scholarly journals Adaptive Mutagenesis at ebgR Is Regulated by PhoPQ

1998 ◽  
Vol 180 (11) ◽  
pp. 2862-2865 ◽  
Author(s):  
Barry G. Hall

ABSTRACT Adaptive mutations are mutations that occur in nondividing or very slowly dividing microbial cells during prolonged nonlethal selection and that are specific to the challenge of the selection in the sense that the only mutations that can be detected are those that provide a growth advantage to the cell. The phoPQ genes encode a two-component positively acting regulatory system that controls expression of at least 25 to 30 genes in Escherichia coliand Salmonella typhimurium. PhoPQ responds to a variety of environmental stress signals including Mg2+ starvation and nutritional deprivation. Here I show that disruption ofphoP or phoQ by Tn10dCam significantly reduces the adaptive mutation rate to ebgR, indicating that the adaptive mutagenesis machinery is regulated, directly or indirectly, byphoPQ. The finding that it is regulated implies that adaptive mutagenesis does not simply result from a failure of various error correction mechanisms during prolonged starvation.

2018 ◽  
Vol 186 (2) ◽  
pp. 335-349 ◽  
Author(s):  
Sambandam Ravikumar ◽  
Yokimiko David ◽  
Si Jae Park ◽  
Jong-il Choi

PLoS ONE ◽  
2018 ◽  
Vol 13 (9) ◽  
pp. e0203497 ◽  
Author(s):  
Coral Pardo-Esté ◽  
Alejandro A. Hidalgo ◽  
Camila Aguirre ◽  
Alan C. Briones ◽  
Carolina E. Cabezas ◽  
...  

2002 ◽  
Vol 184 (20) ◽  
pp. 5599-5608 ◽  
Author(s):  
Cesar Rodriguez ◽  
Joshua Tompkin ◽  
Jill Hazel ◽  
Patricia L. Foster

ABSTRACT Adaptive mutation to Lac+ in Escherichia coli strain FC40 depends on recombination functions and is enhanced by the expression of conjugal functions. To test the hypothesis that the conjugal function that is important for adaptive mutation is the production of a single-strand nick at the conjugal origin, we supplied an exogenous nicking enzyme, the gene II protein (gIIp) of bacteriophage f1, and placed its target sequence near the lac allele. When both gIIp and its target site were present, adaptive mutation was stimulated three- to fourfold. Like normal adaptive mutations, gIIp-induced mutations were recA+ and ruvC+ dependent and were mainly single-base deletions in runs of iterated bases. In addition, gIIp with its target site could substitute for conjugal functions in adaptive mutation. These results support the hypothesis that nicking at the conjugal origin initiates the recombination that produces adaptive mutations in this strain of E. coli, and they suggest that nicking may be the only conjugal function required for adaptive mutation.


2008 ◽  
Vol 75 (3) ◽  
pp. 573-582 ◽  
Author(s):  
Christopher D. Rice ◽  
Jacob E. Pollard ◽  
Zachery T. Lewis ◽  
William R. McCleary

ABSTRACT Expression of the Pho regulon in Escherichia coli is induced in response to low levels of environmental phosphate (Pi). Under these conditions, the high-affinity PstSCAB2 protein (i.e., with two PstB proteins) is the primary Pi transporter. Expression from the pstSCAB-phoU operon is regulated by the PhoB/PhoR two-component regulatory system. PhoU is a negative regulator of the Pho regulon; however, the mechanism by which PhoU accomplishes this is currently unknown. Genetic studies of phoU have proven to be difficult because deletion of the phoU gene leads to a severe growth defect and creates strong selection for compensatory mutations resulting in confounding data. To overcome the instability of phoU deletions, we employed a promoter-swapping technique that places expression of the phoBR two-component system under control of the Ptac promoter and the lacO ID regulatory module. This technique may be generally applicable for controlling expression of other chromosomal genes in E. coli. Here we utilized PphoB ::Ptac and PpstS ::Ptac strains to characterize phenotypes resulting from various ΔphoU mutations. Our results indicate that PhoU controls the activity of the PstSCAB2 transporter, as well as its abundance within the cell. In addition, we used the PphoB ::Ptac ΔphoU strain as a platform to begin characterizing new phoU mutations in plasmids.


1998 ◽  
Vol 180 (20) ◽  
pp. 5421-5425 ◽  
Author(s):  
Evelyn Zientz ◽  
Johannes Bongaerts ◽  
Gottfried Unden

ABSTRACT In Escherichia coli the genes encoding the anaerobic fumarate respiratory system are transcriptionally regulated by C4-dicarboxylates. The regulation is effected by a two-component regulatory system, DcuSR, consisting of a sensory histidine kinase (DcuS) and a response regulator (DcuR). DcuS and DcuR are encoded by the dcuSR genes (previouslyyjdHG) at 93.7 min on the calculated E. coli map. Inactivation of the dcuR anddcuS genes caused the loss of C4-dicarboxylate-stimulated synthesis of fumarate reductase (frdABCD genes) and of the anaerobic fumarate-succinate antiporter DcuB (dcuB gene). DcuS is predicted to contain a large periplasmic domain as the supposed site for C4-dicarboxylate sensing. Regulation by DcuR and DcuS responded to the presence of the C4-dicarboxylates fumarate, succinate, malate, aspartate, tartrate, and maleate. Since maleate is not taken up by the bacteria under these conditions, the carboxylates presumably act from without. Genes of the aerobic C4-dicarboxylate pathway encoding succinate dehydrogenase (sdhCDAB) and the aerobic succinate carrier (dctA) are only marginally or negatively regulated by the DcuSR system. The CitAB two-component regulatory system, which is highly similar to DcuSR, had no effect on C4-dicarboxylate regulation of any of the genes.


1999 ◽  
Vol 181 (17) ◽  
pp. 5263-5272 ◽  
Author(s):  
Tracy L. Raivio ◽  
Daniel L. Popkin ◽  
Thomas J. Silhavy

ABSTRACT In Escherichia coli, the Cpx two-component regulatory system activates expression of protein folding and degrading factors in response to misfolded proteins in the bacterial envelope (inner membrane, periplasm, and outer membrane). It is comprised of the histidine kinase CpxA and the response regulator CpxR. This response plays a role in protection from stresses, such as elevated pH, as well as in the biogenesis of virulence factors. Here, we show that the Cpx periplasmic stress response is subject to amplification and repression through positive and negative autofeedback mechanisms. Western blot and operon fusion analyses demonstrated that the cpxRA operon is autoactivated. Conditions that lead to elevated levels of phosphorylated CpxR cause a concomitant increase in transcription ofcpxRA. Conversely, overproduction of CpxP, a small, Cpx-regulated protein of previously unknown function, represses the regulon and can block activation of the pathway. This repression is dependent on an intact CpxA sensing domain. The ability to autoactivate and then subsequently repress allows for a temporary amplification of the Cpx response that may be important in rescuing cells from transitory stresses and cueing the appropriately timed elaboration of virulence factors.


2007 ◽  
Vol 74 (2) ◽  
pp. 535-539 ◽  
Author(s):  
Erwin G. Zoetendal ◽  
Alexandra H. Smith ◽  
Monica A. Sundset ◽  
Roderick I. Mackie

ABSTRACT The gene expression profiles of Escherichia coli strains grown anaerobically with or without Acacia mearnsii (black wattle) extract were compared to identify tannin resistance strategies. The cell envelope stress protein gene spy and the multidrug transporter-encoding operon mdtABCD, both under the control of the BaeSR two-component regulatory system, were significantly up-regulated in the presence of tannins. BaeSR mutants were more tannin sensitive than their wild-type counterparts.


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