scholarly journals DNA supercoiling and the anaerobic and growth phase regulation of tonB gene expression.

1988 ◽  
Vol 170 (6) ◽  
pp. 2816-2826 ◽  
Author(s):  
C J Dorman ◽  
G C Barr ◽  
N N Bhriain ◽  
C F Higgins
2006 ◽  
Vol 189 (5) ◽  
pp. 1866-1873 ◽  
Author(s):  
Timothy C. Barnett ◽  
Julia V. Bugrysheva ◽  
June R. Scott

ABSTRACT The impressive disease spectrum of Streptococcus pyogenes (the group A streptococcus [GAS]) is believed to be determined by its ability to modify gene expression in response to environmental stimuli. Virulence gene expression is controlled tightly by several different transcriptional regulators in this organism. In addition, expression of most, if not all, GAS genes is determined by a global mechanism dependent on growth phase. To begin an analysis of growth-phase regulation, we compared the transcriptome 2 h into stationary phase to that in late exponential phase of a serotype M3 GAS strain. We identified the arc transcript as more abundant in stationary phase in addition to the sag and sda transcripts that had been previously identified. We found that in stationary phase, the stability of sagA, sda, and arcT transcripts increased dramatically. We found that polynucleotide phosphorylase (PNPase [encoded by pnpA]) is rate limiting for decay of sagA and sda transcripts in late exponential phase, since the stability of these mRNAs was greater in a pnpA mutant, while stability of control mRNAs was unaffected by this mutation. Complementation restored the wild-type decay rate. Furthermore, in a pnpA mutant, the sagA mRNA appeared to be full length, as determined by Northern hybridization. It seems likely that mRNAs abundant in stationary phase are insensitive to the normal decay enzyme(s) and instead require PNPase for this process. It is possible that PNPase activity is limited in stationary phase, allowing persistence of these important virulence factor transcripts at this phase of growth.


Nature ◽  
1990 ◽  
Vol 344 (6268) ◽  
pp. 789-792 ◽  
Author(s):  
Charles J. Dorman ◽  
Niamh Ni Bhriain ◽  
Christopher F. Higgins

BMC Genomics ◽  
2014 ◽  
Vol 15 (1) ◽  
pp. 291 ◽  
Author(s):  
Wiebke Schröder ◽  
Jörg Bernhardt ◽  
Gabriella Marincola ◽  
Ludger Klein-Hitpass ◽  
Alexander Herbig ◽  
...  

1986 ◽  
Vol 6 (6) ◽  
pp. 2262-2266 ◽  
Author(s):  
J A Lewis ◽  
D A Matkovich

We have constructed a chimeric thymidine kinase (TK) minigene, pHe delta 6Ha, which combines the complete coding and 3' noncoding regions of a Chinese hamster TK cDNA with the promoter region and 5' untranslated region of the TK gene of herpes simplex virus type 1. We have transformed rat 4 cells to Tk+ with this gene and analyzed the pattern of TK gene expression in these transformants under various conditions of in vitro cell culture. We find that TK gene expression in these Tk+ transformants is growth phase dependent, responsive to adenovirus 5 infection, and indistinguishable in character under a variety of cell culture conditions from the pattern of TK gene expression in rat 4 cells transformed to Tk+ with the genomic Chinese hamster TK gene clone lambda HaTK.5. We are led to the conclusion that the genetic elements which mediate growth phase-dependent TK gene expression are contained entirely within the sequences of the mature cytoplasmic hamster TK mRNA.


2004 ◽  
Vol 72 (9) ◽  
pp. 5506-5510 ◽  
Author(s):  
John T. Loh ◽  
Mark H. Forsyth ◽  
Timothy L. Cover

ABSTRACT LuxS plays a role in the synthesis of an extracellular signaling molecule, autoinducer 2 (AI-2). To analyze a possible role of AI-2 in regulating Helicobacter pylori gene expression, we constructed a panel of transcriptional reporter strains. We show that the expression of H. pylori flaA is growth phase dependent and that flaA transcription increases in association with increased culture density. Mutating the luxS gene eliminates growth-phase-dependent control of flaA, and this growth phase dependence is restored when the luxS mutant strain is complemented with the wild-type luxS gene.


2018 ◽  
Vol 200 (8) ◽  
Author(s):  
Stephan Brouwer ◽  
Amanda J. Cork ◽  
Cheryl-Lynn Y. Ong ◽  
Timothy C. Barnett ◽  
Nicholas P. West ◽  
...  

ABSTRACTStreptococcus pyogenes(group AStreptococcus[GAS]) causes a wide range of human infections. The pathogenesis of GAS infections is dependent on the temporal expression of numerous secreted and surface-associated virulence factors that interact with host proteins. Streptococcal pyrogenic exotoxin B (SpeB) is one of the most extensively studied toxins produced by GAS, and the coordinate growth phase-dependent regulation ofspeBexpression is linked to disease severity phenotypes. Here, we identified the endopeptidase PepO as a novel growth phase-dependent regulator of SpeB in the invasive GAS M1 serotype strain 5448. By using transcriptomics followed by quantitative reverse transcriptase PCR and Western blot analyses, we demonstrate through targeted mutagenesis that PepO influences growth phase-dependent induction ofspeBgene expression. Compared to wild-type and complemented mutant strains, we demonstrate that the 5448ΔpepOmutant strain is more susceptible to killing by human neutrophils and is attenuated in virulence in a murine model of invasive GAS infection. Our results expand the complex regulatory network that is operating in GAS to control SpeB production and suggest that PepO is a virulence requirement during GAS M1T1 strain 5448 infections.IMPORTANCEDespite the continuing susceptibility ofS. pyogenesto penicillin, this bacterial pathogen remains a leading infectious cause of global morbidity and mortality. A particular subclone of the M1 serotype (M1T1) has persisted globally for decades as the most frequently isolated serotype from patients with invasive and noninvasive diseases in Western countries. One of the key GAS pathogenicity factors is the potent broad-spectrum cysteine protease SpeB. Although there has been extensive research interest on the regulatory mechanisms that controlspeBgene expression, its genetic regulation is not fully understood. Here, we identify the endopeptidase PepO as a new regulator ofspeBgene expression in the globally disseminated M1T1 clone and as being essential for virulence.


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