The role of the temperature-regulated acyltransferase (PA3242) on growth, antibiotic resistance and virulence in Pseudomonas aeruginosa

Increased ParB level affects expression of stress response, adaptation and virulence operons and potentiates repression of promoters adjacent to the high affinity binding sites parS3 and parS4 in Pseudomonas aeruginosa

“…Since inactivation of either of the htrB genes in P . aeruginosa PAO1 leads to motility defects [77,79], this could explain the impaired motility seen both when ParB is missing and when it is present in excess. Notably, also other genes adjacent to parS3 and parS4 encode proteins with putative roles in response to cellular stress.…”

An outer membrane determinant for RNA phage genome entry in Pseudomonas aeruginosa

“…For example, disruption of htrB in Escherichia coli inhibited the growth above 33°C, resulting in filamentous or bulging morphology, 30 increased antibiotic susceptibility 31 and decreased capability to colonize human airway epithelium. 32 In case of PA, which harbors two htrB genes ( htrB1 and htrB2 ), lipid A secondary acylation is crucial to survive the stressful environmental conditions: 33 the htrB2 and, to the lesser extent, the htrB1 mutants displayed increased membrane permeability, and increased chemical susceptibility to some antibiotics and cationic antimicrobial peptides, suggesting a role of these enzymes in maintaining the OM organization and integrity in PA as well. However, a little is known about the involvement of the OM integrity in the phage resistance, despite the potential contribution of the OM remodeling in the uptake of the chemicals and macromolecules.…”

Increased ParB level affects expression of stress response, adaptation and virulence operons and potentiates repression of promoters adjacent to the high affinity binding sitesparS3andparS4inPseudomonas aeruginosa

“…Conversely, expression of another HtrB homolog ( PA3242 ) is significantly reduced in parB null mutant [39]. Since inactivation of either of the htrB genes in P. aeruginosa PAO1 leads to motility defects [77,79], this could explain the impaired motility seen both when ParB is missing and when it is present in excess. Notably, also other genes adjacent to parS3 and parS4 encode proteins with putative roles in response to cellular stress.…”