Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1115109 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Flavobacterium columnare, the causative agent of columnaris disease causes substantial mortality worldwide in numerous freshwater finfish species. Due to its global significance and impact on the aquaculture industry continual efforts to better understand basic mechanisms that contribute to disease are urgently needed. F. columnare naturally occurs in a planktonic, free living state where it can survive for long periods of time, even in the absence of nutrients. In contrast, F. columnare also possesses the ability to form biofilms, broadly defined as surface bound microbial communities inhabiting an organic matrix composed of autogenously derived extracellular polymeric substances. The advantages of adopting this life stage are not completely clear for F. columnare, but biofilm formation could increase virulence by offering protection from desiccation, augment resistance to antimicrobials, improve nutrient acquisition, and protection against other bacteria. To examine gene expression between F. columnare planktonic cells and biofilms, we conducted a study where both phases were grown with and without stimulation and then sampled for RNA sequencing.
2018-10-16 | GSE109937 | GEO
Project description:Tracing autotroph and heterotroph photosynthetic catalytic carbon cycling within a microbial mat, confirming biomass 13C incorporation into extracellular polymeric substances through proteomics.
2023-07-20 | PXD012190 | Pride
Project description:Microalgae associated bacteria Metagenome
| PRJNA578303 | ENA
Project description:With the global increase in the use of carbapenems, several gram-negative bacteria have acquired carbapenem resistance, thereby limiting treatment options. Klebsiella pneumoniae is one of such notorious pathogen that is being widely studied to find novel resistance mechanisms and drug targets. These antibiotic-resistant clinical isolates generally harbor many genetic alterations, and identification of causal mutations will provide insights into the molecular mechanisms of antibiotic resistance. We propose a method to prioritize mutated genes responsible for antibiotic resistance, in which mutated genes that also show significant expression changes among their functionally coupled genes become more likely candidates. For network-based analyses, we developed a genome-scale co-functional network of K. pneumoniae genes, KlebNet (www.inetbio.org/klebnet). Using KlebNet, we could reconstruct functional modules for antibiotic-resistance, and virulence, and retrieved functional association between them. With complementation assays with top candidate genes, we could validate a gene for negative regulation of meropenem resistance and four genes for positive regulation of virulence in Galleria mellonella larvae. Therefore, our study demonstrated the feasibility of network-based identification of genes required for antimicrobial resistance and virulence of human pathogenic bacteria with genomic and transcriptomic profiles from antibiotic-resistant clinical isolates.
2018-06-10 | GSE115539 | GEO
Project description:Antibiotic resistance is a growing global health threat. Most research has focused on understanding how mobile genetic elements are acquired by pathogenic bacteria. However, bacteria have intrinsic chromosomally encoded systems to protect themselves against antimicrobial assault. Our lab has uncovered such a system in uropathogenic E. coli. PmrAB and QseBC are connected two component systems that confer resistance to polymyxins, a last resort antibiotic. The histidine kinase PmrB responds to ferric iron and activates its cognate response regulator PmrA, as well as the non-cognate response regulator QseB. QseC, the other histidine kinase plays an important role in resetting the system. To better understand how PmrAB and QseBC mediate polymyxin resistance, this project aimed to elucidate the regulon of the two response regulators QseB and PmrA in the uropathogenic E. coli strain UTI89. In this strain, isogenic mutants were made lacking qseB and pmrA singly and together. These strains and wild-type UTI89 were stimulated with ferric iron and samples for RNA sequencing were taken prior to stimulation and at 15 and 60 minutes post stimulation. Samples were then sent for sequencing on the Illumina platform and analyzed using Rockhopper software.
2020-10-23 | E-MTAB-9277 | biostudies-arrayexpress
Project description:Characterization and significance of extracellular polymeric substances, reactive oxygen species, and extracellular electron transfer in methanogenic biocathode
| PRJNA736414 | ENA
Project description:Background: Antibiotic resistance is an urgent threat to public health. Prior to the evolution of antibiotic resistance, bacteria frequently undergo response and tend to develop a state of adaption to the antibiotic. Ciprofloxacin is a broad-spectrum antibiotic by damaging DNA. With the widespread clinical application, the resistance of bacteria to ciprofloxacin continues to increase. This study aimed to investigate the transcriptome changes under the action of high concentration of ciprofloxacin in Escherichia coli. Results: We identified 773 up-regulated differentially expressed genes (DEGs) and 645 down-regulated DEGs in ciprofloxacin treated cells. Enriched biological pathways reflected the up-regulation of biological process such as DNA damage and repair system, toxin/antitoxin systems, formaldehyde detoxification system, peptide biosynthetic process and cellular protein metabolic process. With KEGG pathway analysis, up-regulated DEGs of kdsA and waa operon were associated with “LPS biosynthesis”. rfbABC operon was related to “streptomycin biosynthesis” and “polyketide sugar unit biosynthesis ”. Down-regulated DEGs of thrABC and fliL operons were associated with “flagellum-dependent cell motility” and “bacterial-type flagellum” in GO terms, and enriched into “biosynthesis of amino acids” and “flagellar assembly” in KEGG pathways. After treatment of ciprofloxacin, bacterial lipopolysacchride (LPS) release was increased by two times, and the mRNA expression level of LPS synthesis genes, waaB, waaP and waaG were elevated (P < 0.05). Conclusions: Characterization of the gene clusters by RNA-seq showed high dose of ciprofloxacin not only lead to damage of bacterial macromolecules and components, but also induce protective response against antibiotic action by up-regulating the SOS system, toxin/antitoxin system and formaldehyde detoxification system. Moreover, genes related to biosynthesis of LPS were also upregulated by the treatment indicating that ciprofloxacin can enhance the production of endotoxin on the level of transcription. These results demonstrated that transient exposure of high dose ciprofloxacin is double edged. Cautions should be taken when administering the high dose antibiotic treatment for infectious diseases.
2020-06-16 | GSE152445 | GEO