Burian, Heloisa2025-01-152025-01-152025-01-15http://hdl.handle.net/10393/50097https://doi.org/10.20381/ruor-30860Antibiotic resistance is a major problem in the 21st century. Opportunistic bacterial infections caused by Pseudomonas aeruginosa (PA) impact individuals with compromised immune systems, like those with cystic fibrosis (CF). Due to PA's capacity to become resistant to antibiotics through many mechanisms, including the formation of biofilms, this is a pathogen to be concerned about. PA's antibiotic resistance mechanisms built into the organism's genome play a role in this resistance. Prior research involved screening a sub-library of transposon-insertion mutants (tn-mutants) to identify transcriptional regulators (TRs) deemed important to biofilm antibiotic resistance. Thirteen such TRs were identified, and these were thought to be potentially relevant in intrinsic antibiotic resistance. Among these TRs, the tn-mutant PA1759 stood out due to having the strongest biofilm antibiotic susceptibility phenotype. PA1759 is found in an operon with PA1760, so a ΔPA1759-60 double deletion mutant was constructed and analyzed. Compared to the wild-type (WT) biofilm, the ΔPA1759-60 mutant is four times more susceptible to Tobramycin (Tb) when its biofilm is exposed to antibiotics. This suggested that PA1759-60 is an important regulator of antibiotic resistance, necessitating further research into its processes and potential as a therapeutic target. This research aimed to analyze the ΔPA1759-60 mutant to determine its growth and biofilm formation potential under aerobic as well as anaerobic conditions compared to the WT. Given that PA often resides in anaerobic environments, such as within the CF lung, characterization under the two conditions is important in assessing potential clinical outcome. The ΔPA1759-60 mutant had much reduced growth and biofilm formation compared to the WT under anaerobic conditions, consistent with prior observations under aerobic conditions. These findings emphasize the reduced biofilm formation of ΔPA1759-60, providing useful insights for future development of targeted therapies for PA infections in anaerobic conditions.enAttribution 4.0 Internationalhttp://creativecommons.org/licenses/by/4.0/Pseudomonas aeruginosamutant strainanaerobic conditionsbiofilm formationCharacterization of Anaerobic Growth and Biofilm Formation in Pseudomonas aeruginosa Mutant Strain Lacking Genes PA1759 and PA1760Thesis