DNA supercoiling and environmental regulation of virulence gene expression in Shigella flexneri

Nature ◽  
1990 ◽  
Vol 344 (6268) ◽  
pp. 789-792 ◽  
Author(s):  
Charles J. Dorman ◽  
Niamh Ni Bhriain ◽  
Christopher F. Higgins
Keyword(s):  
Gene Expression ◽  
Environmental Regulation ◽  
Shigella Flexneri ◽  
Virulence Gene ◽  
Dna Supercoiling ◽  
Virulence Gene Expression

scholarly journals Formate PromotesShigellaIntercellular Spread and Virulence Gene Expression

mBio ◽  
2018 ◽  
Vol 9 (5) ◽  
Author(s):  
Benjamin J. Koestler ◽  
Carolyn R. Fisher ◽  
Shelley M. Payne
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Host Cell ◽  
Shigella Flexneri ◽  
Virulence Gene ◽  
Plaque Size ◽  
Acid Fermentation ◽  
Content Type ◽  
Virulence Gene Expression ◽  
Cell Spread

ABSTRACTThe intracellular human pathogenShigella flexneriinvades the colon epithelium, replicates to high cell density within the host cell, and then spreads to adjacent epithelial cells. WhenS. flexnerigains access to the host cytosol, the bacteria metabolize host cytosolic carbon using glycolysis and mixed acid fermentation, producing formate as a by-product. We show thatS. flexneriinfection results in the accumulation of formate within the host cell. Loss of pyruvate formate lyase (PFL; ΔpflB), which converts pyruvate to acetyl coenzyme A (CoA) and formate, eliminatesS. flexneriformate production and reduces the ability ofS. flexnerito form plaques in epithelial cell monolayers. This defect in PFL does not decrease the intracellular growth rate ofS. flexneri; rather, it affects cell-to-cell spread. TheS. flexneriΔpflBmutant plaque defect is complemented by supplying exogenous formate; conversely, deletion of theS. flexneriformate dehydrogenase genefdnGincreases host cell formate accumulation andS. flexneriplaque size. Furthermore, exogenous formate increases plaque size of the wild-type (WT)S. flexneristrain and promotesS. flexnericell-to-cell spread. We also demonstrate that formate increases the expression ofS. flexnerivirulence genesicsAandipaJ. IntracellularS. flexneriicsAandipaJexpression is dependent on the presence of formate, andipaJexpression correlates withS. flexneriintracellular density during infection. Finally, consistent with elevatedipaJ, we show that formate altersS. flexneri-infected host interferon- and tumor necrosis factor (TNF)-stimulated gene expression. We propose thatShigella-derived formate is an intracellular signal that modulates virulence in response to bacterial metabolism.IMPORTANCEShigellais an intracellular pathogen that invades the human host cell cytosol and exploits intracellular nutrients for growth, enabling the bacterium to create its own metabolic niche. ForShigellato effectively invade and replicate within the host cytoplasm, it must sense and adapt to changing environmental conditions; however, the mechanisms and signals sensed byS. flexneriare largely unknown. We have found that the secretedShigellametabolism by-product formate regulatesShigellaintracellular virulence gene expression and its ability to spread among epithelial cells. We propose thatShigellasenses formate accumulation in the host cytosol as a way to determine intracellularShigelladensity and regulate secreted virulence factors accordingly, enabling spatiotemporal regulation of effectors important for dampening the host immune response.

974 Bile Salt Exposure Regulates Shigella flexneri Virulence Gene Expression to Facilitate Mucosal Interaction and Colonic Infection

2016 ◽  
Vol 150 (4) ◽  
pp. S198 ◽  
Author(s):  
Kourtney Nickerson ◽  
Rachael B. Chanin ◽  
Jeticia R. Sistrunk ◽  
David A. Rasko ◽  
Christina S. Faherty
Keyword(s):  
Gene Expression ◽  
Bile Salt ◽  
Shigella Flexneri ◽  
Virulence Gene ◽  
Virulence Gene Expression

scholarly journals Shigella flexneri LuxS Quorum-Sensing System Modulates virB Expression but Is Not Essential for Virulence

2001 ◽  
Vol 69 (1) ◽  
pp. 15-23 ◽  
Author(s):  
William A. Day ◽  
Anthony T. Maurelli
Keyword(s):  
Gene Expression ◽  
Quorum Sensing ◽  
Stationary Phase ◽  
Shigella Flexneri ◽  
Virulence Gene ◽  
Maximal Activity ◽  
Conditioned Media ◽  
Virulence Gene Expression ◽  
Animal Pathogens ◽  
Operon Expression

ABSTRACT Quorum-sensing systems regulate the expression of virulence factors in a wide variety of plant and animal pathogens, including members of the Enterobacteriaceae. Studies of Shigellavirulence gene expression have demonstrated that maximal expression of genes encoding the type III secretion system and its substrates and maximal activity of this virulence organelle occur at high cell density. In these studies, we demonstrate that the expression ofipa, mxi, and spa invasion operons is maximal in stationary-phase bacteria and that conditioned media derived from stationary-phase cultures enhance the expression of these loci. In contrast, expression of virB, a transcription factor essential for the expression of invasion loci, peaks in late log phase; accordingly, virB expression is enhanced by a signal(s) present in conditioned media derived from late-log-phase cultures. Autoinducer 2 (AI-2), a quorum signaling molecule active in late log phase, was synthesized by Shigella species and enteroinvasive Escherichia coli and shown to be responsible for the observed peak of virB expression. However, AI-2 does not influence invasion operon expression and is not required forShigella virulence, as mutants deficient in AI-2 synthesis are fully virulent. The implications of these findings with regard to both virB and invasion operon expression and the evolution of circuitries governing virulence gene expression are discussed.

Vibrio harveyi virulence gene expression in vitro and in vivo during infection in black tiger shrimp Penaeus monodon

2020 ◽  
Vol 139 ◽  
pp. 153-160
Author(s):  
S Peeralil ◽  
TC Joseph ◽  
V Murugadas ◽  
PG Akhilnath ◽  
VN Sreejith ◽  
...  
Keyword(s):  
Gene Expression ◽  
Virulence Genes ◽  
Vibrio Harveyi ◽  
Penaeus Monodon ◽  
Challenge Test ◽  
Virulence Gene ◽  
Economic Losses ◽  
Virulence Gene Expression

Luminescent Vibrio harveyi is common in sea and estuarine waters. It produces several virulence factors and negatively affects larval penaeid shrimp in hatcheries, resulting in severe economic losses to shrimp aquaculture. Although V. harveyi is an important pathogen of shrimp, its pathogenicity mechanisms have yet to be completely elucidated. In the present study, isolates of V. harveyi were isolated and characterized from diseased Penaeus monodon postlarvae from hatcheries in Kerala, India, from September to December 2016. All 23 tested isolates were positive for lipase, phospholipase, caseinase, gelatinase and chitinase activity, and 3 of the isolates (MFB32, MFB71 and MFB68) showed potential for significant biofilm formation. Based on the presence of virulence genes, the isolates of V. harveyi were grouped into 6 genotypes, predominated by vhpA+ flaB+ ser+ vhh1- luxR+ vopD- vcrD+ vscN-. One isolate from each genotype was randomly selected for in vivo virulence experiments, and the LD50 ranged from 1.7 ± 0.5 × 103 to 4.1 ± 0.1 × 105 CFU ml-1. The expression of genes during the infection in postlarvae was high in 2 of the isolates (MFB12 and MFB32), consistent with the result of the challenge test. However, in MFB19, even though all genes tested were present, their expression level was very low and likely contributed to its lack of virulence. Because of the significant variation in gene expression, the presence of virulence genes alone cannot be used as a marker for pathogenicity of V. harveyi.

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