cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.15468/dl.7z2whk
title: Occurrence Download

description: A dataset containing 208 species occurrences available in GBIF matching the query:
{
 "and" : [
 "OccurrenceStatus is Present",
 "TaxonKey is Galidia elegans",
 "Year 1985-2026"
 ]
}

 The dataset includes 208 records from 8 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003547-260120142942310/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.5281/zenodo.18331219
title: dentatherina_merceri_zanfona_1.fasta.gz
DOI: 10.5281/zenodo.18331220
title: dentatherina_merceri_zanfona_1.fasta.gz
DOI: 10.6084/m9.figshare.28216618
title: Decarboxylase mediated oxalic acid metabolism is important to antioxidation and detoxification rather than pathogenicity in <i>Magnaporthe oryzae</i>

description: Oxalic acid (OA), an essential pathogenic factor, has been identified in several plant pathogens, and researchers are currently pursuing studies on interference with OA metabolism as a treatment for related diseases. However, the metabolic route in <i>Magnaporthe oryzae</i> remains unknown. In this study, we describe D-erythroascorbic acid-mediated OA synthesis and its metabolic and clearance pathways in rice blast fungus. By knocking out the D-arabino-1,4-lactone oxidase gene (<i>Moalo1</i>), one-third of oxalic acid remained in <i>M. oryzae</i>, indicating a main pathway for oxalic acid production. <i>M. oryzae</i> OxdC (MoOxdC) is an oxalate decarboxylase that appears to play a role in relieving oxalic acid toxicity. Loss of <i>Mooxdc</i> does not affect mycelial growth, conidiophore development, or appressorium formation in <i>M. oryzae</i>; however, the antioxidant and pathogenic abilities of the mutant were enhanced. This is owing to <i>Mooxdc</i> deletion upregulated a series of OA metabolic genes, including the oxalate oxidase gene (<i>Mooxo</i>) and <i>Moalo1</i>, as well as both OA transporter genes. Simultaneously, as feedback to the tricarboxylic acid (TCA) cycle, the decrease of formic acid in Δ<i>Mooxdc</i> leads to the reduction of acetyl-CoA content, and two genes involved in the β-oxidation of fatty acids were also upregulated, which enhanced the fatty acid metabolism of the Δ<i>Mooxdc</i>. Overall, this work reveals the role of OA in <i>M. oryzae</i>. We found that OA metabolism was mainly involved in the growth and development of <i>M. oryzae</i>, OA as a byproduct of D-erythroascorbic acid after removing H<sub>2</sub>O<sub>2</sub>, the OA-associated pathway ensures the TCA process and ATP supply.
DOI: 10.6084/m9.figshare.28216618.v2
title: Decarboxylase mediated oxalic acid metabolism is important to antioxidation and detoxification rather than pathogenicity in <i>Magnaporthe oryzae</i>

description: Oxalic acid (OA), an essential pathogenic factor, has been identified in several plant pathogens, and researchers are currently pursuing studies on interference with OA metabolism as a treatment for related diseases. However, the metabolic route in <i>Magnaporthe oryzae</i> remains unknown. In this study, we describe D-erythroascorbic acid-mediated OA synthesis and its metabolic and clearance pathways in rice blast fungus. By knocking out the D-arabino-1,4-lactone oxidase gene (<i>Moalo1</i>), one-third of oxalic acid remained in <i>M. oryzae</i>, indicating a main pathway for oxalic acid production. <i>M. oryzae</i> OxdC (MoOxdC) is an oxalate decarboxylase that appears to play a role in relieving oxalic acid toxicity. Loss of <i>Mooxdc</i> does not affect mycelial growth, conidiophore development, or appressorium formation in <i>M. oryzae</i>; however, the antioxidant and pathogenic abilities of the mutant were enhanced. This is owing to <i>Mooxdc</i> deletion upregulated a series of OA metabolic genes, including the oxalate oxidase gene (<i>Mooxo</i>) and <i>Moalo1</i>, as well as both OA transporter genes. Simultaneously, as feedback to the tricarboxylic acid (TCA) cycle, the decrease of formic acid in Δ<i>Mooxdc</i> leads to the reduction of acetyl-CoA content, and two genes involved in the β-oxidation of fatty acids were also upregulated, which enhanced the fatty acid metabolism of the Δ<i>Mooxdc</i>. Overall, this work reveals the role of OA in <i>M. oryzae</i>. We found that OA metabolism was mainly involved in the growth and development of <i>M. oryzae</i>, OA as a byproduct of D-erythroascorbic acid after removing H<sub>2</sub>O<sub>2</sub>, the OA-associated pathway ensures the TCA process and ATP supply.
DOI: 10.6084/m9.figshare.28216618.v1
title: <i>Importance of oxalic acid to antioxidation and detoxification in M. oryzae, not to pathogenicity in M.Oryzae</i>Decarboxylase mediated oxalic acid metabolism is important to antioxidation and detoxification rather than pathogenicity in <i>magnaporthe oryzae</i>

description: Oxalic acid (OA), an essential pathogenic factor, has been identified in several plant pathogens, and researchers are currently pursuing studies on interference with OA metabolism as a treatment for related diseases. However, the metabolic route in <i>Magnaporthe oryzae</i> remains unknown. In this study, we describe D-erythroascorbic acid-mediated OA synthesis and its metabolic and clearance pathways in rice blast fungus. By knocking out the D-arabino-1,4-lactone oxidase gene (<i>Moalo1</i>), one-third of oxalic acid remained in <i>M. oryzae</i>, indicating a main pathway for oxalic acid production. <i>M. oryzae</i> OxdC (MoOxdC) is an oxalate decarboxylase that appears to play a role in relieving oxalic acid toxicity. Loss of <i>Mooxdc</i> does not affect mycelial growth, conidiophore development, or appressorium formation in <i>M. oryzae</i>; however, the antioxidant and pathogenic abilities of the mutant were enhanced. This is owing to <i>Mooxdc</i> deletion upregulated a series of OA metabolic genes, including the oxalate oxidase gene (<i>Mooxo</i>) and <i>Moalo1</i>, as well as both OA transporter genes. Simultaneously, as feedback to the tricarboxylic acid (TCA) cycle, the decrease of formic acid in Δ<i>Mooxdc</i> leads to the reduction of acetyl-CoA content, and two genes involved in the β-oxidation of fatty acids were also upregulated, which enhanced the fatty acid metabolism of the Δ<i>Mooxdc</i>. Overall, this work reveals the role of OA in <i>M. oryzae</i>. We found that OA metabolism was mainly involved in the growth and development of <i>M. oryzae</i>, OA as a byproduct of D-erythroascorbic acid after removing H<sub>2</sub>O<sub>2</sub>, the OA-associated pathway ensures the TCA process and ATP supply.
DOI: 10.6084/m9.figshare.30273826
title: Stem cell-derived brain-like endothelial cells to interrogate <i>Streptococcus pneumoniae</i> interaction with brain endothelium

description: <i>Streptococcus pneumoniae</i> (pneumococcus) is an opportunistic pathogen that remains the leading cause of bacterial meningitis worldwide. For meningitis to occur, pneumococcus must breach the blood-brain barrier (BBB), a highly specialized network of brain endothelial cells that comprise the microvasculature of the brain. Here, we report the use of human induced pluripotent stem cell-derived brain-like endothelial cells (iBECs) to model the BBB during pneumococcal infection. iBECs were infected with the <i>S. pneumoniae</i> strain TIGR4. Adherence assays showed that pneumococcal adherence to iBECs was a saturable process. Moreover, deletion of two pneumococcal adhesins resulted in an adherence defect, supporting a receptor-mediated interaction between pneumococcus and iBECs. Next, the integrity of several tight junction components was assessed via western blot and RT-qPCR, revealing the loss of abundance and expression in iBECs during infection with pneumococcus. Simultaneously, the expression of <i>VEGFA</i> and the tight junction repressor <i>SNAI1</i> was upregulated. Semi-automated analysis of junction images also demonstrated a loss of ZO-1 and occludin continuity during pneumococcal infection. Consistent with these findings, the loss of TEER and the increase in barrier permeability were observed in pneumococcus-infected iBECs. The toxin pneumolysin (Ply) was important for this disruption, as the loss of Ply in pneumococcus partially arrested the reduction of TEER and the increase in permeability. Finally, RT-qPCR showed that pneumococcus was sufficient to upregulate a panel of inflammatory cytokines in iBECs. Taken together, these findings show that pneumococcus interacts with and disrupts iBECs during infection, supporting iBECs as an important model for studying pneumococcus-BBB interactions.
DOI: 10.6084/m9.figshare.30273826.v1
title: Stem cell-derived brain-like endothelial cells to interrogate <i>Streptococcus pneumoniae</i> interaction with brain endothelium

description: <i>Streptococcus pneumoniae</i> (pneumococcus) is an opportunistic pathogen that remains the leading cause of bacterial meningitis worldwide. For meningitis to occur, pneumococcus must breach the blood-brain barrier (BBB), a highly specialized network of brain endothelial cells that comprise the microvasculature of the brain. Here, we report the use of human induced pluripotent stem cell-derived brain-like endothelial cells (iBECs) to model the BBB during pneumococcal infection. iBECs were infected with the <i>S. pneumoniae</i> strain TIGR4. Adherence assays showed that pneumococcal adherence to iBECs was a saturable process. Moreover, deletion of two pneumococcal adhesins resulted in an adherence defect, supporting a receptor-mediated interaction between pneumococcus and iBECs. Next, the integrity of several tight junction components was assessed via western blot and RT-qPCR, revealing the loss of abundance and expression in iBECs during infection with pneumococcus. Simultaneously, the expression of <i>VEGFA</i> and the tight junction repressor <i>SNAI1</i> was upregulated. Semi-automated analysis of junction images also demonstrated a loss of ZO-1 and occludin continuity during pneumococcal infection. Consistent with these findings, the loss of TEER and the increase in barrier permeability were observed in pneumococcus-infected iBECs. The toxin pneumolysin (Ply) was important for this disruption, as the loss of Ply in pneumococcus partially arrested the reduction of TEER and the increase in permeability. Finally, RT-qPCR showed that pneumococcus was sufficient to upregulate a panel of inflammatory cytokines in iBECs. Taken together, these findings show that pneumococcus interacts with and disrupts iBECs during infection, supporting iBECs as an important model for studying pneumococcus-BBB interactions.
DOI: 10.6084/m9.figshare.30460203.v1
title: Culture breakthrough enables goose circovirus (GoCV) isolation and pathogenic gosling modeling to uncover the association between viral infection and vaccine failure

description: Goose circovirus (GoCV), recognized as the most economically significant immunosuppressive pathogen in global waterfowl production, causes considerable economic losses annually, and multiprovincial surveillance studies have documented high seroprevalence rates. The critical barrier to combating GoCV has persisted in the complete absence of viable in vitro culture systems, fundamentally limiting pathogenesis studies and vaccine development. In a breakthrough advancement, this study pioneers the first successful establishment of a stable primary goose embryo kidney (GEK) cell culture system for GoCV propagation, achieving sustained viral replication through innovative culture protocol optimization. Comprehensive virological characterization via synchronized growth curve analysis, transmission electron microscopy, and IFA quantification not only confirms efficient viral proliferation but also resolves longstanding debates regarding the intracellular replication mechanisms of GoCV, termed GoCV/369/2020. Pathogenesis trials involving gosling with the novel isolated GoCV revealed unprecedented clinicopathological correlations, revealing severe growth retardation, feather disorders, persistent fecal shedding, and biphasic organ damage progression from acute hypertrophy to chronic atrophy. Most critically, we provide the first experimental evidence linking GoCV infection to catastrophic vaccine failure, showing reductions in the antibody titers of avian influenza virus and Newcastle disease virus. This breakthrough has led to the establishment of poultry industry solutions, such as standardized viral isolation for diagnostics, optimized vaccination schedules, and targeted biosecurity against fecal-oral transmission. This study established a stable in vitro culture system and a pathogenic gosling model for GoCV, elucidating its replication, pathogenesis, and vaccine interference, providing crucial insights for future research and control strategies.
DOI: 10.6084/m9.figshare.29932152
title: Isopropyl paraben targets type III secretion to inhibit <i>Salmonella enterica</i> serovar typhimurium infection

description: <i>Salmonella enterica</i>, a food- and water-borne pathogen, triggers food poisoning and enteric infections. The effectiveness of antibiotics against <i>Salmonella</i> infections is decreasing due to bacterial resistance. Developing novel antimicrobial agents is crucial and urgent. Here, we screened 550 natural compounds and found that isopropyl paraben (IPPB) effectively inhibited <i>Salmonella enterica</i> serovar Typhimurium (ST) invasion of host cells without impacting bacterial growth, reducing the risk of developing bacterial resistance. Further investigation revealed that IPPB bound to the regulatory protein HilD and inhibited the transcription of the type III protein secretion system 1 (T3SS–1) regulatory genes <i>hilD</i>, <i>hilC</i> and <i>rtsA</i>. This interference blocked the production of T3SS–1 effectors. Importantly, IPPB exerted certain therapeutic effects on both <i>G. mellonella</i> larvae and murine models infected with ST and improved the ST-induced gut microbiota dysbiosis in mice. These findings suggest that IPPB has potential as a novel antimicrobial agent, targeting the T3SS–1 of <i>Salmonella</i>.
DOI: 10.6084/m9.figshare.29932152.v2
title: Isopropyl paraben targets type III secretion to inhibit <i>Salmonella enterica</i> serovar typhimurium infection

description: <i>Salmonella enterica</i>, a food- and water-borne pathogen, triggers food poisoning and enteric infections. The effectiveness of antibiotics against <i>Salmonella</i> infections is decreasing due to bacterial resistance. Developing novel antimicrobial agents is crucial and urgent. Here, we screened 550 natural compounds and found that isopropyl paraben (IPPB) effectively inhibited <i>Salmonella enterica</i> serovar Typhimurium (ST) invasion of host cells without impacting bacterial growth, reducing the risk of developing bacterial resistance. Further investigation revealed that IPPB bound to the regulatory protein HilD and inhibited the transcription of the type III protein secretion system 1 (T3SS–1) regulatory genes <i>hilD</i>, <i>hilC</i> and <i>rtsA</i>. This interference blocked the production of T3SS–1 effectors. Importantly, IPPB exerted certain therapeutic effects on both <i>G. mellonella</i> larvae and murine models infected with ST and improved the ST-induced gut microbiota dysbiosis in mice. These findings suggest that IPPB has potential as a novel antimicrobial agent, targeting the T3SS–1 of <i>Salmonella</i>.
DOI: 10.6084/m9.figshare.30460203
title: Culture breakthrough enables goose circovirus (GoCV) isolation and pathogenic gosling modeling to uncover the association between viral infection and vaccine failure

description: Goose circovirus (GoCV), recognized as the most economically significant immunosuppressive pathogen in global waterfowl production, causes considerable economic losses annually, and multiprovincial surveillance studies have documented high seroprevalence rates. The critical barrier to combating GoCV has persisted in the complete absence of viable in vitro culture systems, fundamentally limiting pathogenesis studies and vaccine development. In a breakthrough advancement, this study pioneers the first successful establishment of a stable primary goose embryo kidney (GEK) cell culture system for GoCV propagation, achieving sustained viral replication through innovative culture protocol optimization. Comprehensive virological characterization via synchronized growth curve analysis, transmission electron microscopy, and IFA quantification not only confirms efficient viral proliferation but also resolves longstanding debates regarding the intracellular replication mechanisms of GoCV, termed GoCV/369/2020. Pathogenesis trials involving gosling with the novel isolated GoCV revealed unprecedented clinicopathological correlations, revealing severe growth retardation, feather disorders, persistent fecal shedding, and biphasic organ damage progression from acute hypertrophy to chronic atrophy. Most critically, we provide the first experimental evidence linking GoCV infection to catastrophic vaccine failure, showing reductions in the antibody titers of avian influenza virus and Newcastle disease virus. This breakthrough has led to the establishment of poultry industry solutions, such as standardized viral isolation for diagnostics, optimized vaccination schedules, and targeted biosecurity against fecal-oral transmission. This study established a stable in vitro culture system and a pathogenic gosling model for GoCV, elucidating its replication, pathogenesis, and vaccine interference, providing crucial insights for future research and control strategies.
DOI: 10.6084/m9.figshare.28229358
title: Excessive activation of JAK-STAT signaling contributes to inflammation induced by acute <i>Vibrio</i> infection in shrimp

description: Uncontrolled immune responses resulting from overactivated cellular signaling pathways, leading to inflammation and tissue injury, are a major cause of death in pathogen-infected individuals. This phenomenon has been well studied in mammals but is less explored in invertebrates. Bacteria of the genus <i>Vibrio</i> are among the most harmful pathogens to humans and aquatic animals. In shrimp, <i>Vibrio</i> infection is generally characterized by the sudden onset of disease, with pathological signs of opaque and whitish muscle tissue. The current study shows that shrimp acutely infected with high dose of <i>Vibrio parahaemolyticus</i> develop inflammation-like pathological changes, leading to rapid death. Excessive activation of JAK-STAT signaling, rather than the Dorsal and Relish pathways, results in overactivation of shrimp immunity and is a major cause of inflammation induced by acute <i>Vibrio</i> infection. Weakening JAK-STAT signaling attenuates the inflammatory response and reduces mortality caused by acute <i>Vibrio</i> infection in shrimp, whereas enhancing JAK-STAT signaling can convert a normal infection into an acute one, accelerating shrimp death. Therefore, this study indicates that, similar to that in mammals, the pathogenesis of infectious diseases in invertebrates is complicated by inflammatory responses triggered by dysregulated immune signaling.
DOI: 10.6084/m9.figshare.28229358.v1
title: Excessive activation of JAK-STAT signaling contributes to inflammation induced by acute <i>Vibrio</i> infection in shrimp

description: Uncontrolled immune responses resulting from overactivated cellular signaling pathways, leading to inflammation and tissue injury, are a major cause of death in pathogen-infected individuals. This phenomenon has been well studied in mammals but is less explored in invertebrates. Bacteria of the genus <i>Vibrio</i> are among the most harmful pathogens to humans and aquatic animals. In shrimp, <i>Vibrio</i> infection is generally characterized by the sudden onset of disease, with pathological signs of opaque and whitish muscle tissue. The current study shows that shrimp acutely infected with high dose of <i>Vibrio parahaemolyticus</i> develop inflammation-like pathological changes, leading to rapid death. Excessive activation of JAK-STAT signaling, rather than the Dorsal and Relish pathways, results in overactivation of shrimp immunity and is a major cause of inflammation induced by acute <i>Vibrio</i> infection. Weakening JAK-STAT signaling attenuates the inflammatory response and reduces mortality caused by acute <i>Vibrio</i> infection in shrimp, whereas enhancing JAK-STAT signaling can convert a normal infection into an acute one, accelerating shrimp death. Therefore, this study indicates that, similar to that in mammals, the pathogenesis of infectious diseases in invertebrates is complicated by inflammatory responses triggered by dysregulated immune signaling.
DOI: 10.6084/m9.figshare.29627546
title: Amino acid mutations of porcine circovirus type 2 (PCV2) capsid protein increase virus binding to host and evade immune responses: An evaluation of viral evolution

description: Porcine circovirus type 2 (PCV2), the causative agent of porcine circovirus-associated diseases (PCVAD), has caused huge economic losses in the swine industry. Despite a worldwide disease distribution and numerous reports of the field epidemiology of PCV2, the molecular epidemiology and genetic evolution of PCV2 are not well characterized. In this study, 72 complete genomes of PCV2 strains sequenced from 2016 to 2022 in China were produced; phylogenetic analyses demonstrated three genotypes (PCV2a, PCV2b, and PCV2d). Strains PCV2b and PCV2d were equally represented (30/72, 41.6%) whereas the remainder were PCV2a strains (12/72, 16.6%). Therefore, PCV2b and PCV2d have become dominant genotypes in China. Based on the 1682 capsid protein (Cap) sequences, 27 high-frequency amino acid mutations occurred in Cap, with 18 of 27 mutated amino acids exposed on the capsid surface. That amino acid mutations with increasing positively charged polar amino acids occurred on the capsid surface implied PCV2 may have evolved to better adapt to hosts by enhancing the binding capacity of PCV2 to negatively charged cell receptors. Moreover, these mutations probably enable PCV2 to evade host immune responses by changing epitope antigenicity and decreasing epitope accessibility to the immune system. This study characterized the genotypic evolution of PCV2 and assessed the adaptive value of viral mutations in evading host defences, providing powerful insights to elucidate potential mechanisms of immune evasion and evidence to inform effective prevention and control strategies.
DOI: 10.6084/m9.figshare.29627546.v1
title: Amino acid mutations of porcine circovirus type 2 (PCV2) capsid protein increase virus binding to host and evade immune responses: An evaluation of viral evolution

description: Porcine circovirus type 2 (PCV2), the causative agent of porcine circovirus-associated diseases (PCVAD), has caused huge economic losses in the swine industry. Despite a worldwide disease distribution and numerous reports of the field epidemiology of PCV2, the molecular epidemiology and genetic evolution of PCV2 are not well characterized. In this study, 72 complete genomes of PCV2 strains sequenced from 2016 to 2022 in China were produced; phylogenetic analyses demonstrated three genotypes (PCV2a, PCV2b, and PCV2d). Strains PCV2b and PCV2d were equally represented (30/72, 41.6%) whereas the remainder were PCV2a strains (12/72, 16.6%). Therefore, PCV2b and PCV2d have become dominant genotypes in China. Based on the 1682 capsid protein (Cap) sequences, 27 high-frequency amino acid mutations occurred in Cap, with 18 of 27 mutated amino acids exposed on the capsid surface. That amino acid mutations with increasing positively charged polar amino acids occurred on the capsid surface implied PCV2 may have evolved to better adapt to hosts by enhancing the binding capacity of PCV2 to negatively charged cell receptors. Moreover, these mutations probably enable PCV2 to evade host immune responses by changing epitope antigenicity and decreasing epitope accessibility to the immune system. This study characterized the genotypic evolution of PCV2 and assessed the adaptive value of viral mutations in evading host defences, providing powerful insights to elucidate potential mechanisms of immune evasion and evidence to inform effective prevention and control strategies.