The <scp>S</scp>almonella enterica serovar <scp>T</scp>yphi <scp>ltrR</scp>‐<scp>ompR</scp>‐<scp>ompC</scp>‐<scp>ompF</scp> genes are involved in resistance to the bile salt sodium deoxycholate and in bacterial transformation

Villarreal, José Miguel; Becerra-Lobato, Noé; Rebollar-Flores, Javier E; Medina-Aparicio, Liliana; Carbajal-Gómez, E.; Zavala-García, M. L.; Vázquez, Arturo Pérez; Gutiérrez-Rı́os, Rosa Marı́a; Olvera, Leticia; Encarnación, Sergio; Martínez-Batallar, A. G.; Calva, Edmundo; Hernández-Lucas, Ismael

doi:10.1111/mmi.12610

Cited by 27 publications

(33 citation statements)

References 94 publications

(111 reference statements)

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“…Although some bacteria, i.e. Salmonella enterica , can grow in the presence of sodium deoxycholate concentrations (5% = 120 mM) (Villareal et al ., 2014), which are well above the critical micelle concentration (2–4 mM) for deoxycholate (Neugebauer, 1990), C. crescentus is more sensitive to this detergent and experiments were performed at 1 mg ml −1 (2.5 mM). As shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

Five structural genes required for ceramide synthesis in Caulobacter and for bacterial survival

Olea‐Ozuna

Poggio

EdBergström

et al. 2020

Environmental Microbiology

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Summary Sphingolipids are essential and common membrane components in eukaryotic organisms, participating in many important cellular functions. Only a few bacteria are thought to harbour sphingolipids in their membranes, among them the well‐studied α‐proteobacterium Caulobacter crescentus, a model organism for asymmetric cell division and cellular differentiation. Here, we report that C. crescentus wild type produces several molecular species of dihydroceramides, which are not produced in a mutant lacking the structural gene for serine palmitoyltransferase (spt). Whereas growth of a spt‐deficient mutant and wild type are indistinguishable during the exponential phase of growth, survival of the spt‐deficient mutant is much reduced, in comparison with wild type, during stationary phase of growth, especially at elevated temperatures. The structural gene for spt is located within a genomic cluster, comprising another 16 genes and which, like spt, are important for fitness of C. crescentus. Mutants deficient in genes linked to spt by high cofitness were unable to produce dihydroceramide or to survive in stationary phase of growth at elevated temperatures. At least five structural genes are required for dihydroceramide biosynthesis in C. crescentus and sphingolipid biosynthesis is needed for survival of this bacterium and the integrity of its outer membrane.

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Section: Resultsmentioning

confidence: 99%

Five structural genes required for ceramide synthesis in Caulobacter and for bacterial survival

Olea‐Ozuna

Poggio

EdBergström

et al. 2020

Environmental Microbiology

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“…Previous observation reported changes on the amount of OMPs in an ompF null mutant of a clinical isolate of S. Typhi. However, in this mutant main porins, such as ompC and ompA did not change their migration pattern (Villarreal et al, 2014). It could be the case that the extend of changes produced after ompF is mutated differs between isolates of S. Typhi.…”

Section: Inactivation Of Glna Gene Increases the Expression Of Ompfmentioning

confidence: 75%

Inactivation of Glutamine Synthetase-Coding Gene glnA Increases Susceptibility to Quinolones Through Increasing Outer Membrane Protein F in Salmonella enterica Serovar Typhi

et al. 2020

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Ciprofloxacin is the choice treatment for infections caused by Salmonella Typhi, however, reduced susceptibility to ciprofloxacin has been reported for this pathogen. Considering the decreased approbation of new antimicrobials and the crisis of resistance, one strategy to combat this problem is to find new targets that enhances the antimicrobial activity for approved antimicrobials. In search of mutants with increased susceptibility to ciprofloxacin; 3,216 EZ-Tn5 transposon mutants of S. Typhi were screened. S. Typhi zxx::EZ-Tn5 mutants susceptible to ciprofloxacin were confirmed by agar diffusion and MIC assays. The genes carrying EZ-Tn5 transposon insertions were sequenced. Null mutants of interrupted genes, as well as inducible genetic constructs, were produced using site-directed mutagenesis, to corroborate phenotypes. SDS-PAGE and Real-time PCR were used to evaluate the expression of proteins and genes, respectively. Five mutants with increased ciprofloxacin susceptibility were found in the screening. The first confirmed mutant was the glutamine synthetase-coding gene glnA. Analysis of outer membrane proteins revealed increased OmpF, a channel for the influx of ciprofloxacin and nalidixic acid, in the glnA mutant. Expression of ompF increased four times in the glnA null mutant compared to WT strain. To understand the relationship between the expression of glnA and ompF, a strain with the glnA gene under control of the tetracycline-inducible P tet promoter was created, to modulate glnA expression. Induction of glnA decreased expression of ompF, at the same time that reduced susceptibility to ciprofloxacin. Expression of sRNA MicF, a negative regulator of OmpF was reduced to one-fourth in the glnA mutant, compared to WT strain. In addition, expression of glnL and glnG genes (encoding the two-component system NtrC/B that may positively regulate OmpF) were increased in the glnA mutant. Further Frontiers in Microbiology | www.frontiersin.org 1 March 2020 | Volume 11 | Article 428Millanao et al.glnA Inactivation Increases Quinolones Susceptibility studies indicate that deletion of glnG decreases susceptibility to CIP, while deletion of micF gene increases susceptibility CIP. Our findings indicate that glnA inactivation promotes ompF expression, that translates into increased OmpF protein, facilitating the entry of ciprofloxacin, thus increasing susceptibility to ciprofloxacin through 2 possible mechanisms.

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“…Consistent with the disruption in OM lipid asymmetry, cells lacking OmpC are known to exhibit OM permeability defects, including increased sensitivity to SDS/EDTA (Nichols et al ., ) and bile salts such as deoxycholate (Thanassi et al ., ; Nichols et al ., ; Villarreal et al ., ). Despite having similar levels of PL accumulation in their OMs (Fig.…”

Section: Resultsmentioning

confidence: 97%

Osmoporin OmpC forms a complex with MlaA to maintain outer membrane lipid asymmetry in Escherichia coli

Chong

Woo

Chng

2015

Molecular Microbiology

129

186

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SummaryGram-negative bacteria can survive in harsh environments in part because the asymmetric outer membrane (OM) hinders the entry of toxic compounds. Lipid asymmetry is established by having phospholipids (PLs) confined to the inner leaflet of the membrane and lipopolysaccharides (LPS) to the outer leaflet. Perturbation of OM lipid asymmetry, characterized by PL accumulation in the outer leaflet, disrupts proper LPS packing and increases membrane permeability. The multi-component Mla system prevents PL accumulation in the outer leaflet of the OM via an unknown mechanism. Here, we demonstrate that in Escherichia coli, the Mla system maintains OM lipid asymmetry with the help of osmoporin OmpC. We show that the OM lipoprotein MlaA interacts specifically with OmpC and OmpF. This interaction is sufficient to localize MlaA lacking its lipid anchor to the OM. Removing OmpC, but not OmpF, causes accumulation of PLs in the outer leaflet of the OM in stationary phase, as was previously observed for MlaA. We establish that OmpC is an additional component of the Mla system; the OmpC-MlaA complex may function to remove PLs directly from the outer leaflet to maintain OM lipid asymmetry. Our work reveals a novel function for the general diffusion channel OmpC in lipid transport.

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The Salmonella enterica serovar Typhi ltrR‐ompR‐ompC‐ompF genes are involved in resistance to the bile salt sodium deoxycholate and in bacterial transformation

Cited by 27 publications

References 94 publications

Five structural genes required for ceramide synthesis in Caulobacter and for bacterial survival

Five structural genes required for ceramide synthesis in Caulobacter and for bacterial survival

Inactivation of Glutamine Synthetase-Coding Gene glnA Increases Susceptibility to Quinolones Through Increasing Outer Membrane Protein F in Salmonella enterica Serovar Typhi

Osmoporin OmpC forms a complex with MlaA to maintain outer membrane lipid asymmetry in Escherichia coli

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