cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.29433842
title: 3D2_6.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.29433842.v1
title: 3D2_6.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.29433839
title: 2D2_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.29433845
title: 3D2_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.29433845.v1
title: 3D2_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.29433848
title: WTD2_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.29433848.v1
title: WTD2_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.29433851
title: N3.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.29433851.v1
title: N3.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.29433854.v1
title: N4.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.28946063
title: Transcriptomic Insights into Metabolic Differences Between Toxic and Non-toxic <i>Alexandrium minutum</i> Strains

description: This study used publicly available RNA-seq libraries to explore the metabolic differences between toxic and non-toxic mutants of the dinoflagellate <i>Alexandrium minutum</i>. We identified genes differentially expressed between the two groups, and clusters of co-expressed genes correlated with the toxicity phenotype.
DOI: 10.6084/m9.figshare.29433854
title: N4.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.28946063.v1
title: Transcriptomic Insights into Metabolic Differences Between Toxic and Non-toxic <i>Alexandrium minutum</i> Strains

description: This study used publicly available RNA-seq libraries to explore the metabolic differences between toxic and non-toxic mutants of the dinoflagellate <i>Alexandrium minutum</i>. We identified genes differentially expressed between the two groups, and clusters of co-expressed genes correlated with the toxicity phenotype.
DOI: 10.6084/m9.figshare.28946063.v2
title: Transcriptomic Insights into Metabolic Differences Between Toxic and Non-toxic <i>Alexandrium minutum</i> Strains

description: This study used publicly available RNA-seq libraries to explore the metabolic differences between toxic and non-toxic mutants of the dinoflagellate <i>Alexandrium minutum</i>. We identified genes differentially expressed between the two groups, and clusters of co-expressed genes correlated with the toxicity phenotype.
DOI: 10.7266/n7mw2f20
title: Dataset for: Protein-Assisted Assembly of pi-Conjugated Polymers