Transcriptomic analysis of the response of Pseudomonas fluorescens to epigallocatechin gallate by RNA-seq

Liu, Xiaoxiang; Bimiao, Shen; Du, Peng; Wang, Nan; Wang, Jiaxue; Lǐ, Jiànróng; Sun, Aijun

doi:10.1371/journal.pone.0177938

Cited by 23 publications

(21 citation statements)

References 77 publications

(93 reference statements)

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“…The expression profiles of the examined genes were consistent with the transcriptome sequencing (RNA-seq) results (Fig. 7), although observed fold changes differed in qRT-PCR and RNA-seq data, which may reflect sensitivity and specificity differences between qRT-PCR and RNA-sequencing technology (21).…”

Section: Figsupporting

confidence: 79%

Contributions of a LysR Transcriptional Regulator to Listeria monocytogenes Virulence and Identification of Its Regulons

et al. 2020

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The capacity of Listeria monocytogenes to adapt to environmental changes is facilitated by a large number of regulatory proteins encoded by its genome. Among these proteins are the uncharacterized LysR-type transcriptional regulators (LTTRs). LTTRs can work as positive and/or negative transcription regulators at both local and global genetic levels. Previously, our group determined by comparative genome analysis that one member of the LTTRs (NCBI accession no. WP_003734782) was present in pathogenic strains but absent from nonpathogenic strains. The goal of the present study was to assess the importance of this transcription factor in the virulence of L. monocytogenes strain F2365 and to identify its regulons. An L. monocytogenes strain lacking lysR (the F2365ΔlysR strain) displayed significant reductions in cell invasion of and adhesion to Caco-2 cells. In plaque assays, the deletion of lysR resulted in a 42.86% decrease in plaque number and a 13.48% decrease in average plaque size. Furthermore, the deletion of lysR also attenuated the virulence of L. monocytogenes in mice following oral and intraperitoneal inoculation. The analysis of transcriptomics revealed that the transcript levels of 139 genes were upregulated, while 113 genes were downregulated in the F2365ΔlysR strain compared to levels in the wild-type bacteria. lysR-repressed genes included ABC transporters, important for starch and sucrose metabolism as well as glycerolipid metabolism, flagellar assembly, quorum sensing, and glycolysis/gluconeogenesis. Conversely, lysR activated the expression of genes related to fructose and mannose metabolism, cationic antimicrobial peptide (CAMP) resistance, and beta-lactam resistance. These data suggested that lysR contributed to L. monocytogenes virulence by broad impact on multiple pathways of gene expression. IMPORTANCE Listeria monocytogenes is the causative agent of listeriosis, an infectious and fatal disease of animals and humans. In this study, we have shown that lysR contributes to Listeria pathogenesis and replication in cell lines. We also highlight the importance of lysR in regulating the transcription of genes involved in different pathways that might be essential for the growth and persistence of L. monocytogenes in the host or under nutrient limitation. Better understanding L. monocytogenes pathogenesis and the role of various virulence factors is necessary for further development of prevention and control strategies.

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Section: Figsupporting

confidence: 79%

Contributions of a LysR Transcriptional Regulator to Listeria monocytogenes Virulence and Identification of Its Regulons

et al. 2020

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“…The analysis of genes differentially expressed in the presence of EGCG also revealed components of several pathways (katB, ahpB, trxB2, PA2826, PA3237, PA3287) that are associated in P. aeruginosa with the response to oxidative stress and exposure to H 2 O 2 (25). These findings provide an insight into the antimicrobial mode of action of epigallocatechin gallate and agree with reports of the intercellular release of H 2 O 2 in E. coli O157:H7 treated with subinhibitory levels of EGCG (47) and the results of Liu et al (48), who profiled the transcriptomic response of P. fluorescens to EGCG. Surprisingly, apart from the oxidative stress genes, our RNA-seq data did not significantly overlap the P. fluorescens data set, which had over 400 genes whose expression was altered in response to EGCG.…”

Section: Discussionsupporting

confidence: 90%

“…Surprisingly, apart from the oxidative stress genes, our RNA-seq data did not significantly overlap the P. fluorescens data set, which had over 400 genes whose expression was altered in response to EGCG. We attribute these discrepancies to differences in the biology of the two Pseudomonas species, the higher concentrations of EGCG used by Liu et al (48), and the more stringent fold change cutoff (|log 2 FC| Ն 1.5 versus |log 2 FC| Ն 1) that we used to identify the differentially expressed P. aeruginosa genes.…”

Section: Discussionmentioning

confidence: 97%

Antimicrobial Activity of, and Cellular Pathways Targeted by, p -Anisaldehyde and Epigallocatechin Gallate in the Opportunistic Human Pathogen Pseudomonas aeruginosa

Adewunmi

Namjilsuren

Walker

et al. 2020

Appl Environ Microbiol

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Plant-derived aldehydes are constituents of essential oils that possess broad-spectrum antimicrobial activity and kill microorganisms without promoting resistance. In our previous study, we incorporated p-anisaldehyde from star anise into a polymer network called proantimicrobial networks via degradable acetals (PANDAs) and used it as a novel drug delivery platform. PANDAs released p-anisaldehyde upon a change in pH and humidity and controlled the growth of the multidrug-resistant pathogen Pseudomonas aeruginosa PAO1. In this study, we identified the cellular pathways targeted by p-anisaldehyde by generating 10,000 transposon mutants of PAO1 and screened them for hypersensitivity to p-anisaldehyde. To improve the antimicrobial efficacy of p-anisaldehyde, we combined it with epigallocatechin gallate (EGCG), a polyphenol from green tea, and demonstrated that it acts synergistically with p-anisaldehyde in killing P. aeruginosa. We then used transcriptome sequencing to profile the responses of P. aeruginosa to p-anisaldehyde, EGCG, and their combination. The exposure to p-anisaldehyde altered the expression of genes involved in modification of the cell envelope, membrane transport, drug efflux, energy metabolism, molybdenum cofactor biosynthesis, and the stress response. We also demonstrate that the addition of EGCG reversed many p-anisaldehyde-coping effects and induced oxidative stress. Our results provide insight into the antimicrobial activity of p-anisaldehyde and its interactions with EGCG and may aid in the rational identification of new synergistically acting combinations of plant metabolites. Our study also confirms the utility of the thiol-ene polymer platform for the sustained and effective delivery of hydrophobic and volatile antimicrobial compounds. IMPORTANCE Essential oils (EOs) are plant-derived products that have long been exploited for their antimicrobial activities in medicine, agriculture, and food preservation. EOs represent a promising alternative to conventional antibiotics due to their broad-range antimicrobial activity, low toxicity to human commensal bacteria, and capacity to kill microorganisms without promoting resistance. Despite the progress in the understanding of the biological activity of EOs, our understanding of many aspects of their mode of action remains inconclusive. The overarching aim of this work was to address these gaps by studying the molecular interactions between an antimicrobial plant aldehyde and the opportunistic human pathogen Pseudomonas aeruginosa. The results of this study identify the microbial genes and associated pathways involved in the response to antimicrobial phytoaldehydes and provide insights into the molecular mechanisms governing the synergistic effects of individual constituents within essential oils.

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“…If this were the case, biofilm growth could be inhibited by inhibitors of amyloid formation. Indeed, there is evidence that inhibitors of aggregation also tend to inhibit biofilm formation (48, 49). In the context of Parkinson’s and Alzheimer’s disease, the inhibition of amyloid formation is a major therapeutic target, with the inhibition of self-replication by secondary nucleation being the most promising candidate (36).…”

Section: Discussionmentioning

confidence: 99%

Physical Determinants of Amyloid Assembly in Biofilm Formation

Andreasen

Meisl

Taylor

et al. 2019

mBio

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Biofilms are generated by bacteria, embedded in the formed extracellular matrix. The biofilm's function is to improve the survival of a bacterial colony through, for example, increased resistance to antibiotics or other environmental stresses. Proteins secreted by the bacteria act as a major structural component of this extracellular matrix, as they self-assemble into highly stable amyloid fibrils, making the biofilm very difficult to degrade by physical and chemical means once formed. By studying the self-assembly mechanism of the fibrils from their monomeric precursors in two unrelated bacteria, our experimental and theoretical approaches shed light on the mechanism of functional amyloid assembly in the context of biofilm formation. Our results suggest that fibril formation may be a rate-limiting step in biofilm formation, which in turn has implications on the protein self-assembly reaction as a target for potential antibiotic drugs.

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Transcriptomic analysis of the response of Pseudomonas fluorescens to epigallocatechin gallate by RNA-seq

Cited by 23 publications

References 77 publications

Contributions of a LysR Transcriptional Regulator to Listeria monocytogenes Virulence and Identification of Its Regulons

Contributions of a LysR Transcriptional Regulator to Listeria monocytogenes Virulence and Identification of Its Regulons

Antimicrobial Activity of, and Cellular Pathways Targeted by, p -Anisaldehyde and Epigallocatechin Gallate in the Opportunistic Human Pathogen Pseudomonas aeruginosa

Physical Determinants of Amyloid Assembly in Biofilm Formation

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