Involvement of AmpG in mediating a dynamic relationship between serine beta-lactamase induction and biofilm-forming ability of Escherichia coli

Mallik, Dhriti; Pal, Shilpa; Ghosh, Anindya S.

doi:10.1093/femsle/fny065

Cited by 13 publications

(14 citation statements)

References 23 publications

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“…Similarly, the Δ ampE strain showed a 2-fold increased sensitivity to amoxicillin, cefalothin and cefoxitin. In line with this observation, the effect of elevation of the beta-lactam susceptibility was also reported in the case of the Δ ampG mutant [ 20 ].…”

Section: Resultssupporting

confidence: 64%

“…Upon activity of beta-lactams, possibly at the sub-inhibitory level, the PG fragments are transported back to cytoplasm with the assistance of AmpG permease. Recently, it has also been reported that suppression of AmpG permease can efficiently inhibit both BLA induction and biofilm formation [ 20 ]. The accumulated cytoplasmic PG fragments help in the triggering of the AmpC induction via a transcriptional regulator, AmpR (a lysR type of regulator) [ 15 , 16 ].…”

Section: Resultsmentioning

confidence: 99%

“…The strategy for genetic manipulations followed here was devised by Datsenko and Wanner (2000) [ 38 ] with certain modifications as adopted from Mallik et al (2018) [ 20 ]. All the strains and plasmids used/created in the study are given in Table 3 .…”

Section: Methodsmentioning

confidence: 99%

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Role of AmpC-Inducing Genes in Modulating Other Serine Beta-Lactamases in Escherichia coli

et al. 2022

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The consistently mutating bacterial genotypes appear to have accelerated the global challenge with antimicrobial resistance (AMR); it is therefore timely to investigate certain less-explored fields of targeting AMR mechanisms in bacterial pathogens. One of such areas is beta-lactamase (BLA) induction that can provide us with a collection of prospective therapeutic targets. The key genes (ampD, ampE and ampG) to which the AmpC induction mechanism is linked are also involved in regulating the production of fragmented muropeptides generated during cell-wall peptidoglycan recycling. Although the involvement of these genes in inducing class C BLAs is apparent, their effect on serine beta-lactamase (serine-BLA) induction is little known. Here, by using ∆ampD and ∆ampE mutants of E. coli, we attempted to elucidate the effects of ampD and ampE on the expression of serine-BLAs originating from Enterobacteriaceae, viz., CTX-M-15, TEM-1 and OXA-2. Results show that cefotaxime is the preferred inducer for CTX-M-15 and amoxicillin for TEM-1, whereas oxacillin for OXA-2. Surprisingly, exogenous BLA expressions are elevated in ∆ampD and ∆ampE mutants but do not always alter their beta-lactam susceptibility. Moreover, the beta-lactam resistance is increased upon in trans expression of ampD, whereas the same is decreased upon ampE expression, indicating a differential effect of ampD and ampE overexpression. In a nutshell, depending on the BLA, AmpD amidase moderately facilitates a varying level of serine-BLA expression whereas AmpE transporter acts likely as a negative regulator of serine-BLA.

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Section: Resultssupporting

confidence: 64%

Section: Resultsmentioning

confidence: 99%

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Role of AmpC-Inducing Genes in Modulating Other Serine Beta-Lactamases in Escherichia coli

et al. 2022

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“…388,389 Nonetheless, it is evident that the full breadth of the roles of AmpG in muropeptide recycling, β -lactam susceptibility, and biofilm formation has yet to be determined. 390 A complementary approach to AmpG inhibition, given that this permease is driven by the proton-motive force (PMF), 277 is inhibition of this force. Indeed, this may be the mechanism of the structures identified through screening.…”

Section: Resultsmentioning

confidence: 99%

Cell-Wall Recycling of the Gram-Negative Bacteria and the Nexus to Antibiotic Resistance

2018

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The importance of the cell wall to the viability of the bacterium is underscored by the breadth of antibiotic structures that act by blocking key enzymes that are tasked with cell-wall creation, preservation, and regulation. The interplay between cell-wall integrity, and the summoning forth of resistance mechanisms to deactivate cell-wall-targeting antibiotics, involves exquisite orchestration among cell-wall synthesis and remodeling and the detection of and response to the antibiotics through modulation of gene regulation by specific effectors. Given the profound importance of antibiotics to the practice of medicine, the assertion that understanding this interplay is among the most fundamentally important questions in bacterial physiology is credible. The enigmatic regulation of the expression of the AmpC β-lactamase, a clinically significant and highly regulated resistance response of certain Gram-negative bacteria to the β-lactam antibiotics, is the exemplar of this challenge. This review gives a current perspective to this compelling, and still not fully solved, 35-year enigma.

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“…It has been previously shown that AmpG inactivation prevents the entrance of NAG-anhNAM-peptides and consequently the cytosolic accumulation of AmpC-activator signals, thereby disabling ampC overexpression (47, 76–80). These facts are confirmed by our results, in which ampG deletion drastically decreased the intracellular accumulation of anhNAM-P3 and anhNAM-P5 in PAO1 but also in the high-level hyperproducer mutants in comparison with the respective parent strain, which leads to a block of ampC expression.…”

Section: Discussionmentioning

confidence: 99%

Regulation of AmpC-Driven β-Lactam Resistance in Pseudomonas aeruginosa: Different Pathways, Different Signaling

et al. 2019

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The extensive use of β-lactam antibiotics and the bacterial adaptive capacity have led to the apparently unstoppable increase of antimicrobial resistance, one of the current major global health challenges. In the leading nosocomial pathogen Pseudomonas aeruginosa, the mutation-driven AmpC β-lactamase hyperproduction stands out as the main resistance mechanism, but the molecular cues enabling this system have remained elusive until now. Here, we provide for the first time direct and quantitative information about the soluble cell wall-derived fragments accounting for the different levels and pathways of AmpC hyperproduction. Based on these results, we propose a hierarchical model of signals which ultimately govern ampC hyperexpression and resistance.

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Involvement of AmpG in mediating a dynamic relationship between serine beta-lactamase induction and biofilm-forming ability of Escherichia coli

Cited by 13 publications

References 23 publications

Role of AmpC-Inducing Genes in Modulating Other Serine Beta-Lactamases in Escherichia coli

Role of AmpC-Inducing Genes in Modulating Other Serine Beta-Lactamases in Escherichia coli

Cell-Wall Recycling of the Gram-Negative Bacteria and the Nexus to Antibiotic Resistance

Regulation of AmpC-Driven β-Lactam Resistance in Pseudomonas aeruginosa: Different Pathways, Different Signaling

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