Global Regulator of Virulence A (GrvA) Coordinates Expression of Discrete Pathogenic Mechanisms in Enterohemorrhagic Escherichia coli through Interactions with GadW-GadE

Morgan, Jason K.; O’Carroll, Ronan; Harro, Carly M.; Vendura, Khoury W.; Shaw, Lindsey N.; Riordan, James T.

doi:10.1128/jb.00556-15

Cited by 13 publications

(27 citation statements)

References 93 publications

(112 reference statements)

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“…It could be that the downregulation gadEAB is related to virulence gene expression, because in the TW14359 EHEC O157:H7 strain, gadE is one of the master regulators of the LEE pathogenicity island (Morgan et al . ).…”

Section: Resultsmentioning

confidence: 97%

The antibiotics potentiator bicarbonate causes upregulation of tryptophanase and iron acquisition proteins inEscherichia coli

Gutiérrez‐Huante

Martínez‐Duncker

Sauceda

et al. 2018

Lett Appl Microbiol

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Significance and Impact of the Study: Bicarbonate (NaHCO 3 ) can enhance the activity of various antibiotics. This work investigated its action mechanism. We carried out a transcriptional analysis in Escherichia coli with the aim of defining initial bacterial changes potentially linked to the enhancing activity of NaHCO 3 . Our approach differed from the longer term exposure to NaHCO 3 recently used by other researchers, who noticed changes in the bacterial proton motive force. Based on our analysis, we propose two routes possibly linked to the effect of NaHCO 3 . Conceivably, those routes are potential targets that could be manipulated by alternative means to augment the effect of antibiotics. AbstractWe have reported that bicarbonate (NaHCO 3 ) potentiates the activity of aminoglycosides in Escherichia coli, but the action mechanism was not identified. To eventually understand how NaHCO 3 can potentiate antibiotics, we thought that a rational first step was to examine the effect of NaHCO 3 separately and to inspect initial gene expression changes triggered by it. In this work, we started by confirming that NaHCO 3 can reduce the number of viable E. coli bacteria. We then investigated, via RNAseq, gene expression changes induced by NaHCO 3 . There were upregulated and downregulated genes, among the top upregulated genes c. 10-fold increase in expression) was tnaA, the gene encoding tryptophanase, the enzyme that degrades tryptophan to indole. Considering that higher expression of tnaA likely led to increases in indole, we tested the effect of indole and found both growth inhibition and synergy with NaHCO 3 . We suggest that indole may participate in growth inhibition of E. coli. The RNAseq analysis also revealed upregulation (≥4-fold) of genes encoding proteins for the acquisition of iron and downregulation (≥16-fold) of genes encoding iron-sulphur-holding proteins; hence NaHCO 3 apparently triggered also an iron-deficit response. We suggest that iron deficiency may also be involved in growth inhibition by NaHCO 3 .

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Section: Resultsmentioning

confidence: 97%

The antibiotics potentiator bicarbonate causes upregulation of tryptophanase and iron acquisition proteins inEscherichia coli

Gutiérrez‐Huante

Martínez‐Duncker

Sauceda

et al. 2018

Lett Appl Microbiol

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“…GrvA (global regulator of virulence A), a Tox-R family transcriptional regulator, is also involved in the regulation of the LEE. GrvA works in conjunction with RcsB, a regulator which has been shown to activate and repress the LEE; however, until recently it has not been understood how this mechanism works [55,56]. grvA is directly activated by RcsB, with RcsB hypothesised to bind at grvA promoter region, although this is temperature sensitive [56].…”

Section: Cellular Regulation That Affects Upon the Leementioning

confidence: 99%

“…GrvA works in conjunction with RcsB, a regulator which has been shown to activate and repress the LEE; however, until recently it has not been understood how this mechanism works [55,56]. grvA is directly activated by RcsB, with RcsB hypothesised to bind at grvA promoter region, although this is temperature sensitive [56]. GrvA positively regulates the LEE by indirectly down-regulating GadE, a regulator of acid tolerance and known repressor of ler [56,57].…”

Section: Cellular Regulation That Affects Upon the Leementioning

confidence: 99%

“…grvA is directly activated by RcsB, with RcsB hypothesised to bind at grvA promoter region, although this is temperature sensitive [56]. GrvA positively regulates the LEE by indirectly down-regulating GadE, a regulator of acid tolerance and known repressor of ler [56,57]. GrvA repression of gadE was dependent on an intact gadW [56].…”

Section: Cellular Regulation That Affects Upon the Leementioning

confidence: 99%

“…GrvA positively regulates the LEE by indirectly down-regulating GadE, a regulator of acid tolerance and known repressor of ler [56,57]. GrvA repression of gadE was dependent on an intact gadW [56].…”

Section: Cellular Regulation That Affects Upon the Leementioning

confidence: 99%

See 2 more Smart Citations

Control freaks—signals and cues governing the regulation of virulence in attaching and effacing pathogens

Turner

Connolly

Roe

2018

Biochemical Society Transactions

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Enterohaemorrhagic Escherichia coli (EHEC) mediates disease using a type 3 secretion system (T3SS), which is encoded on the locus of enterocyte effacement (LEE) and is tightly controlled by master regulators. This system is further modulated by a number of signals that help to fine-tune virulence, including metabolic, environmental and chemical signals. Since the LEE and its master regulator, Ler, were established, there have been numerous scientific advancements in understanding the regulation and expression of virulence factors in EHEC. This review will discuss the recent advancements in this field since our previous review, with a focus on the transcriptional regulation of the LEE.

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Enterohemorrhagic Escherichia coli outwits hosts through sensing small molecules

Carlson-Banning

Sperandio

2018

Current Opinion in Microbiology

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Small molecules help intestinal pathogens navigate the complex human gastrointestinal tract to exploit favorable microhabitats. These small molecules provide spatial landmarks for pathogens to regulate synthesis of virulence caches and are derived from the host, ingested plant and animal material, and the microbiota. Their concentrations and fluxes vary along the length of the gut and provide molecular signatures that are beginning to be explored through metabolomics and genetics. However, while many small molecules have been identified and are reviewed here, there are undoubtedly others that may also profoundly affect how enteric pathogens infect their hosts.

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Global Regulator of Virulence A (GrvA) Coordinates Expression of Discrete Pathogenic Mechanisms in Enterohemorrhagic Escherichia coli through Interactions with GadW-GadE

Cited by 13 publications

References 93 publications

The antibiotics potentiator bicarbonate causes upregulation of tryptophanase and iron acquisition proteins inEscherichia coli

The antibiotics potentiator bicarbonate causes upregulation of tryptophanase and iron acquisition proteins inEscherichia coli

Control freaks—signals and cues governing the regulation of virulence in attaching and effacing pathogens

Enterohemorrhagic Escherichia coli outwits hosts through sensing small molecules

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