Analysis of the organization and expression patterns of the convergent Pseudomonas aeruginosa lasR/rsaL gene pair uncovers mutual influence

Abstract

Pseudomonas aeruginosa is a ubiquitous environmental bacterium, which has emerged as an opportunistic pathogen of major clinical relevance (Bassetti et al., 2018). Its extensive metabolic versatility facilitates survival not only in different aquatic and terrestrial habitats, but also in the human host. P. aeruginosa infections can become established at various host sites and progress into life threatening acute or chronic infections (Lorenz et al., 2019;Moradali et al., 2017;Turner et al., 2014). The pathogen is equipped with a large arsenal of virulence factors. Expression of many of the respective P. aeruginosa virulence genes is orchestrated by two hierarchical organized homoserine lactone (HSL)-dependent quorum-sensing (QS) systems, the las and the rhl system (

Distinct Long- and Short-Term Adaptive Mechanisms in Pseudomonas aeruginosa

“…SCV24 was passaged in rich LB medium for seven times overall, and bacteria from each passage were harvested for RNA sequencing at an OD 600 of 2 (in duplicates). cDNA libraries were prepared as previously described ( 68 ). Libraries were sequenced on an Illumina NovaSeq 6000 (paired-end mode; 2 × 50 bp).…”

RsaL is a self‐regulatory switch that controls alternative biosynthesis of two AHL‐type quorum sensing signals in Pseudomonas aeruginosa PA1201

“…Besides its role in QS, RsaL is also a global regulator controlling the expression of numerous genes involved in bacterial functions such as virulence, including the phz1 cluster, phzM, and cdpR, and in antibiotic resistance, including the narK1K2GHJI operon 8, 14,[17][18][19] . Consequently, the rsaL mutation in the P. aeruginosa strain PAO1 enhances the production of virulence factors, such as elastase, hemolysins, hydrogen cyanide, and phenazine metabolites, increases ciprofloxacin and carbenicillin resistance and decreases the ability of the bacteria to cause chronic lung infections in mice 15,[19][20][21][22] . Therefore, understanding the RsaL-dependent regulation of gene expression may uncover new ways to control the harmful effects of P. aeruginosa in clinics and agriculture.…”

“…Consequently, the rsaL mutation in the P . aeruginosa strain PAO1 enhances the production of virulence factors, such as elastase, hemolysins, hydrogen cyanide, and phenazine metabolites, increases ciprofloxacin and carbenicillin resistance and decreases the ability of the bacteria to cause chronic lung infections in mice 15 , 19 , 20 , 21 , 22 . Therefore, understanding the RsaL‐dependent regulation of gene expression may uncover new ways to control the harmful effects of P .…”