scholarly journals Molecular basis for the differential expression of the global regulator VieA inVibrio choleraebiotypes directed by H-NS, LeuO and quorum sensing

2017 ◽  
Vol 107 (3) ◽  
pp. 330-343 ◽  
Author(s):  
Julio C. Ayala ◽  
Hongxia Wang ◽  
Jorge A. Benitez ◽  
Anisia J. Silva
2008 ◽  
Vol 76 (4) ◽  
pp. 1358-1367 ◽  
Author(s):  
A. L. Moyer ◽  
R. T. Ramadan ◽  
J. Thurman ◽  
A. Burroughs ◽  
M. C. Callegan

ABSTRACT Most Bacillus cereus toxin production is controlled by the quorum-sensing-dependent, pleiotropic global regulator plcR, which contributes to the organism's virulence in the eye. The purpose of this study was to analyze the effects of B. cereus infection and plcR-regulated toxins on the barrier function of retinal pigment epithelium (RPE) cells, the primary cells of the blood-retina barrier. Human ARPE-19 cells were apically inoculated with wild-type or quorum-sensing-deficient B. cereus, and cytotoxicity was analyzed. plcR-regulated toxins were not required for B. cereus-induced RPE cytotoxicity, but these toxins did increase the rate of cell death, primarily by necrosis. B. cereus infection of polarized RPE cell monolayers resulted in increased barrier permeability, independent of plcR-regulated toxins. Loss of both occludin and ZO-1 expression occurred by 8 h postinfection, but alterations in tight junctions appeared to precede cytotoxicity. Of the several proinflammatory cytokines analyzed, only interleukin-6 was produced in response to B. cereus infection. These results demonstrate the deleterious effects of B. cereus infection on RPE barrier function and suggest that plcR-regulated toxins may not contribute significantly to RPE barrier permeability during infection.


2016 ◽  
Vol 45 (2) ◽  
pp. 699-710 ◽  
Author(s):  
Huaping Kang ◽  
Jianhua Gan ◽  
Jingru Zhao ◽  
Weina Kong ◽  
Jing Zhang ◽  
...  

2020 ◽  
Vol 117 (39) ◽  
pp. 24494-24502
Author(s):  
Glenn C. Capodagli ◽  
Kaitlyn M. Tylor ◽  
Jason T. Kaelber ◽  
Vasileios I. Petrou ◽  
Michael J. Federle ◽  
...  

Regulator gene of glucosyltransferase (Rgg) family proteins, such as Rgg2 and Rgg3, have emerged as primary quorum-sensing regulated transcription factors in Streptococcus species, controlling virulence, antimicrobial resistance, and biofilm formation. Rgg2 and Rgg3 function is regulated by their interaction with oligopeptide quorum-sensing signals called short hydrophobic peptides (SHPs). The molecular basis of Rgg–SHP and Rgg–target DNA promoter specificity was unknown. To close this gap, we determined the cryoelectron microscopy (cryo-EM) structure of Streptococcus thermophilus Rgg3 bound to its quorum-sensing signal, SHP3, and the X-ray crystal structure of Rgg3 alone. Comparison of these structures with that of an Rgg in complex with cyclosporin A (CsA), an inhibitor of SHP-induced Rgg activity, reveals the molecular basis of CsA function. Furthermore, to determine how Rgg proteins recognize DNA promoters, we determined X-ray crystal structures of both Streptococcus dysgalactiae Rgg2 and S. thermophilus Rgg3 in complex with their target DNA promoters. The physiological importance of observed Rgg–DNA interactions was dissected using in vivo genetic experiments and in vitro biochemical assays. Based on these structure–function studies, we present a revised unifying model of Rgg regulatory interplay. In contrast to existing models, where Rgg2 proteins are transcriptional activators and Rgg3 proteins are transcriptional repressors, we propose that both are capable of transcriptional activation. However, when Rgg proteins with different activation requirements compete for the same DNA promoters, those with more stringent activation requirements function as repressors by blocking promoter access of SHP-bound conformationally active Rgg proteins. While a similar gene expression regulatory scenario has not been previously described, in all likelihood it is not unique to streptococci.


2005 ◽  
Vol 58 (2) ◽  
pp. 552-564 ◽  
Author(s):  
Yi-Hu Dong ◽  
Xi-Fen Zhang ◽  
Jin-Ling Xu ◽  
Ai-Tee Tan ◽  
Lian-Hui Zhang

1994 ◽  
Vol 21 (3-4) ◽  
pp. 312-320 ◽  
Author(s):  
Rachel Grossman ◽  
Lyle E. Fox ◽  
Rena Gorovits ◽  
Iris Ben-Dror ◽  
Smadar Reisfeld ◽  
...  

2010 ◽  
Vol 23 (10) ◽  
pp. 1316-1323 ◽  
Author(s):  
Asita Chatterjee ◽  
Yaya Cui ◽  
Pranjib Chakrabarty ◽  
Arun K. Chatterjee

Erwinia carotovora subsp. carotovora causes soft-rotting (tissue-macerating) disease in many plants and plant organs. Although pectinases are the primary determinants of virulence, several ancillary factors that augment bacterial virulence have also been identified. One such factor is bacterial motility. Flagellum formation and bacterial movement are regulated in many enterobacteria, including E. carotovora subsp. carotovora, by FlhDC, the master regulator of flagellar genes and FliA, a flagellum-specific σ factor. We document here that motility of E. carotovora subsp. carotovora is positively regulated by the quorum-sensing signal, N-acylhomoserine lactone (AHL), and negatively regulated by RsmA, a post-transcriptional regulator. RsmA, an RNA-binding protein, causes translational repression and promotes RNA decay. Our data show that RsmA negatively regulates flhDC and fliA expression. Moreover, the chemical stabilities of transcripts of these genes are greater in an RsmA– mutant than in RsmA+ bacteria. These observations contrast with positive regulation of flhDC and motility by CsrA (= RsmA) in Escherichia coli. In the absence of AHL, the AHL receptors ExpR1/ExpR2 (= AhlR) in Erwinia carotovora subsp. carotovora negatively regulate motility and expression of flhDC and fliA by activating RsmA production. In the presence of AHL, regulatory effects of ExpR1/ExpR2 are neutralized, resulting in reduced levels of rsmA expression and enhanced motility.


2007 ◽  
Vol 66 (6) ◽  
pp. 1557-1565 ◽  
Author(s):  
Giordano Rampioni ◽  
Martin Schuster ◽  
Everett Peter Greenberg ◽  
Iris Bertani ◽  
Marco Grasso ◽  
...  

2017 ◽  
Author(s):  
Claire E. Price ◽  
Filipe Branco dos Santos ◽  
Anne Hesseling ◽  
Jaakko J. Uusitalo ◽  
Herwig Bachmann ◽  
...  

ABSTRACTA central theme in biology is to understand the molecular basis of fitness: which strategies succeed under which conditions; how are they mechanistically implemented; and which constraints shape trade-offs between alternative strategies. We approached these questions with parallel bacterial evolution experiments in chemostats. Chemostats provide a constant environment with a defined resource limitation (glucose), in which the growth rate can be controlled. UsingLactococcus lactis, we found a single mutation in a global regulator of carbon metabolism, CcpA, to confer predictable fitness improvements across multiple growth rates.In silicoprotein structural analysis complemented with biochemical and phenotypic assays, show that the mutation reprograms the CcpA regulon, specifically targeting transporters. This supports that membrane occupancy, rather than biosynthetic capacity, is the dominant constraint for the observed fitness enhancement. It also demonstrates that cells can modulate a pleiotropic regulator to work around limiting constraints.


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