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Chapter 9 : Enterohemorrhagic Virulence Gene Regulation

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Enterohemorrhagic Virulence Gene Regulation, Page 1 of 2

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Abstract:

As a species, is highly successful, adapting to inhabit the lower intestine of warm-blooded animals. Commensal , part of the normal biota, resides harmlessly in the gut, producing vitamin K. However, also causes three types of disease in humans: urinary tract infections, sepsis in newborns, and diarrheal disease. Enterohemorrhagic (EHEC) plays a prominent role in the third type of illness. It has been estimated that, for the pan genome of the nonpathogenic and pathogenic strains only contain a core set of genes comprising approximately 20% of any one genome ( ). Much of the horizontally acquired genetic information is clustered within genomic islands in pathogens. As for EHEC, this has allowed the organism to not only attach and colonize the large intestine of humans and other animals, to outcompete commensal and other bacteria at the site of infection, but also to cause serious disease.

Citation: Mellies J, Lorenzen E. 2015. Enterohemorrhagic Virulence Gene Regulation, p 199-209. In Sperandio V, Hovde C (ed), Enterohemorrhagic and Other Shiga Toxin-Producing . ASM Press, Washington, DC. doi: 10.1128/microbiolspec.EHEC-0004-2013

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Type III Secretion System
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Outer Membrane Protein A
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Type III Secretion System
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Outer Membrane Protein A
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Figures

Image of Figure 1
Figure 1

Control of acid tolerance by EHEC. Resident flora produce AHL signaling molecules that stimulate expression of the glutamate-dependent acid resistance system ( ). The GAD system removes excess protons by exchanging the alpha-carboxyl groups of glutamate with a proton. The resulting GABA molecules are transported out of the cell in exchange for additional glutamate ( ). doi:10.1128/microbiolspec.EHEC-0004-2013.f1

Citation: Mellies J, Lorenzen E. 2015. Enterohemorrhagic Virulence Gene Regulation, p 199-209. In Sperandio V, Hovde C (ed), Enterohemorrhagic and Other Shiga Toxin-Producing . ASM Press, Washington, DC. doi: 10.1128/microbiolspec.EHEC-0004-2013
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Image of Figure 2
Figure 2

Regulation of flagellar biosynthesis and motility. Extracellular signals norepinephrine, epinephrine, and AI-3 stimulate expression of (motility) and (biosynthesis) through the two-component system QseBC ( ). Following induction of the operons, inhibits expression of and ( ). Blunted arrow indicates negative control. doi:10.1128/microbiolspec.EHEC-0004-2013.f2

Citation: Mellies J, Lorenzen E. 2015. Enterohemorrhagic Virulence Gene Regulation, p 199-209. In Sperandio V, Hovde C (ed), Enterohemorrhagic and Other Shiga Toxin-Producing . ASM Press, Washington, DC. doi: 10.1128/microbiolspec.EHEC-0004-2013
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Image of Figure 3
Figure 3

Inhibition of EHEC effector molecules in the cattle rumen and human small intestine. Resident flora in the rumen produce the signaling molecule AHL that causes SdiA to fold and inhibit transcription of ( ). Glycolytic conditions in the small intestine inhibit the transcriptional activators KdpE and Cra ( ). Fucose, a component of cell-surface glycans, signals through the two-component system FusKR to inhibit Ler expression ( ). The transcriptional silencer H-NS maintains Ler downregulation ( ). Blunted arrows indicate negative control. doi:10.1128/microbiolspec.EHEC-0004-2013.f3

Citation: Mellies J, Lorenzen E. 2015. Enterohemorrhagic Virulence Gene Regulation, p 199-209. In Sperandio V, Hovde C (ed), Enterohemorrhagic and Other Shiga Toxin-Producing . ASM Press, Washington, DC. doi: 10.1128/microbiolspec.EHEC-0004-2013
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Image of Figure 4
Figure 4

Stimulation of LEE and non-LEE effector molecules required for infection by EHEC. In the large intestine of humans and RAJ, the host-produced hormones norepinephrine and epinephrine, EHEC-derived signaling molecule AI-3, and sulfate and phosphate trigger the two-component sensors QseC,F and/or QseEF to upregulate and transcription ( ). In addition, ethanolamine, a cell membrane component, stimulates production through EutR and QseC ( ). Gluconeogenic conditions of the large intestine activate the activators KdpE and Cra, and butyrate directly activates LEE transcriptional activity ( ). The RNA chaperone Hfq affects LEE expression through interactions with Ler mRNA but has negative or positive effects depending on the strain of EHEC, as indicated by a dashed arrow ( ). Finally, nutrient deprivation associated with the infection site activates the stringent response leading to production of ppGpp, which promotes expression of the LEE transcriptional activators and and the non-LEE effector NleA ( ). The asterisk indicates that () expression is upregulated by several other factors, including temperature, pH, iron, ammonium, calcium, bicarbonate, and the regulatory proteins IHF, Fis, BipA, PerC, and GadX (previously reviewed in reference 45). Blunted arrow indicates negative control. doi:10.1128/microbiolspec.EHEC-0004-2013.f4

Citation: Mellies J, Lorenzen E. 2015. Enterohemorrhagic Virulence Gene Regulation, p 199-209. In Sperandio V, Hovde C (ed), Enterohemorrhagic and Other Shiga Toxin-Producing . ASM Press, Washington, DC. doi: 10.1128/microbiolspec.EHEC-0004-2013
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Figure 5

Stimulation of Shiga toxin expression. Low iron levels lead to upregulation of ( ). Hydrogen peroxide and antibiotics targeting DNA synthesis, such as mytomycin C and quinolines, lead to DNA damage and activate RecA to induce Stx1 production ( ). Sulfate, phosphate, and epinephrine molecules signal through the two-component system QseCF to RecA, thus leading activation of Stx2 production. Ethanolamine also upregulates through the transcription factor EutR ( ). doi:10.1128/microbiolspec.EHEC-0004-2013.f5

Citation: Mellies J, Lorenzen E. 2015. Enterohemorrhagic Virulence Gene Regulation, p 199-209. In Sperandio V, Hovde C (ed), Enterohemorrhagic and Other Shiga Toxin-Producing . ASM Press, Washington, DC. doi: 10.1128/microbiolspec.EHEC-0004-2013
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Tables

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TABLE 1

Regulation of non-LEE adhesins and factors involved in EHEC adherence

Citation: Mellies J, Lorenzen E. 2015. Enterohemorrhagic Virulence Gene Regulation, p 199-209. In Sperandio V, Hovde C (ed), Enterohemorrhagic and Other Shiga Toxin-Producing . ASM Press, Washington, DC. doi: 10.1128/microbiolspec.EHEC-0004-2013

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