The Association of Cell Division Regulated by DicC With the Formation of Viable but Non-culturable Escherichia coli O157:H7

Pan, Hanxu; Dong, Kai; Rao, Lei; Zhao, Liang; Wang, Yongtao; Liao, Xiaojun

doi:10.3389/fmicb.2019.02850

Cited by 13 publications

(7 citation statements)

References 60 publications

(79 reference statements)

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“…Recent work in E. coli O157:H7 showed that overexpression of DicC repressed dicA's transcription, similar to Cro repression of cI (39). Additionally, deletion of dicC led to a reduction in dicB levels while overexpression induced dicB expression (39). Our results show that DicC is important for the spontaneous induction phenotype of dicBp, as deletion of dicC results in a reduction in the frequency of cells that have induced dicBp.…”

Section: Discussionsupporting

confidence: 74%

“…A study by Yun et al in E. coli MG1655 showed that by binding to dicCp, DicA blocks dicC transcription and activates its own transcription (47). Recent work in E. coli O157:H7 showed that overexpression of DicC repressed dicA's transcription, similar to Cro repression of cI (39). Additionally, deletion of dicC led to a reduction in dicB levels while overexpression induced dicB expression (39).…”

Section: Discussionmentioning

confidence: 86%

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Mechanisms of regulation of cryptic prophage-encoded gene products inEscherichia coli

Ragunathan

Kim²,

et al. 2023

Preprint

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The dicBF operon of Qin cryptic prophage in Escherichia coli K12 encodes the small RNA (sRNA) DicF and small protein DicB, which regulate host cell division and are toxic when overexpressed. While new functions of DicB and DicF have been identified in recent years, the mechanisms controlling the expression of the dicBF operon have remained unclear. Under standard laboratory growth conditions, transcription from dicBp, the major promoter of the dicBF operon, is repressed by DicA. Here, we discovered that transcription of the dicBF operon and processing of the polycistronic mRNA is regulated by multiple mechanisms. DicF sRNA accumulates during stationary phase and is processed from the polycistronic dicBF mRNA by the action of both RNase III and RNase E. DicA-mediated transcriptional repression of dicBp can be relieved by an antirepressor protein, Rem, encoded on the Qin prophage. Ectopic production of Rem results in cell filamentation due to strong induction of the dicBF operon and filamentation is mediated by DicF and DicB. Spontaneous derepression of dicBp occurs in a subpopulation of cells independent of the antirepressor. This phenomenon is reminiscent of the bistable switch of λ phage with DicA and DicC performing functions similar to CI and Cro, respectively. Additional experiments demonstrate stress-dependent induction of the dicBF operon. Collectively, our results illustrate that toxic genes encoded on cryptic prophages are subject to layered mechanisms of control, some that are derived from the ancestral phage and some that are likely later adaptations.

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Section: Discussionsupporting

confidence: 74%

Section: Discussionmentioning

confidence: 86%

Mechanisms of regulation of cryptic prophage-encoded gene products inEscherichia coli

Ragunathan

Kim²,

et al. 2023

Preprint

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Section: Resultsmentioning

confidence: 99%

“…In our study, the sulA gene was significantly upregulated as shown in Figure 2g. DicB is another cell division inhibition protein, [53] which was also significantly upregulated in E. coli treated with EPGNs (Figure 2g). All these results showed that the cell division of E. coli was largely inhibited by the treatment of EPGNs, confirming the cell division inhibitory effect of EPGNs.…”

Section: Epgns Cause Bacterial Cell Expansionmentioning

confidence: 98%

Expand and Sensitize: Guanidine‐Functionalized Exopolysaccharide Nanoparticles Cause Bacterial Cell Expansion and Antibiotic Sensitization

Li,

Jia,

Seidi

et al. 2023

Adv Funct Materials

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Conventional antibacterial agents and mechanisms are frequently observed to be ineffective due to the evolution of bacteria to the strains with stronger antibiotic resistance, and hence developing alternative antibacterial materials and mechanisms is urgently needed. Here, guanidine‐functionalized exopolysaccharide (EPS) nanoparticles (termed EPGNs) with durable antibacterial and antibiofilm activities are developed. Very interestingly, the EPGNs obtained by the reaction of EPS, epichlorohydrin, and polyhexamethylene guanidine hydrochloride exhibit an unconventional antibacterial mechanism, i.e., they can induce substantial bacterial cell expansion by upregulating the SulA and DicB proteins that are responsible for cell division inhibition, along with the increase of reactive oxygen species production, bacterial cell surface disruption, and bacterial ribosomal RNA degradation. The transcriptome analysis reveals that EPGNs can hinder cell motility, induce loss of cell integrity, decrease the resistance of bacteria to oxidative stress, and finally lead to cell death. Moreover, EPGNs can effectively accelerate the bacteria‐infected wound healing. This work provides the first example that nanomaterials can cause bacterial cell expansion by affecting intracellular structures and inhibiting cell division, and it may inspire other researchers to investigate the effect of antibacterial materials on the change of bacterial volume and design unconventional antibacterial materials/strategies.

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“…Log phase bacteria were used to focus population gates around E. coli or S. aureus cells that were alive and had intact cell membrane. Data were collected using CellQuest software (Becton Dickinson, San Jose, CA, United States; Pan et al, 2019).…”

Section: Fcm Analysismentioning

confidence: 99%

Influence of pressurization rate and mode on cell damage of Escherichia coli and Staphyloccocus aureus by high hydrostatic pressure

Yang

Li²,

Dong³

et al. 2023

Front. Microbiol.

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As a non-thermal technology, high hydrostatic pressure (HHP) has been widely investigated for inactivating microorganisms in food. Few studies have been presented on the pressurization/depressurization rate and mode of microbial inactivation. In this study, effect of pressurization rate and mode on Escherichia coli and Staphylococcus aureus cell damage during HHP treatment was investigated. The results showed that fast pressurization + linear mode (FL) treatment has the best bactericidal effect on E. coli and S. aureus, followed by fast pressurization + stepwise mode (FS) and slow pressurization + stepwise mode (SS) treatments. FL treatment caused more morphological damage to the cell wall, cell membrane, and cytoplasmic components compared with FS and SS treatment detected by SEM and TEM. Additionally, the damage to membrane permeability of them was also enhanced after FL treatment. Therefore, our results indicated that FL treatment could be applied to enhance the bactericidal effect of HHP on bacteria by increasing the damage to cell morphological structure and membrane integrity.

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The Association of Cell Division Regulated by DicC With the Formation of Viable but Non-culturable Escherichia coli O157:H7

Cited by 13 publications

References 60 publications

Mechanisms of regulation of cryptic prophage-encoded gene products inEscherichia coli

Mechanisms of regulation of cryptic prophage-encoded gene products inEscherichia coli

Expand and Sensitize: Guanidine‐Functionalized Exopolysaccharide Nanoparticles Cause Bacterial Cell Expansion and Antibiotic Sensitization

Influence of pressurization rate and mode on cell damage of Escherichia coli and Staphyloccocus aureus by high hydrostatic pressure

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