scholarly journals Crystal structure ofPseudomonas aeruginosaRsaL bound to promoter DNA reaffirms its role as a global regulator involved in quorum-sensing

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


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

2011 ◽  
Vol 108 (38) ◽  
pp. 15763-15768 ◽  
Author(s):  
M. J. Lintz ◽  
K.-I. Oinuma ◽  
C. L. Wysoczynski ◽  
E. P. Greenberg ◽  
M. E. A. Churchill

2005 ◽  
Vol 280 (32) ◽  
pp. 29073-29079 ◽  
Author(s):  
André Schiefner ◽  
Kinga Gerber ◽  
Sabine Seitz ◽  
Wolfram Welte ◽  
Kay Diederichs ◽  
...  

2007 ◽  
Vol 17 (1) ◽  
pp. 159-170 ◽  
Author(s):  
M. C.M. Reddy ◽  
K. Gokulan ◽  
W. R. Jacobs ◽  
T. R. Ioerger ◽  
J. C. Sacchettini

2002 ◽  
Vol 22 (19) ◽  
pp. 6735-6749 ◽  
Author(s):  
Cécile Deluen ◽  
Nicole James ◽  
Laurent Maillet ◽  
Miguel Molinete ◽  
Grégory Theiler ◽  
...  

ABSTRACT The Saccharomyces cerevisiae Ccr4-Not complex is a global regulator of transcription that is thought to regulate TATA binding protein (TBP) function at certain promoters specifically. In this paper, we show interactions between the essential domain of Not1p, which interacts with Not4p and Not5p, and the N-terminal domain of yTAF1. We isolated a temperature-sensitive nonsense allele of TAF1, taf1-4, which is synthetically lethal at the permissive temperature when combined with not4 and not5 mutants and which produces high levels of a C-terminally truncated yTAF1 derivative. Overexpression of C-terminally truncated yTAF1 is toxic in not4 or not5 mutants, whereas overexpression of full-length yTAF1 suppresses not4. Furthermore, mutations in the autoinhibitory N-terminal TAND domain of yTAF1 suppress not5, and the overexpression of similar mutants does not suppress not4. We find that, like Not5p, yTAF1 acts as a repressor of stress response element-dependent transcription. Finally, we have evidence for stress-regulated occupancy of promoter DNA by Not5p and for Not5p-dependent regulation of yTAF1 association with promoter DNA. Taken together with our finding that Not1p copurifies with glutathione S-transferase-yTaf1 in large complexes, these results provide the first molecular evidence that the Ccr4-Not complex might interact with yTAF1 to regulate its association at promoters, a function that might in turn regulate the autoinhibitory N-terminal domain of yTAF1.


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.


Author(s):  
Ryan R Chaparian ◽  
Minh L N Tran ◽  
Laura C Miller Conrad ◽  
Douglas B Rusch ◽  
Julia C van Kessel

Abstract Bacteria coordinate cellular behaviors using a cell–cell communication system termed quorum sensing. In Vibrio harveyi, the master quorum sensing transcription factor LuxR directly regulates >100 genes in response to changes in population density. Here, we show that LuxR derepresses quorum sensing loci by competing with H-NS, a global transcriptional repressor that oligomerizes on DNA to form filaments and bridges. We first identified H-NS as a repressor of bioluminescence gene expression, for which LuxR is a required activator. In an hns deletion strain, LuxR is no longer necessary for transcription activation of the bioluminescence genes, suggesting that the primary role of LuxR is to displace H-NS to derepress gene expression. Using RNA-seq and ChIP-seq, we determined that H-NS and LuxR co-regulate and co-occupy 28 promoters driving expression of 63 genes across the genome. ChIP-PCR assays show that as autoinducer concentration increases, LuxR protein accumulates at co-occupied promoters while H-NS protein disperses. LuxR is sufficient to evict H-NS from promoter DNA in vitro, which is dependent on LuxR DNA binding activity. From these findings, we propose a model in which LuxR serves as a counter-silencer at H-NS-repressed quorum sensing loci by disrupting H-NS nucleoprotein complexes that block transcription.


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