cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.29433995.v1
title: WTD2_2.fastqDivergent Roles of hcp Genes in Salmonella Typhimurium T6SS Shape Gut Microbiota Dysbiosis during InfectionT6SS

description:   
<em>Salmonella enterica </em>subsp.<em> enterica </em>serovar Typhimurium (<em>S. </em>Typhimurium) is a facultative intracellular pathogen causing significant gastrointestinal infections in humans and animals. The type VI secretion system (T6SS) plays a crucial role in its virulence, facilitating competition with host gut microbiota and promoting infection. While <em>S.</em> Typhimurium possesses a single T6SS, it encodes three <em>hcp</em> genes, which are crucial for its functionality and may exhibit non-redundant roles. In this study, we used 16S rRNA sequencing to analyze gut microbiota in BALB/c mice after infection with wild-type (WT) <em>S.</em> Typhimurium or mutant strains (Δ<em>hcp1</em>, Δ<em>hcp2</em>, Δ<em>hcp3</em>). Our findings revealed that <em>S</em>. Typhimurium infection induced severe gut dysbiosis especially on the second day post-infection. Specifically, the infection led to a notable increase in Firmicutes and activated the energy pathways that promotes the breakdown of short chain fatty acids. Wild type <em>S.</em> Typhimurium infection caused a sharp increase in <em>Escherichia-Shigella</em> levels, indicating inflammation-related dysbiosis, while the Δ<em>hcp</em>1, Δ<em>hcp</em>2, and Δ<em>hcp</em>3 groups showed milder changes, suggesting less disruption to gut microbiota. Deletion of individual <em>hcp</em> genes led to distinct bacterial taxa changes, underscoring the non-redundant functions of each <em>hcp</em>. Despite having only one T6SS, <em>S.</em> Typhimurium achieves precise modulation of its functions through the divergent roles of its Hcp proteins, enabling efficient colonization and persistence in the host gut.  These findings provide insights into the intricate mechanisms of bacterial adaptation and host-pathogen interactions, offering potential avenues for therapeutic interventions targeting T6SS-mediated dysbiosis.
DOI: 10.6084/m9.figshare.29433998
title: 2D5_1.fastqDivergent Roles of hcp Genes in Salmonella Typhimurium T6SS Shape Gut Microbiota Dysbiosis during InfectionT6SS

description:   
<em>Salmonella enterica </em>subsp.<em> enterica </em>serovar Typhimurium (<em>S. </em>Typhimurium) is a facultative intracellular pathogen causing significant gastrointestinal infections in humans and animals. The type VI secretion system (T6SS) plays a crucial role in its virulence, facilitating competition with host gut microbiota and promoting infection. While <em>S.</em> Typhimurium possesses a single T6SS, it encodes three <em>hcp</em> genes, which are crucial for its functionality and may exhibit non-redundant roles. In this study, we used 16S rRNA sequencing to analyze gut microbiota in BALB/c mice after infection with wild-type (WT) <em>S.</em> Typhimurium or mutant strains (Δ<em>hcp1</em>, Δ<em>hcp2</em>, Δ<em>hcp3</em>). Our findings revealed that <em>S</em>. Typhimurium infection induced severe gut dysbiosis especially on the second day post-infection. Specifically, the infection led to a notable increase in Firmicutes and activated the energy pathways that promotes the breakdown of short chain fatty acids. Wild type <em>S.</em> Typhimurium infection caused a sharp increase in <em>Escherichia-Shigella</em> levels, indicating inflammation-related dysbiosis, while the Δ<em>hcp</em>1, Δ<em>hcp</em>2, and Δ<em>hcp</em>3 groups showed milder changes, suggesting less disruption to gut microbiota. Deletion of individual <em>hcp</em> genes led to distinct bacterial taxa changes, underscoring the non-redundant functions of each <em>hcp</em>. Despite having only one T6SS, <em>S.</em> Typhimurium achieves precise modulation of its functions through the divergent roles of its Hcp proteins, enabling efficient colonization and persistence in the host gut.  These findings provide insights into the intricate mechanisms of bacterial adaptation and host-pathogen interactions, offering potential avenues for therapeutic interventions targeting T6SS-mediated dysbiosis.
DOI: 10.6084/m9.figshare.29433998.v1
title: 2D5_1.fastqDivergent Roles of hcp Genes in Salmonella Typhimurium T6SS Shape Gut Microbiota Dysbiosis during InfectionT6SS

description:   
<em>Salmonella enterica </em>subsp.<em> enterica </em>serovar Typhimurium (<em>S. </em>Typhimurium) is a facultative intracellular pathogen causing significant gastrointestinal infections in humans and animals. The type VI secretion system (T6SS) plays a crucial role in its virulence, facilitating competition with host gut microbiota and promoting infection. While <em>S.</em> Typhimurium possesses a single T6SS, it encodes three <em>hcp</em> genes, which are crucial for its functionality and may exhibit non-redundant roles. In this study, we used 16S rRNA sequencing to analyze gut microbiota in BALB/c mice after infection with wild-type (WT) <em>S.</em> Typhimurium or mutant strains (Δ<em>hcp1</em>, Δ<em>hcp2</em>, Δ<em>hcp3</em>). Our findings revealed that <em>S</em>. Typhimurium infection induced severe gut dysbiosis especially on the second day post-infection. Specifically, the infection led to a notable increase in Firmicutes and activated the energy pathways that promotes the breakdown of short chain fatty acids. Wild type <em>S.</em> Typhimurium infection caused a sharp increase in <em>Escherichia-Shigella</em> levels, indicating inflammation-related dysbiosis, while the Δ<em>hcp</em>1, Δ<em>hcp</em>2, and Δ<em>hcp</em>3 groups showed milder changes, suggesting less disruption to gut microbiota. Deletion of individual <em>hcp</em> genes led to distinct bacterial taxa changes, underscoring the non-redundant functions of each <em>hcp</em>. Despite having only one T6SS, <em>S.</em> Typhimurium achieves precise modulation of its functions through the divergent roles of its Hcp proteins, enabling efficient colonization and persistence in the host gut.  These findings provide insights into the intricate mechanisms of bacterial adaptation and host-pathogen interactions, offering potential avenues for therapeutic interventions targeting T6SS-mediated dysbiosis.
DOI: 10.15468/dl.4wktzz
title: Occurrence Download

description: A dataset containing 1874 species occurrences available in GBIF matching the query:
{
 "and" : [
 "TaxonKey is one of (Ethmalosa fimbriata (Bowdich, 1825))",
 "BasisOfRecord is one of (Specimen, Human Observation, Observation, Machine Observation)",
 "HasCoordinate is true",
 "HasGeospatialIssue is false"
 ]
}

 The dataset includes 1874 records from 31 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0079129-250525065834625/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.29433992.v1
title: 1D2_4.fastqDivergent Roles of hcp Genes in Salmonella Typhimurium T6SS Shape Gut Microbiota Dysbiosis during InfectionT6SS

description:   
<em>Salmonella enterica </em>subsp.<em> enterica </em>serovar Typhimurium (<em>S. </em>Typhimurium) is a facultative intracellular pathogen causing significant gastrointestinal infections in humans and animals. The type VI secretion system (T6SS) plays a crucial role in its virulence, facilitating competition with host gut microbiota and promoting infection. While <em>S.</em> Typhimurium possesses a single T6SS, it encodes three <em>hcp</em> genes, which are crucial for its functionality and may exhibit non-redundant roles. In this study, we used 16S rRNA sequencing to analyze gut microbiota in BALB/c mice after infection with wild-type (WT) <em>S.</em> Typhimurium or mutant strains (Δ<em>hcp1</em>, Δ<em>hcp2</em>, Δ<em>hcp3</em>). Our findings revealed that <em>S</em>. Typhimurium infection induced severe gut dysbiosis especially on the second day post-infection. Specifically, the infection led to a notable increase in Firmicutes and activated the energy pathways that promotes the breakdown of short chain fatty acids. Wild type <em>S.</em> Typhimurium infection caused a sharp increase in <em>Escherichia-Shigella</em> levels, indicating inflammation-related dysbiosis, while the Δ<em>hcp</em>1, Δ<em>hcp</em>2, and Δ<em>hcp</em>3 groups showed milder changes, suggesting less disruption to gut microbiota. Deletion of individual <em>hcp</em> genes led to distinct bacterial taxa changes, underscoring the non-redundant functions of each <em>hcp</em>. Despite having only one T6SS, <em>S.</em> Typhimurium achieves precise modulation of its functions through the divergent roles of its Hcp proteins, enabling efficient colonization and persistence in the host gut.  These findings provide insights into the intricate mechanisms of bacterial adaptation and host-pathogen interactions, offering potential avenues for therapeutic interventions targeting T6SS-mediated dysbiosis.
DOI: 10.6084/m9.figshare.29434001
title: 1D5_2.fastqDivergent Roles of hcp Genes in Salmonella Typhimurium T6SS Shape Gut Microbiota Dysbiosis during InfectionT6SS

description:   
<em>Salmonella enterica </em>subsp.<em> enterica </em>serovar Typhimurium (<em>S. </em>Typhimurium) is a facultative intracellular pathogen causing significant gastrointestinal infections in humans and animals. The type VI secretion system (T6SS) plays a crucial role in its virulence, facilitating competition with host gut microbiota and promoting infection. While <em>S.</em> Typhimurium possesses a single T6SS, it encodes three <em>hcp</em> genes, which are crucial for its functionality and may exhibit non-redundant roles. In this study, we used 16S rRNA sequencing to analyze gut microbiota in BALB/c mice after infection with wild-type (WT) <em>S.</em> Typhimurium or mutant strains (Δ<em>hcp1</em>, Δ<em>hcp2</em>, Δ<em>hcp3</em>). Our findings revealed that <em>S</em>. Typhimurium infection induced severe gut dysbiosis especially on the second day post-infection. Specifically, the infection led to a notable increase in Firmicutes and activated the energy pathways that promotes the breakdown of short chain fatty acids. Wild type <em>S.</em> Typhimurium infection caused a sharp increase in <em>Escherichia-Shigella</em> levels, indicating inflammation-related dysbiosis, while the Δ<em>hcp</em>1, Δ<em>hcp</em>2, and Δ<em>hcp</em>3 groups showed milder changes, suggesting less disruption to gut microbiota. Deletion of individual <em>hcp</em> genes led to distinct bacterial taxa changes, underscoring the non-redundant functions of each <em>hcp</em>. Despite having only one T6SS, <em>S.</em> Typhimurium achieves precise modulation of its functions through the divergent roles of its Hcp proteins, enabling efficient colonization and persistence in the host gut.  These findings provide insights into the intricate mechanisms of bacterial adaptation and host-pathogen interactions, offering potential avenues for therapeutic interventions targeting T6SS-mediated dysbiosis.
DOI: 10.6084/m9.figshare.29434001.v1
title: 1D5_2.fastqDivergent Roles of hcp Genes in Salmonella Typhimurium T6SS Shape Gut Microbiota Dysbiosis during InfectionT6SS

description:   
<em>Salmonella enterica </em>subsp.<em> enterica </em>serovar Typhimurium (<em>S. </em>Typhimurium) is a facultative intracellular pathogen causing significant gastrointestinal infections in humans and animals. The type VI secretion system (T6SS) plays a crucial role in its virulence, facilitating competition with host gut microbiota and promoting infection. While <em>S.</em> Typhimurium possesses a single T6SS, it encodes three <em>hcp</em> genes, which are crucial for its functionality and may exhibit non-redundant roles. In this study, we used 16S rRNA sequencing to analyze gut microbiota in BALB/c mice after infection with wild-type (WT) <em>S.</em> Typhimurium or mutant strains (Δ<em>hcp1</em>, Δ<em>hcp2</em>, Δ<em>hcp3</em>). Our findings revealed that <em>S</em>. Typhimurium infection induced severe gut dysbiosis especially on the second day post-infection. Specifically, the infection led to a notable increase in Firmicutes and activated the energy pathways that promotes the breakdown of short chain fatty acids. Wild type <em>S.</em> Typhimurium infection caused a sharp increase in <em>Escherichia-Shigella</em> levels, indicating inflammation-related dysbiosis, while the Δ<em>hcp</em>1, Δ<em>hcp</em>2, and Δ<em>hcp</em>3 groups showed milder changes, suggesting less disruption to gut microbiota. Deletion of individual <em>hcp</em> genes led to distinct bacterial taxa changes, underscoring the non-redundant functions of each <em>hcp</em>. Despite having only one T6SS, <em>S.</em> Typhimurium achieves precise modulation of its functions through the divergent roles of its Hcp proteins, enabling efficient colonization and persistence in the host gut.  These findings provide insights into the intricate mechanisms of bacterial adaptation and host-pathogen interactions, offering potential avenues for therapeutic interventions targeting T6SS-mediated dysbiosis.
DOI: 10.6084/m9.figshare.29434004
title: 2D5_8.fastqDivergent Roles of hcp Genes in Salmonella Typhimurium T6SS Shape Gut Microbiota Dysbiosis during InfectionT6SS

description:   
<em>Salmonella enterica </em>subsp.<em> enterica </em>serovar Typhimurium (<em>S. </em>Typhimurium) is a facultative intracellular pathogen causing significant gastrointestinal infections in humans and animals. The type VI secretion system (T6SS) plays a crucial role in its virulence, facilitating competition with host gut microbiota and promoting infection. While <em>S.</em> Typhimurium possesses a single T6SS, it encodes three <em>hcp</em> genes, which are crucial for its functionality and may exhibit non-redundant roles. In this study, we used 16S rRNA sequencing to analyze gut microbiota in BALB/c mice after infection with wild-type (WT) <em>S.</em> Typhimurium or mutant strains (Δ<em>hcp1</em>, Δ<em>hcp2</em>, Δ<em>hcp3</em>). Our findings revealed that <em>S</em>. Typhimurium infection induced severe gut dysbiosis especially on the second day post-infection. Specifically, the infection led to a notable increase in Firmicutes and activated the energy pathways that promotes the breakdown of short chain fatty acids. Wild type <em>S.</em> Typhimurium infection caused a sharp increase in <em>Escherichia-Shigella</em> levels, indicating inflammation-related dysbiosis, while the Δ<em>hcp</em>1, Δ<em>hcp</em>2, and Δ<em>hcp</em>3 groups showed milder changes, suggesting less disruption to gut microbiota. Deletion of individual <em>hcp</em> genes led to distinct bacterial taxa changes, underscoring the non-redundant functions of each <em>hcp</em>. Despite having only one T6SS, <em>S.</em> Typhimurium achieves precise modulation of its functions through the divergent roles of its Hcp proteins, enabling efficient colonization and persistence in the host gut.  These findings provide insights into the intricate mechanisms of bacterial adaptation and host-pathogen interactions, offering potential avenues for therapeutic interventions targeting T6SS-mediated dysbiosis.
DOI: 10.6084/m9.figshare.29434004.v1
title: 2D5_8.fastqDivergent Roles of hcp Genes in Salmonella Typhimurium T6SS Shape Gut Microbiota Dysbiosis during InfectionT6SS

description:   
<em>Salmonella enterica </em>subsp.<em> enterica </em>serovar Typhimurium (<em>S. </em>Typhimurium) is a facultative intracellular pathogen causing significant gastrointestinal infections in humans and animals. The type VI secretion system (T6SS) plays a crucial role in its virulence, facilitating competition with host gut microbiota and promoting infection. While <em>S.</em> Typhimurium possesses a single T6SS, it encodes three <em>hcp</em> genes, which are crucial for its functionality and may exhibit non-redundant roles. In this study, we used 16S rRNA sequencing to analyze gut microbiota in BALB/c mice after infection with wild-type (WT) <em>S.</em> Typhimurium or mutant strains (Δ<em>hcp1</em>, Δ<em>hcp2</em>, Δ<em>hcp3</em>). Our findings revealed that <em>S</em>. Typhimurium infection induced severe gut dysbiosis especially on the second day post-infection. Specifically, the infection led to a notable increase in Firmicutes and activated the energy pathways that promotes the breakdown of short chain fatty acids. Wild type <em>S.</em> Typhimurium infection caused a sharp increase in <em>Escherichia-Shigella</em> levels, indicating inflammation-related dysbiosis, while the Δ<em>hcp</em>1, Δ<em>hcp</em>2, and Δ<em>hcp</em>3 groups showed milder changes, suggesting less disruption to gut microbiota. Deletion of individual <em>hcp</em> genes led to distinct bacterial taxa changes, underscoring the non-redundant functions of each <em>hcp</em>. Despite having only one T6SS, <em>S.</em> Typhimurium achieves precise modulation of its functions through the divergent roles of its Hcp proteins, enabling efficient colonization and persistence in the host gut.  These findings provide insights into the intricate mechanisms of bacterial adaptation and host-pathogen interactions, offering potential avenues for therapeutic interventions targeting T6SS-mediated dysbiosis.
DOI: 10.6084/m9.figshare.29434007
title: WTD5_8.fastqDivergent Roles of hcp Genes in Salmonella Typhimurium T6SS Shape Gut Microbiota Dysbiosis during InfectionT6SS

description:   
<em>Salmonella enterica </em>subsp.<em> enterica </em>serovar Typhimurium (<em>S. </em>Typhimurium) is a facultative intracellular pathogen causing significant gastrointestinal infections in humans and animals. The type VI secretion system (T6SS) plays a crucial role in its virulence, facilitating competition with host gut microbiota and promoting infection. While <em>S.</em> Typhimurium possesses a single T6SS, it encodes three <em>hcp</em> genes, which are crucial for its functionality and may exhibit non-redundant roles. In this study, we used 16S rRNA sequencing to analyze gut microbiota in BALB/c mice after infection with wild-type (WT) <em>S.</em> Typhimurium or mutant strains (Δ<em>hcp1</em>, Δ<em>hcp2</em>, Δ<em>hcp3</em>). Our findings revealed that <em>S</em>. Typhimurium infection induced severe gut dysbiosis especially on the second day post-infection. Specifically, the infection led to a notable increase in Firmicutes and activated the energy pathways that promotes the breakdown of short chain fatty acids. Wild type <em>S.</em> Typhimurium infection caused a sharp increase in <em>Escherichia-Shigella</em> levels, indicating inflammation-related dysbiosis, while the Δ<em>hcp</em>1, Δ<em>hcp</em>2, and Δ<em>hcp</em>3 groups showed milder changes, suggesting less disruption to gut microbiota. Deletion of individual <em>hcp</em> genes led to distinct bacterial taxa changes, underscoring the non-redundant functions of each <em>hcp</em>. Despite having only one T6SS, <em>S.</em> Typhimurium achieves precise modulation of its functions through the divergent roles of its Hcp proteins, enabling efficient colonization and persistence in the host gut.  These findings provide insights into the intricate mechanisms of bacterial adaptation and host-pathogen interactions, offering potential avenues for therapeutic interventions targeting T6SS-mediated dysbiosis.
DOI: 10.6084/m9.figshare.29434007.v1
title: WTD5_8.fastqDivergent Roles of hcp Genes in Salmonella Typhimurium T6SS Shape Gut Microbiota Dysbiosis during InfectionT6SS

description:   
<em>Salmonella enterica </em>subsp.<em> enterica </em>serovar Typhimurium (<em>S. </em>Typhimurium) is a facultative intracellular pathogen causing significant gastrointestinal infections in humans and animals. The type VI secretion system (T6SS) plays a crucial role in its virulence, facilitating competition with host gut microbiota and promoting infection. While <em>S.</em> Typhimurium possesses a single T6SS, it encodes three <em>hcp</em> genes, which are crucial for its functionality and may exhibit non-redundant roles. In this study, we used 16S rRNA sequencing to analyze gut microbiota in BALB/c mice after infection with wild-type (WT) <em>S.</em> Typhimurium or mutant strains (Δ<em>hcp1</em>, Δ<em>hcp2</em>, Δ<em>hcp3</em>). Our findings revealed that <em>S</em>. Typhimurium infection induced severe gut dysbiosis especially on the second day post-infection. Specifically, the infection led to a notable increase in Firmicutes and activated the energy pathways that promotes the breakdown of short chain fatty acids. Wild type <em>S.</em> Typhimurium infection caused a sharp increase in <em>Escherichia-Shigella</em> levels, indicating inflammation-related dysbiosis, while the Δ<em>hcp</em>1, Δ<em>hcp</em>2, and Δ<em>hcp</em>3 groups showed milder changes, suggesting less disruption to gut microbiota. Deletion of individual <em>hcp</em> genes led to distinct bacterial taxa changes, underscoring the non-redundant functions of each <em>hcp</em>. Despite having only one T6SS, <em>S.</em> Typhimurium achieves precise modulation of its functions through the divergent roles of its Hcp proteins, enabling efficient colonization and persistence in the host gut.  These findings provide insights into the intricate mechanisms of bacterial adaptation and host-pathogen interactions, offering potential avenues for therapeutic interventions targeting T6SS-mediated dysbiosis.
DOI: 10.6084/m9.figshare.29434010
title: WTD2_3.fastqDivergent Roles of hcp Genes in Salmonella Typhimurium T6SS Shape Gut Microbiota Dysbiosis during InfectionT6SS

description:   
<em>Salmonella enterica </em>subsp.<em> enterica </em>serovar Typhimurium (<em>S. </em>Typhimurium) is a facultative intracellular pathogen causing significant gastrointestinal infections in humans and animals. The type VI secretion system (T6SS) plays a crucial role in its virulence, facilitating competition with host gut microbiota and promoting infection. While <em>S.</em> Typhimurium possesses a single T6SS, it encodes three <em>hcp</em> genes, which are crucial for its functionality and may exhibit non-redundant roles. In this study, we used 16S rRNA sequencing to analyze gut microbiota in BALB/c mice after infection with wild-type (WT) <em>S.</em> Typhimurium or mutant strains (Δ<em>hcp1</em>, Δ<em>hcp2</em>, Δ<em>hcp3</em>). Our findings revealed that <em>S</em>. Typhimurium infection induced severe gut dysbiosis especially on the second day post-infection. Specifically, the infection led to a notable increase in Firmicutes and activated the energy pathways that promotes the breakdown of short chain fatty acids. Wild type <em>S.</em> Typhimurium infection caused a sharp increase in <em>Escherichia-Shigella</em> levels, indicating inflammation-related dysbiosis, while the Δ<em>hcp</em>1, Δ<em>hcp</em>2, and Δ<em>hcp</em>3 groups showed milder changes, suggesting less disruption to gut microbiota. Deletion of individual <em>hcp</em> genes led to distinct bacterial taxa changes, underscoring the non-redundant functions of each <em>hcp</em>. Despite having only one T6SS, <em>S.</em> Typhimurium achieves precise modulation of its functions through the divergent roles of its Hcp proteins, enabling efficient colonization and persistence in the host gut.  These findings provide insights into the intricate mechanisms of bacterial adaptation and host-pathogen interactions, offering potential avenues for therapeutic interventions targeting T6SS-mediated dysbiosis.