cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.30158630
title: The phenol-2-monooxygenase FgPhm1 regulates DON synthesis, pathogenicity and environmental stress response in <i>Fusarium graminearum</i>

description: <i>Fusarium graminearum</i> is a devastating plant pathogenic fungus that produces mycotoxins and is the predominant pathogen causing Fusarium head blight. Phenol-2-monooxygenase is an oxidoreductase that is responsible for the conversion of phenol to catechol. However, the role of phenol-2-monooxygenase in filamentous fungi remains unclear. This study showed that the deletion of the phenol-2-monooxygenase gene <i>FgPHM1</i> leads to defects in vegetative growth, conidia production, sexual reproduction, and plant infection. FgPhm1 is localized to the nucleoplasm and regulates DON production. In addition, FgPhm1 is required for the formation of toxisomes and regulates the expression of <i>TRI</i> genes. RNA-seq analysis showed that the differentially expressed genes in the mutant were enriched in secondary metabolite biosynthesis, carbon metabolism, and pyruvate metabolism. Interestingly, the <i>FgPHM1</i> deletion mutant was tolerant to phenol stress, whereas it was sensitive to catechol and oxidative stress. FgPhm1 is required for reactive oxygen species production in <i>F. graminearum</i>, and the expression level of <i>FgPHM1</i> gene is induced by H<sub>2</sub>O<sub>2</sub>. Moreover, FgPhm1 regulates autophagy in <i>F. graminearum</i> under nitrogen starvation or rapamycin treatment in <i>F. graminearum</i>. Taken together, this study demonstrated that FgPhm1 is essential for the development and production of DON and plays important roles in the pathogenicity and stress response of <i>F. graminearum</i>, and RNA-seq revealed that FgPhm1 was involved in the biosynthesis of secondary metabolites in <i>F. graminearum</i>.
DOI: 10.6084/m9.figshare.30158630.v2
title: The phenol-2-monooxygenase FgPhm1 regulates DON synthesis, pathogenicity and environmental stress response in <i>Fusarium graminearum</i>

description: <i>Fusarium graminearum</i> is a devastating plant pathogenic fungus that produces mycotoxins and is the predominant pathogen causing Fusarium head blight. Phenol-2-monooxygenase is an oxidoreductase that is responsible for the conversion of phenol to catechol. However, the role of phenol-2-monooxygenase in filamentous fungi remains unclear. This study showed that the deletion of the phenol-2-monooxygenase gene <i>FgPHM1</i> leads to defects in vegetative growth, conidia production, sexual reproduction, and plant infection. FgPhm1 is localized to the nucleoplasm and regulates DON production. In addition, FgPhm1 is required for the formation of toxisomes and regulates the expression of <i>TRI</i> genes. RNA-seq analysis showed that the differentially expressed genes in the mutant were enriched in secondary metabolite biosynthesis, carbon metabolism, and pyruvate metabolism. Interestingly, the <i>FgPHM1</i> deletion mutant was tolerant to phenol stress, whereas it was sensitive to catechol and oxidative stress. FgPhm1 is required for reactive oxygen species production in <i>F. graminearum</i>, and the expression level of <i>FgPHM1</i> gene is induced by H<sub>2</sub>O<sub>2</sub>. Moreover, FgPhm1 regulates autophagy in <i>F. graminearum</i> under nitrogen starvation or rapamycin treatment in <i>F. graminearum</i>. Taken together, this study demonstrated that FgPhm1 is essential for the development and production of DON and plays important roles in the pathogenicity and stress response of <i>F. graminearum</i>, and RNA-seq revealed that FgPhm1 was involved in the biosynthesis of secondary metabolites in <i>F. graminearum</i>.
DOI: 10.6084/m9.figshare.30688059
title: Characterization of the pathogenicity and mechanisms underlying the pathogenesis of <i>Apibacter raozihei</i>, a potential bacterial pathogen

description: <i>Apibacter raozihei</i> is a Gram-negative bacterium isolated from the feces of bats, and there is a scarcity of information regarding its genomic and pathogenicity characteristics. This study systematically evaluated the pathogenic potential of <i>A</i>. <i>raozihei</i> by comparing the survival rates, bacterial loads in the peripheral blood and organs, histopathological lesions, and the production of proinflammatory cytokines in C57BL/6 mice infected with strains HY037 and HY041<sup>T</sup> of <i>A</i>. <i>raozihei</i>. The findings revealed that mice infected with <i>A</i>. <i>raozihei</i> had low survival rates, with significant differences between the HY041<sup>T</sup> and HY037 strains. The mice infected with HY041<sup>T</sup> exhibited more severe pulmonary histopathological damage and higher levels of proinflammatory cytokines compared to those infected with HY037. These results demonstrated that <i>A</i>. <i>raozihei</i> is lethal in mice, causing significant pulmonary histopathological damage accompanied by the dysregulated secretion of proinflammatory cytokines in lung tissues and blood. The molecular mechanisms underlying their virulence were investigated through comparative analyses of the genomic and transcriptional profiles of HY041<sup>T</sup> and HY037. The findings revealed that the genes encoding outer membrane protein A (OmpA), three peptidases, heat shock proteins, and proteins involved in lipopolysaccharide biosynthesis, and iron acquisition represent potential virulence factors of <i>A</i>. <i>raozihei</i>. In conclusion, this study established <i>A</i>. <i>raozihei</i> as a potential pathogen and identified significant differences in virulence across its strains, thereby enhancing our understanding of the pathogenesis of <i>A</i>. <i>raozihei</i>.
DOI: 10.6084/m9.figshare.30688059.v1
title: Characterization of the pathogenicity and mechanisms underlying the pathogenesis of <i>Apibacter raozihei</i>, a potential bacterial pathogen

description: <i>Apibacter raozihei</i> is a Gram-negative bacterium isolated from the feces of bats, and there is a scarcity of information regarding its genomic and pathogenicity characteristics. This study systematically evaluated the pathogenic potential of <i>A</i>. <i>raozihei</i> by comparing the survival rates, bacterial loads in the peripheral blood and organs, histopathological lesions, and the production of proinflammatory cytokines in C57BL/6 mice infected with strains HY037 and HY041<sup>T</sup> of <i>A</i>. <i>raozihei</i>. The findings revealed that mice infected with <i>A</i>. <i>raozihei</i> had low survival rates, with significant differences between the HY041<sup>T</sup> and HY037 strains. The mice infected with HY041<sup>T</sup> exhibited more severe pulmonary histopathological damage and higher levels of proinflammatory cytokines compared to those infected with HY037. These results demonstrated that <i>A</i>. <i>raozihei</i> is lethal in mice, causing significant pulmonary histopathological damage accompanied by the dysregulated secretion of proinflammatory cytokines in lung tissues and blood. The molecular mechanisms underlying their virulence were investigated through comparative analyses of the genomic and transcriptional profiles of HY041<sup>T</sup> and HY037. The findings revealed that the genes encoding outer membrane protein A (OmpA), three peptidases, heat shock proteins, and proteins involved in lipopolysaccharide biosynthesis, and iron acquisition represent potential virulence factors of <i>A</i>. <i>raozihei</i>. In conclusion, this study established <i>A</i>. <i>raozihei</i> as a potential pathogen and identified significant differences in virulence across its strains, thereby enhancing our understanding of the pathogenesis of <i>A</i>. <i>raozihei</i>.
DOI: 10.6084/m9.figshare.28260840
title: Lactic acid in the vaginal milieu modulates the <i>Candida</i>-host interaction

description: Vulvovaginal candidiasis (VVC) is one of the most common infections caused by <i>Candida albicans</i>. VVC is characterized by an inadequate hyperinflammatory response and clinical symptoms associated with <i>Candida</i> colonization of the vaginal mucosa. Compared to other host niches in which <i>C. albicans</i> can cause infection, the vaginal environment is extremely rich in lactic acid that is produced by the vaginal microbiota. We examined how lactic acid abundance in the vaginal niche impacts the interaction between <i>C. albicans</i> and the human immune system using an <i>in vitro</i> culture in vaginal simulative medium (VSM). The presence of lactic acid in VSM (VSM+LA) increased <i>C. albicans</i> proliferation, hyphal length, and its ability to cause damage during subsequent infection of vaginal epithelial cells. The cell wall of <i>C. albicans</i> cells grown in VSM+LA displayed a robust mannan fibrillar structure, β-glucan exposure, and low chitin content. These cell wall changes were associated with altered immune responses and an increased ability of the fungus to induce trained immunity. Neutrophils were compromised in clearing <i>C. albicans</i> grown in VSM+LA conditions, despite mounting stronger oxidative responses. Collectively, we found that fungal adaptation to lactic acid in a vaginal simulative context increases its immunogenicity favouring a pro-inflammatory state. This potentially contributes to the immune response dysregulation and neutrophil recruitment observed during recurrent VVC.
DOI: 10.6084/m9.figshare.28260840.v1
title: Lactic acid in the vaginal milieu modulates the <i>Candida</i>-host interaction

description: Vulvovaginal candidiasis (VVC) is one of the most common infections caused by <i>Candida albicans</i>. VVC is characterized by an inadequate hyperinflammatory response and clinical symptoms associated with <i>Candida</i> colonization of the vaginal mucosa. Compared to other host niches in which <i>C. albicans</i> can cause infection, the vaginal environment is extremely rich in lactic acid that is produced by the vaginal microbiota. We examined how lactic acid abundance in the vaginal niche impacts the interaction between <i>C. albicans</i> and the human immune system using an <i>in vitro</i> culture in vaginal simulative medium (VSM). The presence of lactic acid in VSM (VSM+LA) increased <i>C. albicans</i> proliferation, hyphal length, and its ability to cause damage during subsequent infection of vaginal epithelial cells. The cell wall of <i>C. albicans</i> cells grown in VSM+LA displayed a robust mannan fibrillar structure, β-glucan exposure, and low chitin content. These cell wall changes were associated with altered immune responses and an increased ability of the fungus to induce trained immunity. Neutrophils were compromised in clearing <i>C. albicans</i> grown in VSM+LA conditions, despite mounting stronger oxidative responses. Collectively, we found that fungal adaptation to lactic acid in a vaginal simulative context increases its immunogenicity favouring a pro-inflammatory state. This potentially contributes to the immune response dysregulation and neutrophil recruitment observed during recurrent VVC.
DOI: 10.6084/m9.figshare.29041329
title: Combining whole genome and transcriptome sequencing to analyze the pathogenic mechanism of <i>Diplodia sapinea</i> blight in <i>Pinus sylvestris</i> var. <i>mongolica</i> Litv.

description: <i>Diplodia sapinea</i> (= <i>Sphaeropsis sapinea</i>) is an opportunistic pathogen that usually lives in symbiosis (the coexistence of dissimilar organisms) with its host and can cause disease under extreme climatic or physiological stress. In this study, we generated a high-quality genome map of <i>D. sapinea</i> using PacBio Circular Consensus Sequencing (CCS) technology and analysed the key disease-causing genes of <i>D. sapinea</i> by RNA sequencing (RNA-seq). In the study, a number of cell wall degrading enzyme genes were identified to be up-regulated during pathogen infection, which may be involved in biotic stress response in <i>P. sylvestris</i> var. <i>mongolica</i> Litv. It was also found that the expression of antioxidant-related genes, such as those involved in carotenoid biosynthesis, ascorbate and glutathione metabolism, was up-regulated in the <i>P. s</i>. var. <i>mongolica</i> Litv. after fungus infection. Differently expressed genes (DEGs) -based protein-protein interaction (PPI) network was constructed that included 163 pairs of significantly positively correlated proteins, forming three highly interacting gene clusters, and the PPI network was predicted to be associated with the replication and propagation processes of the fungus. These results provide important information for understanding the pathogenic mechanisms of <i>Diplodia</i> tip blight and developing control strategies in <i>P. s</i>. var. <i>mongolica</i> Litv.
DOI: 10.6084/m9.figshare.29041329.v1
title: Combining whole genome and transcriptome sequencing to analyze the pathogenic mechanism of <i>Diplodia sapinea</i> blight in <i>Pinus sylvestris</i> var. <i>mongolica</i> Litv.

description: <i>Diplodia sapinea</i> (= <i>Sphaeropsis sapinea</i>) is an opportunistic pathogen that usually lives in symbiosis (the coexistence of dissimilar organisms) with its host and can cause disease under extreme climatic or physiological stress. In this study, we generated a high-quality genome map of <i>D. sapinea</i> using PacBio Circular Consensus Sequencing (CCS) technology and analysed the key disease-causing genes of <i>D. sapinea</i> by RNA sequencing (RNA-seq). In the study, a number of cell wall degrading enzyme genes were identified to be up-regulated during pathogen infection, which may be involved in biotic stress response in <i>P. sylvestris</i> var. <i>mongolica</i> Litv. It was also found that the expression of antioxidant-related genes, such as those involved in carotenoid biosynthesis, ascorbate and glutathione metabolism, was up-regulated in the <i>P. s</i>. var. <i>mongolica</i> Litv. after fungus infection. Differently expressed genes (DEGs) -based protein-protein interaction (PPI) network was constructed that included 163 pairs of significantly positively correlated proteins, forming three highly interacting gene clusters, and the PPI network was predicted to be associated with the replication and propagation processes of the fungus. These results provide important information for understanding the pathogenic mechanisms of <i>Diplodia</i> tip blight and developing control strategies in <i>P. s</i>. var. <i>mongolica</i> Litv.
DOI: 10.6084/m9.figshare.30158630.v1
title: The phenol-2-monooxygenase FgPhm1 regulates DON synthesis, pathogenicity and environmental stress response in <i>fusarium graminearum</i>

description: <i>Fusarium graminearum</i> is a devastating plant pathogenic fungus that produces mycotoxins and is the predominant pathogen causing Fusarium head blight. Phenol-2-monooxygenase is an oxidoreductase that is responsible for the conversion of phenol to catechol. However, the role of phenol-2-monooxygenase in filamentous fungi remains unclear. This study showed that the deletion of the phenol-2-monooxygenase gene <i>FgPHM1</i> leads to defects in vegetative growth, conidia production, sexual reproduction, and plant infection. FgPhm1 is localized to the nucleoplasm and regulates DON production. In addition, FgPhm1 is required for the formation of toxisomes and regulates the expression of <i>TRI</i> genes. RNA-seq analysis showed that the differentially expressed genes in the mutant were enriched in secondary metabolite biosynthesis, carbon metabolism, and pyruvate metabolism. Interestingly, the <i>FgPHM1</i> deletion mutant was tolerant to phenol stress, whereas it was sensitive to catechol and oxidative stress. FgPhm1 is required for reactive oxygen species production in <i>F. graminearum</i>, and the expression level of <i>FgPHM1</i> gene is induced by H<sub>2</sub>O<sub>2</sub>. Moreover, FgPhm1 regulates autophagy in <i>F. graminearum</i> under nitrogen starvation or rapamycin treatment in <i>F. graminearum</i>. Taken together, this study demonstrated that FgPhm1 is essential for the development and production of DON and plays important roles in the pathogenicity and stress response of <i>F. graminearum</i>, and RNA-seq revealed that FgPhm1 was involved in the biosynthesis of secondary metabolites in <i>F. graminearum</i>.
DOI: 10.15468/dl.c6rsy7
title: Occurrence Download

description: A dataset containing 150 species occurrences available in GBIF matching the query:
{
 "and" : [
 "OccurrenceStatus is Present",
 "TaxonKey is Trachykele blondeli",
 "Year 2000-2026"
 ]
}

 The dataset includes 150 records from 3 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003550-260120142942310/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.28646388
title: Gut microbiome composition and metabolic activity in metabolic-associated fatty liver disease

description: Metabolic Associated Fatty Liver Disease (MAFLD) impacts approximately 25% of the global population. Between April 2023 and July 2023, 60 patients with MAFLD, along with 60 age, ethnicity, and sex-matched healthy controls (HCs), were enrolled from the Inner Mongolia Autonomous Region, China. Analysis of gut microbiota composition and plasma metabolic profiles was conducted using metagenome sequencing and LC-MS. LEfSe analysis identified five pivotal species: Eubacterium rectale, Dialister invisus, Pseudoruminococcus massiliensis, GGB3278 SGB4328, and Ruminococcaceae bacteria. In subgroup analysis, Eubacterium rectale tended to increase by more than 2 times and more than double in the non-obese MAFLD group, and MAFLD with moderate hepatic steatosis (HS), respectively. Plasma samples identified 172 metabolites mainly composed of fatty acid metabolites such as propionic acid and butyric acid analogues. Ruminococcaceae bacteria have a strong positive correlation with β-alanine, uric acid, and L-valine. Pseudoruminococcus massiliensis has a strong positive correlation with β-alanine. Combinations of phenomics and metabolomics yielded the highest accuracy (AUC = 0.97) in the MAFLD diagnosis. Combinations of phenomics and metagenomics yielded the highest accuracy (AUC = 0.94) in the prediction of the MAFLD HS progress. Increases in Eubacterium rectale and decreases in Dialister invisus seem to be indicative of MAFLD patients. Eubacterium rectale may predict HS degree of MAFLD and play an important role in the development of non-obese MAFLD. Eubacterium rectale can generate more propionic acid and butyric acid analogues to absorb energy and increase lipid synthesis and ultimately cause MAFLD.
DOI: 10.6084/m9.figshare.28646388.v2
title: Gut microbiome composition and metabolic activity in metabolic-associated fatty liver disease

description: Metabolic Associated Fatty Liver Disease (MAFLD) impacts approximately 25% of the global population. Between April 2023 and July 2023, 60 patients with MAFLD, along with 60 age, ethnicity, and sex-matched healthy controls (HCs), were enrolled from the Inner Mongolia Autonomous Region, China. Analysis of gut microbiota composition and plasma metabolic profiles was conducted using metagenome sequencing and LC-MS. LEfSe analysis identified five pivotal species: Eubacterium rectale, Dialister invisus, Pseudoruminococcus massiliensis, GGB3278 SGB4328, and Ruminococcaceae bacteria. In subgroup analysis, Eubacterium rectale tended to increase by more than 2 times and more than double in the non-obese MAFLD group, and MAFLD with moderate hepatic steatosis (HS), respectively. Plasma samples identified 172 metabolites mainly composed of fatty acid metabolites such as propionic acid and butyric acid analogues. Ruminococcaceae bacteria have a strong positive correlation with β-alanine, uric acid, and L-valine. Pseudoruminococcus massiliensis has a strong positive correlation with β-alanine. Combinations of phenomics and metabolomics yielded the highest accuracy (AUC = 0.97) in the MAFLD diagnosis. Combinations of phenomics and metagenomics yielded the highest accuracy (AUC = 0.94) in the prediction of the MAFLD HS progress. Increases in Eubacterium rectale and decreases in Dialister invisus seem to be indicative of MAFLD patients. Eubacterium rectale may predict HS degree of MAFLD and play an important role in the development of non-obese MAFLD. Eubacterium rectale can generate more propionic acid and butyric acid analogues to absorb energy and increase lipid synthesis and ultimately cause MAFLD.
DOI: 10.6084/m9.figshare.30666963
title: Mss2 shapes the virulence of <i>Candida albicans</i> through reactive oxygen species (ROS) and calcium signaling, independent of direct transcriptional control

description: Mitochondrial function is essential for virulence in <i>Candida albicans</i>, yet the mechanism by which mitochondria influence pathogenesis remains largely undefined. Here, we reveal that the mitochondrial-associated factor Mss2 controls invasive growth through the regulation of calcium–reactive oxygen species (ROS) homeostasis. Deletion of <i>MSS2</i> results in impaired invasive growth on solid media without affecting hyphal formation in liquid media, indicating that Mss2 controls contact-specific responses. We demonstrate that the regulation of these processes by Mss2 is linked to the regulation of cytosolic calcium levels and cellular ROS production. Furthermore, transcriptomic profiling identified <i>MSS2</i>-regulated genes, including <i>UME6</i>, <i>SAC1</i>, <i>RIM8</i>, and <i>ORF19.1841</i>, whose expression is dependent on calcium and ROS levels. Restoration of invasive phenotypes through exogenous ROS confirms the functional significance of this calcium-ROS circuit. In systemic infection models, similar to <i>mss2Δ</i>, the Mss2 downstream genes exhibit severe virulence defects. Together, this work is the first to show that mitochondrial regulation of a coordinated calcium-ROS circuit is required for invasive hyphal growth and virulence in <i>C. albicans</i>. These findings refine our understanding of fungal invasion and virulence and reveal that targeting mitochondrial signaling could be an important area for antifungal therapeutic interventions.
DOI: 10.6084/m9.figshare.30666963.v1
title: Mss2 shapes the virulence of <i>Candida albicans</i> through reactive oxygen species (ROS) and calcium signaling, independent of direct transcriptional control

description: Mitochondrial function is essential for virulence in <i>Candida albicans</i>, yet the mechanism by which mitochondria influence pathogenesis remains largely undefined. Here, we reveal that the mitochondrial-associated factor Mss2 controls invasive growth through the regulation of calcium–reactive oxygen species (ROS) homeostasis. Deletion of <i>MSS2</i> results in impaired invasive growth on solid media without affecting hyphal formation in liquid media, indicating that Mss2 controls contact-specific responses. We demonstrate that the regulation of these processes by Mss2 is linked to the regulation of cytosolic calcium levels and cellular ROS production. Furthermore, transcriptomic profiling identified <i>MSS2</i>-regulated genes, including <i>UME6</i>, <i>SAC1</i>, <i>RIM8</i>, and <i>ORF19.1841</i>, whose expression is dependent on calcium and ROS levels. Restoration of invasive phenotypes through exogenous ROS confirms the functional significance of this calcium-ROS circuit. In systemic infection models, similar to <i>mss2Δ</i>, the Mss2 downstream genes exhibit severe virulence defects. Together, this work is the first to show that mitochondrial regulation of a coordinated calcium-ROS circuit is required for invasive hyphal growth and virulence in <i>C. albicans</i>. These findings refine our understanding of fungal invasion and virulence and reveal that targeting mitochondrial signaling could be an important area for antifungal therapeutic interventions.