scholarly journals A mutation in the ftsK gene of Escherichia coli affects cell-cell separation, stationary-phase survival, stress adaptation, and expression of the gene encoding the stress protein UspA.

1997 ◽  
Vol 179 (18) ◽  
pp. 5878-5883 ◽  
Author(s):  
A A Diez ◽  
A Farewell ◽  
U Nannmark ◽  
T Nyström
2004 ◽  
Vol 186 (20) ◽  
pp. 6698-6705 ◽  
Author(s):  
Jason A. Opdyke ◽  
Ju-Gyeong Kang ◽  
Gisela Storz

ABSTRACT A previous bioinformatics-based search for small RNAs in Escherichia coli identified a novel RNA named IS183. The gene encoding this small RNA is located between and on the opposite strand of genes encoding two transcriptional regulators of the acid response, gadX (yhiX) and gadW (yhiW). Given that IS183 is encoded in the gad gene cluster and because of its role in regulating acid response genes reported here, this RNA has been renamed GadY. We show that GadY exists in three forms, a long form consisting of 105 nucleotides and two processed forms, consisting of 90 and 59 nucleotides. The expression of this small RNA is highly induced during stationary phase in a manner that is dependent on the alternative sigma factor σS. Overexpression of the three GadY RNA forms resulted in increased levels of the mRNA encoding the GadX transcriptional activator, which in turn caused increased levels of the GadA and GadB glutamate decarboxylases. A promoter mutation which abolished gadY expression resulted in a reduction in the amount of gadX mRNA during stationary phase. The gadY gene was shown to overlap the 3′ end of the gadX gene, and this overlap region was found to be necessary for the GadY-dependent accumulation of gadX mRNA. We suggest that during stationary phase, GadY forms base pairs with the 3′-untranslated region of the gadX mRNA and confers increased stability, allowing for gadX mRNA accumulation and the increased expression of downstream acid resistance genes.


2007 ◽  
Vol 189 (14) ◽  
pp. 5193-5202 ◽  
Author(s):  
Lisa U. Magnusson ◽  
Bertil Gummesson ◽  
Predrag Joksimović ◽  
Anne Farewell ◽  
Thomas Nyström

ABSTRACT The recent discovery that the protein DksA acts as a coregulator of genes controlled by ppGpp led us to investigate the similarities and differences between the relaxed phenotype of a ppGpp-deficient mutant and the phenotype of a strain lacking DksA. We demonstrate that the absence of DksA and ppGpp has similar effects on many of the observed phenotypes but that DksA and ppGpp also have independent and sometimes opposing roles in the cell. Specifically, we show that overexpression of DksA can compensate for the loss of ppGpp with respect to transcription of the promoters P uspA , P livJ , and P rrnBP1 as well as amino acid auxotrophy, cell-cell aggregation, motility, filamentation, and stationary phase morphology, suggesting that DksA can function without ppGpp in regulating gene expression. In addition, ppGpp and DksA have opposing effects on adhesion. In the course of our analysis, we also discovered new features of the relaxed mutant, namely, defects in cell-cell aggregation and motility.


1998 ◽  
Vol 180 (21) ◽  
pp. 5704-5711 ◽  
Author(s):  
Sara W. Lazar ◽  
Marta Almirón ◽  
Antonio Tormo ◽  
Roberto Kolter

ABSTRACT SurA is a periplasmic peptidyl-prolyl isomerase required for the efficient folding of extracytoplasmic proteins. Although thesurA gene had been identified in a screen for mutants that failed to survive in stationary phase, the role played by SurA in stationary-phase survival remained unknown. The results presented here demonstrate that the survival defect of surA mutants is due to their inability to grow at elevated pH in the absence of ςS. When cultures of Escherichia coli were grown in peptide-rich Luria-Bertani medium, the majority of the cells lost viability during the first two to three days of incubation in stationary phase as the pH rose to pH 9. At this time the surviving cells resumed growth. In cultures of surA rpoS double mutants the survivors lysed as they attempted to resume growth at the elevated pH. Cells lacking penicillin binding protein 3 and ςS had a survival defect similar to that of surA rpoS double mutants, suggesting that SurA foldase activity is important for the proper assembly of the cell wall-synthesizing apparatus.


2006 ◽  
Vol 188 (9) ◽  
pp. 3175-3181 ◽  
Author(s):  
Celeste N. Peterson ◽  
Valerie J. Carabetta ◽  
Tahmeena Chowdhury ◽  
Thomas J. Silhavy

ABSTRACT Regulation of the Escherichia coli stationary-phase sigma factor RpoS is complex and occurs at multiple levels in response to different environmental stresses. One protein that reduces RpoS levels is the transcription factor LrhA, a global regulator of flagellar synthesis. Here we clarify the mechanism of this repression and provide insight into the signaling pathways that feed into this regulation. We show that LrhA represses RpoS at the level of translation in a manner that is dependent on the small RNA (sRNA) chaperone Hfq. Although LrhA also represses the transcription of the sRNA RprA, its regulation of RpoS mainly occurs independently of RprA. To better understand the physiological signals affecting this pathway, a transposon mutagenesis screen was carried out to find factors affecting LrhA activity levels. The RcsCDB phosphorelay system, a cell envelope stress-sensing pathway, was found to repress lrhA synthesis. In addition, mutations in the gene encoding the DNA motor protein FtsK induce lrhA synthesis, which may explain why such strains fail to accumulate RpoS in stationary phase.


2009 ◽  
Vol 191 (9) ◽  
pp. 3177-3182 ◽  
Author(s):  
Ilana Kolodkin-Gal ◽  
Hanna Engelberg-Kulka

ABSTRACT Escherichia coli mazEF is a toxin-antitoxin gene module that mediates cell death during exponential-phase cellular growth through either reactive oxygen species (ROS)-dependent or ROS-independent pathways. Here, we found that the stationary-phase sigma factor σS was responsible for the resistance to mazEF-mediated cell death during stationary growth phase. Deletion of rpoS, the gene encoding σS from the bacterial chromosome, permitted mazEF-mediated cell death during stationary growth phase.


1996 ◽  
Vol 178 (7) ◽  
pp. 2159.1-2159
Author(s):  
Chuan Li ◽  
Jeffrey K. Ichikawa ◽  
Jeffrey J. Ravetto ◽  
Hung-Chih Kuo ◽  
June C. Fu ◽  
...  

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