology and antifungal resistance in China remain poorly understood. This study analysed 204 <i>N. glabrata</i> isolates from VVC patients in Suzhou, Eastern China, using multi-locus sequence typing (MLST) and microsatellite genotyping, alongside antifungal susceptibility testing. A total of 46 sequence types (STs) were identified by MLST, as well as 146 genotypes (GTs) revealed by microsatellite. According to MLST, ST7 was the predominant ST in vaginal <i>N. glabrata</i> isolates, along with a considerably high proportion (32/46, 69.6%) of novel STs. Notably, 27 STs were unique singletons, of which 25 unique STs were newly defined in this investigation. Microsatellite genotyping revealed a similar pattern as MLST with high variability. Population genetic analysis revealed evidence of recombination and ST7 could be the founding population of other related STs. However, there was no significant association between the genotypes and resistance phenotypes. Molecular epidemiology of <i>N. glabrata</i> associated with VVC revealed high genetic variability and the presence of novel genotypes in China. This study highlights the unique genetic profile of vaginal <i>N. glabrata</i> isolates in Suzhou, with the majority of resistant strains belonging to ST7.
DOI: 10.6084/m9.figshare.29975804
title: Roles of the lipopolysaccharide biosynthesis-related gene <i>HP0858</i> in the fitness of <i>Helicobacter pylori</i> and its virulence in <i>Galleria mellonella</i>

description: <i>Helicobacter pylori</i> is a pathogenic bacterium associated with the development of gastric cancer and other gastric disorders. One of its major virulence factors, lipopolysaccharide (LPS), plays a crucial role in maintaining bacterial integrity, mediating host adhesion, and modulating the immune response. Recent studies have indicated that ADP-heptose, an intermediate in the heptose biosynthetic pathway involved in the LPS synthesis cascade, is a novel pathogen-associated molecular pattern for <i>H. pylori</i>. This study focuses on the <i>HP0858</i> gene, which is predicted to encode RfaE/HldE, an enzyme with kinase and ADP-transferase activities essential for heptose production. An <i>HP0858</i> gene-disrupted mutant was first generated, and the resulting mutant exhibited a truncated LPS structure, confirming its role in LPS biosynthesis. The <i>HP0858</i>-deficient mutant displayed increased sensitivity to the detergent SDS and the antibiotic novobiocin, heightened surface hydrophobicity, and a propensity for autoaggregation. Additionally, the mutant exhibited reduced adhesion and internalization capabilities, a diminished elongation phenotype, and failed to induce IL-8 secretion in infected gastric AGS cells. In an <i>in vivo Galleria mellonella</i> infection model, the <i>HP0858</i> knockout mutant showed significantly attenuated virulence, as no bacterial load was detectable in the larvae’s hemolymph 48 h post-infection, unlike the wild-type strain. Finally, we provided evidence that the enzyme encoded by <i>HP0858</i> is involved in a general protein glycosylation system linked to LPS biosynthesis, specifically glycosylating the adhesin AlpA. These findings highlight the essential role of RfaE/HldE/HP0858 in LPS biosynthesis and bacterial virulence, making it a promising target for future therapeutic interventions against <i>H. pylori</i> infections.
DOI: 10.6084/m9.figshare.29975804.v1
title: Roles of the lipopolysaccharide biosynthesis-related gene <i>HP0858</i> in the fitness of <i>Helicobacter pylori</i> and its virulence in <i>Galleria mellonella</i>

description: <i>Helicobacter pylori</i> is a pathogenic bacterium associated with the development of gastric cancer and other gastric disorders. One of its major virulence factors, lipopolysaccharide (LPS), plays a crucial role in maintaining bacterial integrity, mediating host adhesion, and modulating the immune response. Recent studies have indicated that ADP-heptose, an intermediate in the heptose biosynthetic pathway involved in the LPS synthesis cascade, is a novel pathogen-associated molecular pattern for <i>H. pylori</i>. This study focuses on the <i>HP0858</i> gene, which is predicted to encode RfaE/HldE, an enzyme with kinase and ADP-transferase activities essential for heptose production. An <i>HP0858</i> gene-disrupted mutant was first generated, and the resulting mutant exhibited a truncated LPS structure, confirming its role in LPS biosynthesis. The <i>HP0858</i>-deficient mutant displayed increased sensitivity to the detergent SDS and the antibiotic novobiocin, heightened surface hydrophobicity, and a propensity for autoaggregation. Additionally, the mutant exhibited reduced adhesion and internalization capabilities, a diminished elongation phenotype, and failed to induce IL-8 secretion in infected gastric AGS cells. In an <i>in vivo Galleria mellonella</i> infection model, the <i>HP0858</i> knockout mutant showed significantly attenuated virulence, as no bacterial load was detectable in the larvae’s hemolymph 48 h post-infection, unlike the wild-type strain. Finally, we provided evidence that the enzyme encoded by <i>HP0858</i> is involved in a general protein glycosylation system linked to LPS biosynthesis, specifically glycosylating the adhesin AlpA. These findings highlight the essential role of RfaE/HldE/HP0858 in LPS biosynthesis and bacterial virulence, making it a promising target for future therapeutic interventions against <i>H. pylori</i> infections.
DOI: 10.6084/m9.figshare.29817972.v1
title: Molecular epidemiology of <i>nakaseomyces glabrata</i> associated with vulvovaginal candidiasis revealed high genetic variability and the presence of novel genotypes in China

description: <i>Nakaseomyces glabrata</i> (former name: <i>candida glabrata</i>) is the second most common cause of vulvovaginal candidiasis (VVC), but its molecular epidemiology and antifungal resistance in China remain poorly understood. This study analysed 204 <i>N. glabrata</i> isolates from VVC patients in Suzhou, Eastern China, using multi-locus sequence typing (MLST) and microsatellite genotyping, alongside antifungal susceptibility testing. A total of 46 sequence types (STs) were identified by MLST, as well as 146 genotypes (GTs) revealed by microsatellite. According to MLST, ST7 was the predominant ST in vaginal <i>N. glabrata</i> isolates, along with a considerably high proportion (32/46, 69.6%) of novel STs. Notably, 27 STs were unique singletons, of which 25 unique STs were newly defined in this investigation. Microsatellite genotyping revealed a similar pattern as MLST with high variability. Population genetic analysis revealed evidence of recombination and ST7 could be the founding population of other related STs. However, there was no significant association between the genotypes and resistance phenotypes. Molecular epidemiology of <i>N. glabrata</i> associated with VVC revealed high genetic variability and the presence of novel genotypes in China. This study highlights the unique genetic profile of vaginal <i>N. glabrata</i> isolates in Suzhou, with the majority of resistant strains belonging to ST7.
DOI: 10.6084/m9.figshare.30247786
title: Metabolic adaptation to host acetate facilitates oxidative stress resistance and intracellular survival of <i>Neisseria meningitidis</i> in macrophages

description: <i>Neisseria meningitidis</i> encounters a dynamic nutrient landscape during host colonization, which necessitates its metabolic adaptation to different host metabolites such as acetate. Acetate, a short chain fatty acid (SCFA) within the host milieu, found to regulate host defense and inflammation during bacterial infection. In macrophage acetate gets converted into acetyl-CoA to provide energy via TCA cycle. Also, acetate is a crucial metabolic intermediate that takes part in lipid biosynthesis and protein acetylation. Acetate acts as an immunomodulator which improves the bactericidal effect of macrophage by activating the inflammasome. Therefore, to persist in nutrient limited conditions encountered in macrophages pathogens should resort to effective utilization of energy sources. We demonstrate that <i>N. meningitidis</i> can potentially utilize host acetate as a carbon source and regulate its virulence. The utilization of acetate enhanced the survival of <i>N. meningitidis</i> in H<sub>2</sub>O<sub>2</sub> induced oxidative stress which can be correlated with the macrophage infection assay. Moreover, our investigation into underlying mechanism suggests that acetate exposure upregulates bacterial oxidative stress response by significantly increasing catalase and superoxide dismutase activity. We demonstrated that acetate metabolism also upregulated expression of nitric oxide detoxification genes <i>fnr, narQ</i> which mitigate reactive oxygen and nitrogen species produced in macrophages. Therefore, we conclude that bacterial utilization of physiologically relevant host acetate levels represents an important strategy to consume or detoxify macrophage-mediated oxidative stress, thereby facilitating bacterial survival.
DOI: 10.6084/m9.figshare.30247786.v1
title: Metabolic adaptation to host acetate facilitates oxidative stress resistance and intracellular survival of <i>Neisseria meningitidis</i> in macrophages

description: <i>Neisseria meningitidis</i> encounters a dynamic nutrient landscape during host colonization, which necessitates its metabolic adaptation to different host metabolites such as acetate. Acetate, a short chain fatty acid (SCFA) within the host milieu, found to regulate host defense and inflammation during bacterial infection. In macrophage acetate gets converted into acetyl-CoA to provide energy via TCA cycle. Also, acetate is a crucial metabolic intermediate that takes part in lipid biosynthesis and protein acetylation. Acetate acts as an immunomodulator which improves the bactericidal effect of macrophage by activating the inflammasome. Therefore, to persist in nutrient limited conditions encountered in macrophages pathogens should resort to effective utilization of energy sources. We demonstrate that <i>N. meningitidis</i> can potentially utilize host acetate as a carbon source and regulate its virulence. The utilization of acetate enhanced the survival of <i>N. meningitidis</i> in H<sub>2</sub>O<sub>2</sub> induced oxidative stress which can be correlated with the macrophage infection assay. Moreover, our investigation into underlying mechanism suggests that acetate exposure upregulates bacterial oxidative stress response by significantly increasing catalase and superoxide dismutase activity. We demonstrated that acetate metabolism also upregulated expression of nitric oxide detoxification genes <i>fnr, narQ</i> which mitigate reactive oxygen and nitrogen species produced in macrophages. Therefore, we conclude that bacterial utilization of physiologically relevant host acetate levels represents an important strategy to consume or detoxify macrophage-mediated oxidative stress, thereby facilitating bacterial survival.
DOI: 10.6084/m9.figshare.30465519
title: Coronaviruses remodel the mature human tRNAome to modulate infection

description: Current research on virus-host interactions primarily focuses on the transcription and translation of viral and host genes. However, there is a major knowledge gap between transcription and translation, known as translational decoding mediated by mature transfer RNAs (tRNAs) charged with amino acids. Codon usage analysis of seven human coronaviruses indicates that they are highly dissimilar from the human host. Quantification of the human tRNAome, consisting of 57 species, demonstrated that infections with these coronaviruses robustly upregulate the global tRNAome landscapes in host cells. Deprivation of individual amino acids or knockdown of TRNT1, the enzyme adding 3’-ACC terminal for tRNA aminoacylation, inhibited coronavirus infection. Integrative analysis of codon usage and the tRNAome landscape identified a prominent role of tRNA-Asn-AUU in translational decoding of different human coronaviruses. Deprivation of asparagine (Asn) or knockdown of Asparaginyl-tRNA Synthetase 1, an enzyme that charges the Asn amino acid onto tRNA-Asn acceptors, including tRNA-Asn-AUU, profoundly inhibited coronavirus 229E infection, but to a much lesser extent for NL63 and SARS-CoV-2. Collectively, we demonstrated that human coronaviruses are capable of remodeling the host mature tRNAome to facilitate infection. However, the regulatory patterns and sensitivities to interference, particularly at the single amino acid or tRNA levels, vary among different coronavirus species. These findings provide a new perspective for understanding virus-host interactions.
DOI: 10.6084/m9.figshare.30465519.v1
title: Coronaviruses remodel the mature human tRNAome to modulate infection

description: Current research on virus-host interactions primarily focuses on the transcription and translation of viral and host genes. However, there is a major knowledge gap between transcription and translation, known as translational decoding mediated by mature transfer RNAs (tRNAs) charged with amino acids. Codon usage analysis of seven human coronaviruses indicates that they are highly dissimilar from the human host. Quantification of the human tRNAome, consisting of 57 species, demonstrated that infections with these coronaviruses robustly upregulate the global tRNAome landscapes in host cells. Deprivation of individual amino acids or knockdown of TRNT1, the enzyme adding 3’-ACC terminal for tRNA aminoacylation, inhibited coronavirus infection. Integrative analysis of codon usage and the tRNAome landscape identified a prominent role of tRNA-Asn-AUU in translational decoding of different human coronaviruses. Deprivation of asparagine (Asn) or knockdown of Asparaginyl-tRNA Synthetase 1, an enzyme that charges the Asn amino acid onto tRNA-Asn acceptors, including tRNA-Asn-AUU, profoundly inhibited coronavirus 229E infection, but to a much lesser extent for NL63 and SARS-CoV-2. Collectively, we demonstrated that human coronaviruses are capable of remodeling the host mature tRNAome to facilitate infection. However, the regulatory patterns and sensitivities to interference, particularly at the single amino acid or tRNA levels, vary among different coronavirus species. These findings provide a new perspective for understanding virus-host interactions.
DOI: 10.15468/dl.pkv8vg
title: Occurrence Download

description: A dataset containing 7217 species occurrences available in GBIF matching the query:
{
 "and" : [
 "OccurrenceStatus is Present",
 "TaxonKey is Macaca mulatta",
 "Year 1000-2026"
 ]
}

 The dataset includes 7217 records from 68 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003556-260120142942310/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.3ctytf
title: Occurrence Download

description: A dataset containing 872 species occurrences available in GBIF matching the query:
{
 "and" : [
 "TaxonKey is Lemur catta",
 "Year 1950-2026"
 ]
}

 The dataset includes 872 records from 40 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003555-260120142942310/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.28771093
title: Identifying sex-based disparities in porcine mitochondrial function

description: In pigs, the effect of sex on production and reproductive traits has been largely reported, however, whether sex exerts its influence through regulating mitochondrial function is still unclear. In this study, we constructed 15 male cells and 15 female fibroblasts derived from 35-day and 50-day fetuses, newborn piglets and 1-year-old pigs to identify the sex effect on mitochondrial functions. Results indicated significant differences on cellular and molecular characteristics between male and female cells, including energy metabolic trait, mitochondrial DNA (mtDNA) replication and transcription, and mRNA expressions of mitochondrial biogenesis genes and mitoprotease genes. Referring to sex, males exhibited significantly higher oxygen consumption rate productions, levels of reactive oxygen species (ROS) and mtDNA copy numbers than those with females in muscle and ear fibroblasts. And the expressions of mtDNA, mitochondrial biogenesis genes (<i>POLG</i>, <i>PPARGC1A</i>, <i>TFAM</i> and <i>TWNK</i>) and <i>XPNPEP3</i> were higher in males than females in ear fibroblasts derived from 1-year-old adult pigs (EFA cells). While, the cell proliferation and expressions of genes related to ROS metabolism were not influenced by sex. The results highlight the effect of sex on mitochondrial function and gene expression, and provide important data for a comprehensive understanding of the mechanisms underlying sex regulation of energy metabolism-related traits in pigs.
DOI: 10.6084/m9.figshare.28771093.v1
title: Identifying sex-based disparities in porcine mitochondrial function

description: In pigs, the effect of sex on production and reproductive traits has been largely reported, however, whether sex exerts its influence through regulating mitochondrial function is still unclear. In this study, we constructed 15 male cells and 15 female fibroblasts derived from 35-day and 50-day fetuses, newborn piglets and 1-year-old pigs to identify the sex effect on mitochondrial functions. Results indicated significant differences on cellular and molecular characteristics between male and female cells, including energy metabolic trait, mitochondrial DNA (mtDNA) replication and transcription, and mRNA expressions of mitochondrial biogenesis genes and mitoprotease genes. Referring to sex, males exhibited significantly higher oxygen consumption rate productions, levels of reactive oxygen species (ROS) and mtDNA copy numbers than those with females in muscle and ear fibroblasts. And the expressions of mtDNA, mitochondrial biogenesis genes (<i>POLG</i>, <i>PPARGC1A</i>, <i>TFAM</i> and <i>TWNK</i>) and <i>XPNPEP3</i> were higher in males than females in ear fibroblasts derived from 1-year-old adult pigs (EFA cells). While, the cell proliferation and expressions of genes related to ROS metabolism were not influenced by sex. The results highlight the effect of sex on mitochondrial function and gene expression, and provide important data for a comprehensive understanding of the mechanisms underlying sex regulation of energy metabolism-related traits in pigs.
DOI: 10.6084/m9.figshare.28908704
title: Transcriptome-wide study of mRNAs modified by m<sup>6</sup>A RNA methylation in the testis development of dairy goats

description: N6-methyladenosine (m<sup>6</sup>A) is an important epigenetic modification in RNA, playing a crucial role in regulating the production and aging of animal testicular sperm. This study extracted mRNA from the testicular tissue of male goats before and after sexual maturity, generating a methylation map through preliminary experiments and methylation immunoprecipitation sequencing. The results showed that during the development of dairy goats, the expression levels of marker genes related to testicular development and methylation-related enzymes changed significantly. A total of 36,602 peaks and 11,223 genes were identified in the two groups, including 2989 differential peaks (427 upregulated and 2562 downregulated) and 1457 differentially expressed genes (833 upregulated and 624 downregulated). The abundance of m<sup>6</sup>A was positively correlated with gene expression levels. This study reports for the first time the mRNA profiles of m<sup>6</sup>A modifications across the entire transcriptome during testicular development in Guanzhong dairy goats, providing a new perspective for genetic improvement in goats.