Solvent tolerance in Gram-negative bacteria

Segura, Ana; Molina, Lázaro; Fillet, Sandy; Krell, Tino; Bernal, Patricia; Muñoz‐Rojas, Jesús; Ramos, Juan L.

doi:10.1016/j.copbio.2011.11.015

Cited by 164 publications

(142 citation statements)

References 52 publications

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“…Alcohols are known to induce hyperfluidization of bacterial membranes and protein denaturation, following an increase of reactive oxygen species levels (19,20). Indeed, a recent genomic study showed that BA upregulated genes responsible for envelope stresses, metabolite transportation, and oxidative stresses (36).…”

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

“…The antimicrobial mechanisms of some organic solvents were also intensively investigated (18)(19)(20). It was suggested that organic solvents accumulate in cellular membranes and disorganize the structures, and the resultant losses of intracellular ions and metabolites lead to cell death (19,20). Organic solvents also induce various cellular responses, including structural changes of the membrane (21,22), and upregulation or downregulation of various other genes, as revealed by transcriptomic analyses (19,23).…”

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confidence: 99%

“…It was suggested that organic solvents accumulate in cellular membranes and disorganize the structures, and the resultant losses of intracellular ions and metabolites lead to cell death (19,20). Organic solvents also induce various cellular responses, including structural changes of the membrane (21,22), and upregulation or downregulation of various other genes, as revealed by transcriptomic analyses (19,23). Nonetheless, with regard to the simultaneous addition of cationic agents and alcohols, many questions remain, such as how each agent acts individually on microbes.…”

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Pentanol and Benzyl Alcohol Attack Bacterial Surface Structures Differently

Yano

Miyahara

Morii

et al. 2016

Appl Environ Microbiol

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bThe genus Methylobacterium tolerates hygiene agents like benzalkonium chloride (BAC), and infection with this organism is an important public health issue. Here, we found that the combination of BAC with particular alcohols at nonlethal concentrations in terms of their solitary uses significantly reduced bacterial viability after only 5 min of exposure. Among the alcohols, Raman spectroscopic analyses showed that pentanol (pentyl alcohol [PeA]) and benzyl alcohol (BzA) accelerated the cellular accumulation of BAC. Fluorescence spectroscopic assays and morphological assays with giant vesicles indicated that PeA rarely attacked membrane structures, while BzA increased the membrane fluidity and destabilized the structures. Other fluorescent spectroscopic assays indicated that PeA and BzA inactivate bacterial membrane proteins, including an efflux pump for BAC transportation. These findings suggested that the inactivation of membrane proteins by PeA and BzA led to the cellular accumulation but that only BzA also enhanced BAC penetration by membrane fluidization at nonlethal concentrations.

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confidence: 99%

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Pentanol and Benzyl Alcohol Attack Bacterial Surface Structures Differently

Yano

Miyahara

Morii

et al. 2016

Appl Environ Microbiol

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“…One well-established toxic effect of ethanol on E. coli is an increase in cell-envelope permeability (7)(8)(9). E. coli exposed to ethanol exhibit reduced peptidoglycan cross-linking, which is detrimental to viability, and altered membrane-lipid composition, which may represent an attempt to cope with ethanol stress (10,11).…”

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Correcting direct effects of ethanol on translation and transcription machinery confers ethanol tolerance in bacteria

Haft

Keating

Schwaegler

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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The molecular mechanisms of ethanol toxicity and tolerance in bacteria, although important for biotechnology and bioenergy applications, remain incompletely understood. Genetic studies have identified potential cellular targets for ethanol and have revealed multiple mechanisms of tolerance, but it remains difficult to separate the direct and indirect effects of ethanol. We used adaptive evolution to generate spontaneous ethanol-tolerant strains of Escherichia coli, and then characterized mechanisms of toxicity and resistance using genome-scale DNAseq, RNAseq, and ribosome profiling coupled with specific assays of ribosome and RNA polymerase function. Evolved alleles of metJ, rho, and rpsQ recapitulated most of the observed ethanol tolerance, implicating translation and transcription as key processes affected by ethanol. Ethanol induced miscoding errors during protein synthesis, from which the evolved rpsQ allele protected cells by increasing ribosome accuracy. Ribosome profiling and RNAseq analyses established that ethanol negatively affects transcriptional and translational processivity. Ethanol-stressed cells exhibited ribosomal stalling at internal AUG codons, which may be ameliorated by the adaptive inactivation of the MetJ repressor of methionine biosynthesis genes. Ethanol also caused aberrant intragenic transcription termination for mRNAs with low ribosome density, which was reduced in a strain with the adaptive rho mutation. Furthermore, ethanol inhibited transcript elongation by RNA polymerase in vitro. We propose that ethanol-induced inhibition and uncoupling of mRNA and protein synthesis through direct effects on ribosomes and RNA polymerase conformations are major contributors to ethanol toxicity in E. coli, and that adaptive mutations in metJ, rho, and rpsQ help protect these central dogma processes in the presence of ethanol.

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