186,958 research outputs found
Appendix_1_revised – Supplemental material for Psychologists psychologizing scientific psychology: An epistemological reading of the replication crisis
No full textSupplemental material, Appendix_1_revised for Psychologists psychologizing scientific psychology: An epistemological reading of the replication crisis by Ivan Flis in Theory & Psychology</p
Table_4_Transcriptomic and metabolomic insights into the role of fliS in the pathogenicity of Pseudomonas plecoglossicida against Epinephelus coioides.docx
No full textPseudomonas plecoglossicida is responsible for visceral white spot disease in economically valuable marine fish such as Larimichthys crocea and Epinephelus coioides. Based on RNA sequencing, we previously showed that P. plecoglossicida fliS gene expression is significantly up-regulated in E. coioides spleens during infection. Here, to explore the role of this gene in pathogenicity, RNA interference (RNAi) was performed to silence fliS in P. plecoglossicida, and the mutant with the best silencing efficiency (89%) was chosen for further studies. Results showed that fliS silencing significantly attenuated motility, chemotaxis, adhesion, and biofilm formation of P. plecoglossicida. Furthermore, E. coioides infected with the fliS-RNAi strain recorded no deaths and showed fewer pathogens in the spleen and fewer white spots on the spleen surface compared to those fish infected with the wild type P. plecoglossicida strain. RNAi of fliS significantly affected the spleen transcriptome and metabolome in infected E. coioides. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that the cytokine-cytokine receptor interaction pathway was the most enriched immune-related pathway, and the arginine biosynthesis pathway was the most enriched metabolism-related pathway. These findings suggest that fliS is a virulence gene of P. plecoglossicida and is involved in the regulation of motility, chemotaxis, adhesion, and biofilm formation, as well as the inflammatory and immune responses of E. coioides to P. plecoglossicida infection.</p
DataSheet_2_Transcriptomic and metabolomic insights into the role of fliS in the pathogenicity of Pseudomonas plecoglossicida against Epinephelus coioides.docx
No full textPseudomonas plecoglossicida is responsible for visceral white spot disease in economically valuable marine fish such as Larimichthys crocea and Epinephelus coioides. Based on RNA sequencing, we previously showed that P. plecoglossicida fliS gene expression is significantly up-regulated in E. coioides spleens during infection. Here, to explore the role of this gene in pathogenicity, RNA interference (RNAi) was performed to silence fliS in P. plecoglossicida, and the mutant with the best silencing efficiency (89%) was chosen for further studies. Results showed that fliS silencing significantly attenuated motility, chemotaxis, adhesion, and biofilm formation of P. plecoglossicida. Furthermore, E. coioides infected with the fliS-RNAi strain recorded no deaths and showed fewer pathogens in the spleen and fewer white spots on the spleen surface compared to those fish infected with the wild type P. plecoglossicida strain. RNAi of fliS significantly affected the spleen transcriptome and metabolome in infected E. coioides. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that the cytokine-cytokine receptor interaction pathway was the most enriched immune-related pathway, and the arginine biosynthesis pathway was the most enriched metabolism-related pathway. These findings suggest that fliS is a virulence gene of P. plecoglossicida and is involved in the regulation of motility, chemotaxis, adhesion, and biofilm formation, as well as the inflammatory and immune responses of E. coioides to P. plecoglossicida infection.</p
Table_5_Transcriptomic and metabolomic insights into the role of fliS in the pathogenicity of Pseudomonas plecoglossicida against Epinephelus coioides.docx
No full textPseudomonas plecoglossicida is responsible for visceral white spot disease in economically valuable marine fish such as Larimichthys crocea and Epinephelus coioides. Based on RNA sequencing, we previously showed that P. plecoglossicida fliS gene expression is significantly up-regulated in E. coioides spleens during infection. Here, to explore the role of this gene in pathogenicity, RNA interference (RNAi) was performed to silence fliS in P. plecoglossicida, and the mutant with the best silencing efficiency (89%) was chosen for further studies. Results showed that fliS silencing significantly attenuated motility, chemotaxis, adhesion, and biofilm formation of P. plecoglossicida. Furthermore, E. coioides infected with the fliS-RNAi strain recorded no deaths and showed fewer pathogens in the spleen and fewer white spots on the spleen surface compared to those fish infected with the wild type P. plecoglossicida strain. RNAi of fliS significantly affected the spleen transcriptome and metabolome in infected E. coioides. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that the cytokine-cytokine receptor interaction pathway was the most enriched immune-related pathway, and the arginine biosynthesis pathway was the most enriched metabolism-related pathway. These findings suggest that fliS is a virulence gene of P. plecoglossicida and is involved in the regulation of motility, chemotaxis, adhesion, and biofilm formation, as well as the inflammatory and immune responses of E. coioides to P. plecoglossicida infection.</p
DataSheet_1_Transcriptomic and metabolomic insights into the role of fliS in the pathogenicity of Pseudomonas plecoglossicida against Epinephelus coioides.docx
No full textPseudomonas plecoglossicida is responsible for visceral white spot disease in economically valuable marine fish such as Larimichthys crocea and Epinephelus coioides. Based on RNA sequencing, we previously showed that P. plecoglossicida fliS gene expression is significantly up-regulated in E. coioides spleens during infection. Here, to explore the role of this gene in pathogenicity, RNA interference (RNAi) was performed to silence fliS in P. plecoglossicida, and the mutant with the best silencing efficiency (89%) was chosen for further studies. Results showed that fliS silencing significantly attenuated motility, chemotaxis, adhesion, and biofilm formation of P. plecoglossicida. Furthermore, E. coioides infected with the fliS-RNAi strain recorded no deaths and showed fewer pathogens in the spleen and fewer white spots on the spleen surface compared to those fish infected with the wild type P. plecoglossicida strain. RNAi of fliS significantly affected the spleen transcriptome and metabolome in infected E. coioides. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that the cytokine-cytokine receptor interaction pathway was the most enriched immune-related pathway, and the arginine biosynthesis pathway was the most enriched metabolism-related pathway. These findings suggest that fliS is a virulence gene of P. plecoglossicida and is involved in the regulation of motility, chemotaxis, adhesion, and biofilm formation, as well as the inflammatory and immune responses of E. coioides to P. plecoglossicida infection.</p
Table_3_Transcriptomic and metabolomic insights into the role of fliS in the pathogenicity of Pseudomonas plecoglossicida against Epinephelus coioides.docx
No full textPseudomonas plecoglossicida is responsible for visceral white spot disease in economically valuable marine fish such as Larimichthys crocea and Epinephelus coioides. Based on RNA sequencing, we previously showed that P. plecoglossicida fliS gene expression is significantly up-regulated in E. coioides spleens during infection. Here, to explore the role of this gene in pathogenicity, RNA interference (RNAi) was performed to silence fliS in P. plecoglossicida, and the mutant with the best silencing efficiency (89%) was chosen for further studies. Results showed that fliS silencing significantly attenuated motility, chemotaxis, adhesion, and biofilm formation of P. plecoglossicida. Furthermore, E. coioides infected with the fliS-RNAi strain recorded no deaths and showed fewer pathogens in the spleen and fewer white spots on the spleen surface compared to those fish infected with the wild type P. plecoglossicida strain. RNAi of fliS significantly affected the spleen transcriptome and metabolome in infected E. coioides. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that the cytokine-cytokine receptor interaction pathway was the most enriched immune-related pathway, and the arginine biosynthesis pathway was the most enriched metabolism-related pathway. These findings suggest that fliS is a virulence gene of P. plecoglossicida and is involved in the regulation of motility, chemotaxis, adhesion, and biofilm formation, as well as the inflammatory and immune responses of E. coioides to P. plecoglossicida infection.</p
Importance of Campylobacter jejuni FliS and FliW in Flagella Biogenesis and Flagellin Secretion
No full textFlagella-driven motility enables bacteria to reach their favorable niche within the host. The human foodborne pathogen Campylobacter jejuni produces two heavily glycosylated structural flagellins (FlaA and FlaB) that form the flagellar filament. It also encodes the non-structural FlaC flagellin which is secreted through the flagellum and has been implicated in host cell invasion. The mechanisms that regulate C. jejuni flagellin biogenesis and guide the proteins to the export apparatus are different from those in most other enteropathogens and are not fully understood. This work demonstrates the importance of the putative flagellar protein FliS in C. jejuni flagella assembly. A constructed fliS knockout strain was non-motile, displayed reduced levels of FlaA/B and FlaC flagellin, and carried severely truncated flagella. Pull-down and Far Western blot assays showed direct interaction of FliS with all three C. jejuni flagellins (FlaA, FlaB, and FlaC). This is in contrast to, the sensor and regulator of intracellular flagellin levels, FliW, which bound to FlaA and FlaB but not to FlaC. The FliS protein but not FliW preferred binding to glycosylated C. jejuni flagellins rather than to their non-glycosylated recombinant counterparts. Mapping of the binding region of FliS and FliW using a set of flagellin fragments showed that the C-terminal subdomain of the flagellin was required for FliS binding, whereas the N-terminal subdomain was essential for FliW binding. The separate binding subdomains required for FliS and FliW, the different substrate specificity, and the differential preference for binding of glycosylated flagellins ensure optimal processing and assembly of the C. jejuni flagellins
Table_1_Transcriptomic and metabolomic insights into the role of fliS in the pathogenicity of Pseudomonas plecoglossicida against Epinephelus coioides.docx
No full textPseudomonas plecoglossicida is responsible for visceral white spot disease in economically valuable marine fish such as Larimichthys crocea and Epinephelus coioides. Based on RNA sequencing, we previously showed that P. plecoglossicida fliS gene expression is significantly up-regulated in E. coioides spleens during infection. Here, to explore the role of this gene in pathogenicity, RNA interference (RNAi) was performed to silence fliS in P. plecoglossicida, and the mutant with the best silencing efficiency (89%) was chosen for further studies. Results showed that fliS silencing significantly attenuated motility, chemotaxis, adhesion, and biofilm formation of P. plecoglossicida. Furthermore, E. coioides infected with the fliS-RNAi strain recorded no deaths and showed fewer pathogens in the spleen and fewer white spots on the spleen surface compared to those fish infected with the wild type P. plecoglossicida strain. RNAi of fliS significantly affected the spleen transcriptome and metabolome in infected E. coioides. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that the cytokine-cytokine receptor interaction pathway was the most enriched immune-related pathway, and the arginine biosynthesis pathway was the most enriched metabolism-related pathway. These findings suggest that fliS is a virulence gene of P. plecoglossicida and is involved in the regulation of motility, chemotaxis, adhesion, and biofilm formation, as well as the inflammatory and immune responses of E. coioides to P. plecoglossicida infection.</p
Table_2_Transcriptomic and metabolomic insights into the role of fliS in the pathogenicity of Pseudomonas plecoglossicida against Epinephelus coioides.docx
No full textPseudomonas plecoglossicida is responsible for visceral white spot disease in economically valuable marine fish such as Larimichthys crocea and Epinephelus coioides. Based on RNA sequencing, we previously showed that P. plecoglossicida fliS gene expression is significantly up-regulated in E. coioides spleens during infection. Here, to explore the role of this gene in pathogenicity, RNA interference (RNAi) was performed to silence fliS in P. plecoglossicida, and the mutant with the best silencing efficiency (89%) was chosen for further studies. Results showed that fliS silencing significantly attenuated motility, chemotaxis, adhesion, and biofilm formation of P. plecoglossicida. Furthermore, E. coioides infected with the fliS-RNAi strain recorded no deaths and showed fewer pathogens in the spleen and fewer white spots on the spleen surface compared to those fish infected with the wild type P. plecoglossicida strain. RNAi of fliS significantly affected the spleen transcriptome and metabolome in infected E. coioides. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that the cytokine-cytokine receptor interaction pathway was the most enriched immune-related pathway, and the arginine biosynthesis pathway was the most enriched metabolism-related pathway. These findings suggest that fliS is a virulence gene of P. plecoglossicida and is involved in the regulation of motility, chemotaxis, adhesion, and biofilm formation, as well as the inflammatory and immune responses of E. coioides to P. plecoglossicida infection.</p
Importance of Campylobacter jejuni FliS and FliW in flagella biogenesis and flagellin secretion
No full textFlagella-driven motility enables bacteria to reach their favorable niche within the host. The human foodborne pathogen Campylobacter jejuni produces two heavily glycosylated structural flagellins (FlaA and FlaB) that form the flagellar filament. It also encodes the non-structural FlaC flagellin which is secreted through the flagellum and has been implicated in host cell invasion. The mechanisms that regulate C. jejuni flagellin biogenesis and guide the proteins to the export apparatus are different from those in most other enteropathogens and are not fully understood. This work demonstrates the importance of the putative flagellar protein FliS in C. jejuni flagella assembly. A constructed fliS knockout strain was non-motile, displayed reduced levels of FlaA/B and FlaC flagellin, and carried severely truncated flagella. Pull-down and Far Western blot assays showed direct interaction of FliS with all three C. jejuni flagellins (FlaA, FlaB, and FlaC). This is in contrast to, the sensor and regulator of intracellular flagellin levels, FliW, which bound to FlaA and FlaB but not to FlaC. The FliS protein but not FliW preferred binding to glycosylated C. jejuni flagellins rather than to their non-glycosylated recombinant counterparts. Mapping of the binding region of FliS and FliW using a set of flagellin fragments showed that the C-terminal subdomain of the flagellin was required for FliS binding, whereas the N-terminal subdomain was essential for FliW binding. The separate binding subdomains required for FliS and FliW, the different substrate specificity, and the differential preference for binding of glycosylated flagellins ensure optimal processing and assembly of the C. jejuni flagellins.</p
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