Project description:Transcriptional profiling of RNA-seq data from two Burkholderia species grown under conditions mimicking the cystic fibrosis lung and the soil environment
Project description:Pseudomonas aeruginosa was repeatedly and intermittently exposed to tobramycin. Bacteria were grown in synthetic cystic fibrosis medium in wells of a 96-well microtiter plate. After 24 hours, more medium with or without tobramycin was added. After another 24 hours of incubation, a subsample of the well content was used to inoculate fresh synthetic cystic fibrosis medium in a 96-well microtiter plate. This was repeated for a total of 15 cycles. Evolved lineages were then DNA-sequenced to screen for genome changes.
Project description:The gene expression of the opportunictic cystic fibrosis lung pathogen Burkholderia multivorans ATCC 17616 was investigated under different growth conditions relevant for growth in the cystic fibrosis lung.
Project description:The gene expression of the opportunictic cystic fibrosis lung pathogen Burkholderia multivorans ATCC 17616 was investigated under different growth conditions relevant for growth in the cystic fibrosis lung.
Project description:The gene expression of the opportunictic cystic fibrosis lung pathogen Burkholderia multivorans ATCC 17616 was investigated under different growth conditions relevant for growth in the cystic fibrosis lung.
Project description:Arrays comparing Pseudomonas aeruginosa growth in a defined synthetic cystic fibrosis sputum medium with and without aromatic amino acids. Additional arrays comparing wild-type Pseudomonas aeruginosa and phhR mutant P. aeruginosa in defined synthetic cystic fibrosis sputum medium.
Project description:The purpose of this study was to explore miRNA mediated Transforming Growth Factor (TGF)-β1 regulation of F508del Cystic Fibrosis Transmembrane Conductance regulator (CFTR). To fulfill this goal, miRNA sequencing was done to see miRNA landscape in Cystic Fibrosis Bronchial Epithelial (CFBE) Cells with homozygous WT-CFTR and F508del mutated CFTR in response to TGFβ1 treatment.
