Biofilm metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA314676 | ENA |
REPOSITORIES: ENA
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Project description:mesocosm stream biofilms Targeted loci environmental
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Project description:Biofilms from various membrane materials Targeted loci environmental
| PRJNA354951 | ENA
Project description:Is there a universal genetically programmed defense providing tolerance to antibiotics when bacteria grow as biofilms? A comparison between biofilms of three different bacterial species by transcriptomic and metabolomic approaches uncovered no evidence of one. Single-species biofilms of three bacterial species (Pseudomonas aeruginosa, Staphylococcus aureus, and Acinetobacter baumannii) were grown in vitro for three days then challenged with respective antibiotics (ciprofloxacin, daptomycin, tigecycline) for an additional 24 h. All three microorganisms displayed reduced susceptibility in biofilms compared to planktonic cultures. Global transcriptomic profiling of gene expression comparing biofilm to planktonic and antibiotic-treated biofilm to untreated biofilm was performed. Extracellular metabolites including 18 amino acids, glucose, lactate, acetate, formate, and ethanol were measured to characterize the utilization of carbon sources between biofilms, treated biofilms, and planktonic cells. While all three bacteria exhibited a species-specific signature of stationary phase, no conserved gene, gene set, or common functional pathway could be identified that changed consistently across the three microorganisms. Across the three species, glucose consumption was increased in biofilms compared to planktonic cells and alanine and aspartic acid utilization were decreased in biofilms compared to planktonic cells. The reasons for these changes were not readily apparent in the transcriptomes. No common shift in the utilization pattern of carbon sources was discerned when comparing untreated to antibiotic-exposed biofilms. Overall, our measurements do not support the existence of a common genetic or biochemical basis for biofilm tolerance against antibiotics. Rather, there are likely myriad genes, proteins, and metabolic pathways that influence the physiological state of microorganisms in biofilms contributing to antibiotic tolerance. The Acinetobacter baumannii microarray data from the study described above is deposited here.
2021-10-18 | GSE186041 | GEO
Project description:Is there a universal genetically programmed defense providing tolerance to antibiotics when bacteria grow as biofilms? A comparison between biofilms of three different bacterial species by transcriptomic and metabolomic approaches uncovered no evidence of one. Single-species biofilms of three bacterial species (Pseudomonas aeruginosa, Staphylococcus aureus, and Acinetobacter baumannii) were grown in vitro for three days then challenged with respective antibiotics (ciprofloxacin, daptomycin, tigecycline) for an additional 24 h. All three microorganisms displayed reduced susceptibility in biofilms compared to planktonic cultures. Global transcriptomic profiling of gene expression comparing biofilm to planktonic and antibiotic-treated biofilm to untreated biofilm was performed. Extracellular metabolites including 18 amino acids, glucose, lactate, acetate, formate, and ethanol were measured to characterize the utilization of carbon sources between biofilms, treated biofilms, and planktonic cells. While all three bacteria exhibited a species-specific signature of stationary phase, no conserved gene, gene set, or common functional pathway could be identified that changed consistently across the three microorganisms. Across the three species, glucose consumption was increased in biofilms compared to planktonic cells and alanine and aspartic acid utilization were decreased in biofilms compared to planktonic cells. The reasons for these changes were not readily apparent in the transcriptomes. No common shift in the utilization pattern of carbon sources was discerned when comparing untreated to antibiotic-exposed biofilms. Overall, our measurements do not support the existence of a common genetic or biochemical basis for biofilm tolerance against antibiotics. Rather, there are likely myriad genes, proteins, and metabolic pathways that influence the physiological state of microorganisms in biofilms contributing to antibiotic tolerance. The Staphylococcus aureus microarray data from the study described above is deposited here.
2021-10-18 | GSE185864 | GEO
Project description:Microarray analysis was used to identify changes in the level of transcription of genes in P. aeruginosa drip flow biofilms in response to ciprofloxacin and tobramycin exposure. This data was evaluated and used to select strains that carry transposon mutations in genes that might play a role in antibiotic tolerance of biofilms. The strains were evaluated for defects in biofilm tolerance.
2015-05-11 | GSE65870 | GEO
Project description:Investigation of the kinetics of whole genome gene expression level changes in Bacillus subtilis NDmed strain during formation of submerged biofilm and pellicle. The Bacillus subtilis NDmed strain analyzed in this study is able to form thick and highly structured submerged biofilms as described in Bridier et al., (2011) The Spatial Architecture of Bacillus subtilis Biofilms Deciphered Using a Surface-Associated Model and In Situ Imaging. PLoS ONE 6(1):e16177.
2021-12-09 | GSE190460 | GEO
Project description:Bacteria growing in biofilms are physiologically heterogeneous, due in part to their adaptation to local environmental conditions. Here, we characterized the local transcriptional responses of Pseudomonas aeruginosa growing in biofilms by using microarray analysis of isolated biofilm subpopulations. The results demonstrated that cells at the top of the biofilms had high mRNA abundances for genes involved in general metabolic functions, while mRNAs for these housekeeping genes were low in cells at the bottom of the biofilms. Selective GFP labeling showed that cells at the top of the biofilm were actively dividing. However, the dividing cells had high mRNAs levels for genes regulated by the hypoxia induced regulator, Anr. Slow-growing cells deep in the biofilms had little expression of Anr-regulated genes and may have experienced long-termanoxia. Transcripts for ribosomal proteins were primarily associated with the metabolically active cell fraction, while ribosomal RNAs were abundant throughout the biofilms, indicating that ribosomes are stably maintained even in slowly growing cells. Consistent with these results was the identification of mRNAs for ribosome hibernation factors (rmf and PA4463) at the bottom of the biofilms. A P. aeruginosa ∆rmf strain had increased uptake of the membrane integrity stain, propidium iodide. Using selective GFP labeling and cell sorting, we showed that the dividing cells were more susceptible to tobramycin and ciprofloxacin than the dormant subpopulation. The results demonstrate that in thick P. aeruginosa biofilms, cells are physiologically distinct spatially, with cells deep in the biofilm in a viable but antibiotic-tolerant slow-growth state.
2012-05-03 | GSE34762 | GEO
Project description:The global transcriptional regulator Hha of Escherichia coli controls hemolysin activity, biofilm formation, and virulence expressions. Earlier, we have reported that Hha represses initial biofilm formation and disperses biofilms as well as controls prophage excision in E. coli. Since biofilm dispersal is a promising area to control biofilms, here we rewired Hha to control biofilm dispersal and formation. The Hha variant Hha13D6 was obtained to have enhanced biofilm dispersal activity along with increased toxicity compared to wild-type Hha (Hha13D6 induces dispersal 60%, whereas wild-type Hha induces dispersal at early biofilms but not at mature biofilms). Toxic Hha13D6 caused cell death probably by the activation of proteases HslUV, Lon, and PrlC, and deletion of protease gene hslV with overproducing Hh13D6 repressed biofilm dispersal, indicating Hha13D6 induces biofilm dispersal through the activity of protease HslV. Furthermore, another Hha variant Hha24E9 was also obtained to decrease biofilm formation 4-fold compared to wild-type Hha by regulation of gadW, glpT, and phnF. However, the dispersal variant Hha13D6 did not decrease biofilm formation, while the biofilm variant Hha24E9 did not induce biofilm dispersal. Hence, Hha may have evolved two ways in response to environmental factors to control biofilm dispersal and formation, but both controlling mechanisms come from different regulatory systems.
2010-10-31 | GSE21604 | GEO
Project description:Biofilms are broadly formed by a diversity of microorganisms that enable them to adapt stressful environments. Biofilms often impose harmful influences in many niches, as they can cause food contamination, antibiotics resistance, and environmental issues. However, eradicating biofilms remains difficult since the formation mechanism of biofilms are still incompletely clarified. In this study, we aimed at exploring the regulatory role of magnesium (Mg2+) on biofilm formation in Escherichia coli (E. coli) using phenotype visualization combined with targeted metabolomics method. We found that Mg2+ could exert significant influence on biofilm formation in a concentration-dependent manner by regulating phenotypic morphology and triggering metabolic modifications of biofilm. Phenotypic imaging revealed that increasing concentration of Mg2+ gradually inhibited biofilm formation, Mg2+ was observed to restore the microstructure of E. coli strain in biofilms to that in the relevant planktonic cells. In addition, our metabolomics analysis characterized 20 differential metabolites and associated 2 metabolic pathways including nucleotide metabolism and amino acid metabolism that were notably modified during biofilm formation under the treatments of different concentrations of Mg2+. Altogether, our work provides a novel insight into the influence of Mg2+ on biofilm formation at a metabolic level, which are implicated in the novel solution to disturb biofilm formation through the regulation of Mg2+ and functional metabolite interaction, then biofilms associated harmful impacts in different niches could be well tangled accordingly.
2021-09-07 | ST001939 | MetabolomicsWorkbench
Project description:Biofilms are broadly formed by a diversity of microorganisms that enable them to adapt stressful environments. Biofilms often impose harmful influences in many niches, as they can cause food contamination, antibiotics resistance, and environmental issues. However, eradicating biofilms remains difficult since the formation mechanism of biofilms are still incompletely clarified. In this study, we aimed at exploring the regulatory role of magnesium (Mg2+) on biofilm formation in Escherichia coli (E. coli) using phenotype visualization combined with targeted metabolomics method. We found that Mg2+ could exert significant influence on biofilm formation in a concentration-dependent manner by regulating phenotypic morphology and triggering metabolic modifications of biofilm. Phenotypic imaging revealed that increasing concentration of Mg2+ gradually inhibited biofilm formation, Mg2+ was observed to restore the microstructure of E. coli strain in biofilms to that in the relevant planktonic cells. In addition, our metabolomics analysis characterized 20 differential metabolites and associated 2 metabolic pathways including nucleotide metabolism and amino acid metabolism that were notably modified during biofilm formation under the treatments of different concentrations of Mg2+. Altogether, our work provides a novel insight into the influence of Mg2+ on biofilm formation at a metabolic level, which are implicated in the novel solution to disturb biofilm formation through the regulation of Mg2+ and functional metabolite interaction, then biofilms associated harmful impacts in different niches could be well tangled accordingly.
2021-09-07 | ST001938 | MetabolomicsWorkbench