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Author (up) Aertsen, A.; Michiels, C.W. file  url
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  Title SulA-dependent hypersensitivity to high pressure and hyperfilamentation after high-pressure treatment of Escherichia coli lon mutants Type Journal Article
  Year 2005 Publication Research in Microbiology Abbreviated Journal Res Microbiol  
  Volume 156 Issue 2 Pages 233-237  
  Keywords Colony Count, Microbial; Culture Media; Escherichia coli--genetics, growth & development; Escherichia coli Proteins--genetics, metabolism; Gene Expression Regulation, Bacterial; Hydrostatic Pressure; Mutation; Protease La--genetics; SOS Response (Genetics); Ultraviolet Rays  
  Abstract High-pressure treatment (>100 MPa) is known to induce several heat shock proteins as well as an SOS response in Escherichia coli. In the current work, we have investigated properties with respect to high-pressure treatment of mutants-deficient in Lon, a pressure-induced ATP-dependent protease that belongs to the heat shock regulon but that also has a link to the SOS regulon. We report that lon mutants show increased pressure sensitivity and exhibit hyperfilamentation during growth after high-pressure treatment. Both phenotypes could be entirely attributed to the action of the SOS protein SulA, a potent inhibitor of the cell division ring protein FtsZ and a specific target of the Lon protease, since they were suppressed by knock-out of SulA. Introduction of the lexA1 allele, which effectively blocks the entire SOS response, also suppressed the high pressure hypersensitivity of lon mutants, but not their UV hypersensitivity. These results indicate the existence of a SulA-dependent pathway of high-pressure-induced cell filamentation, and suggest involvement of the SOS response, and particularly of SulA, in high-pressure-mediated cell death in E. coli strains which are compromised in Lon function.  
  Call Number Serial 301  
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Author (up) Bhattacharya, R.; Beck, D.J. file  url
openurl 
  Title Survival and SOS induction in cisplatin-treated Escherichia coli deficient in Pol II, RecBCD and RecFOR functions Type Journal Article
  Year 2002 Publication DNA Repair Abbreviated Journal DNA Repair (Amst)  
  Volume 1 Issue 11 Pages 955-966  
  Keywords Antineoplastic Agents/*pharmacology; Bacterial Proteins/physiology; Cell Division/drug effects/genetics/radiation effects; Cisplatin/*pharmacology; DNA Damage/drug effects/radiation effects; DNA Polymerase II/*physiology; DNA Polymerase III/physiology; DNA Repair/drug effects/radiation effects; DNA-Binding Proteins/physiology; Dose-Response Relationship, Drug; Drug Resistance, Bacterial/physiology; Escherichia coli/*drug effects/enzymology; Escherichia coli Proteins/pharmacology/*physiology; Exodeoxyribonuclease V; Exodeoxyribonucleases/*physiology; Lac Operon; SOS Response (Genetics)/*physiology; beta-Galactosidase/metabolism  
  Abstract Cisplatin is a potent anticancer agent forming intrastrand-crosslinks in DNA. The efficacy of cisplatin in chemotherapy can be limited by the development of tumor resistances such as elevated DNA repair or damage tolerance. In Escherichia coli, cisplatin treatment causes induction of the SOS regulon resulting in elevated levels of DNA Pol II, DNA Pol IV, DNA Pol V, the cell division inhibitor SfiA (SulA), homologous recombination (HR) and DNA repair. In this work, the roles of Pol II and HR in facilitating resistance of E. coli to cisplatin are studied. SOS induction levels were measured by beta-galactosidase assays in cisplatin-treated and untreated E. coli PQ30 that has the lacZ gene fused to the sfiA promoter. Comparative studies were carried out with derivatives of PQ30 constructed by P1 transduction that have transposon insertions in the polB gene, the recB gene blocking the RecBCD pathway of HR and genes of the RecFOR pathway of HR. Resistance of E. coli strains to cisplatin as determined by plating experiments decreased in the following order: parent PQ30 strain, polB > recO, recR, recF > recB. Both the RecBCD and RecFOR pathways of HR are important for survival when E. coli is exposed to cisplatin, because treatment of double mutants deficient in both pathways reduced colony forming ability to 37% in 6-9min in comparison to 39-120min for single mutants. Pol II and RecF appear to function in two distinct pathways to initiate replication blocked due to damage caused by cisplatin because function of Pol II was required for survival in mutants deficient in the RecFOR pathway after 2h of cisplatin treatment. In contrast, Pol II was not required for survival in recB mutants. SOS induction was delayed in RecFOR deficient mutants but occurred at high levels in the recB mutant soon after cisplatin treatment in a RecFOR-dependent way. An SfiA independent, DNA damage dependent pathway is apparently responsible for the filamentous cells observed after cisplatin or MMC treatments of these SfiA defective strains.  
  Call Number Serial 407  
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Author (up) Finkel, S.E. file  url
openurl 
  Title Long-term survival during stationary phase: evolution and the GASP phenotype Type Journal Article
  Year 2006 Publication Nature Reviews. Microbiology Abbreviated Journal Nat Rev Microbiol  
  Volume 4 Issue 2 Pages 113-120  
  Keywords Bacteria/*genetics/*growth & development; *Evolution, Molecular; Genetic Variation; Mutation; Phenotype; SOS Response (Genetics); Selection, Genetic  
  Abstract The traditional view of the stationary phase of the bacterial life cycle, obtained using standard laboratory culture practices, although useful, might not always provide us with the complete picture. Here, the traditional three phases of the bacterial life cycle are expanded to include two additional phases: death phase and long-term stationary phase. In many natural environments, bacteria probably exist in conditions more akin to those of long-term stationary-phase cultures, in which the expression of a wide variety of stress-response genes and alternative metabolic pathways is essential for survival. Furthermore, stressful environments can result in selection for mutants that express the growth advantage in stationary phase (GASP) phenotype.  
  Call Number Serial 1555  
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Author (up) Finkel, S.E. file  url
openurl 
  Title Long-term survival during stationary phase: evolution and the GASP phenotype Type Journal Article
  Year 2006 Publication Nature Reviews. Microbiology Abbreviated Journal Nat Rev Microbiol  
  Volume 4 Issue 2 Pages 113-120  
  Keywords Bacteria/*genetics/*growth & development; *Evolution, Molecular; Genetic Variation; Mutation; Phenotype; SOS Response (Genetics); Selection, Genetic  
  Abstract The traditional view of the stationary phase of the bacterial life cycle, obtained using standard laboratory culture practices, although useful, might not always provide us with the complete picture. Here, the traditional three phases of the bacterial life cycle are expanded to include two additional phases: death phase and long-term stationary phase. In many natural environments, bacteria probably exist in conditions more akin to those of long-term stationary-phase cultures, in which the expression of a wide variety of stress-response genes and alternative metabolic pathways is essential for survival. Furthermore, stressful environments can result in selection for mutants that express the growth advantage in stationary phase (GASP) phenotype.  
  Call Number Serial 1581  
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Author (up) Wang, L.; Lutkenhaus, J. file  url
openurl 
  Title FtsK is an essential cell division protein that is localized to the septum and induced as part of the SOS response Type Journal Article
  Year 1998 Publication Molecular Microbiology Abbreviated Journal Mol Microbiol  
  Volume 29 Issue 3 Pages 731-740  
  Keywords Bacterial Proteins/*genetics/metabolism/physiology; Binding Sites; *Carrier Proteins; Cell Division; *Cytoskeletal Proteins; DNA Damage; Drug Resistance, Microbial; Escherichia coli/drug effects/*genetics/physiology; *Escherichia coli Proteins; Gene Expression Regulation, Bacterial; Genes, Bacterial; Hexosyltransferases/metabolism; Membrane Proteins/*genetics/metabolism/physiology; Mitomycin/pharmacology; Multienzyme Complexes/metabolism; *Muramoylpentapeptide Carboxypeptidase; Penicillin-Binding Proteins; Peptidyl Transferases/metabolism; Rec A Recombinases; *SOS Response (Genetics); Serine Endopeptidases  
  Abstract The role of ftsK in the growth of Escherichia coli was examined by turning off its expression. This resulted in smooth filaments without constrictions, indicating that FtsK was required at an early step in septation. Consistent with this, FtsK was found to localize to the septum in 70% of the cells, indicating that it was recruited relatively early in this process. FtsK localization required the function of FtsZ and FtsA but not FtsI and FtsQ. Consistent with this, Z rings were present in FtsK-depleted filaments. Subcellular localization of FtsK confirmed that it was a membrane protein. Only the first 202 amino acids of FtsK were essential for its role in membrane localization, cell division and viability. The expression of ftsK increased as part of the SOS response, and increased expression of ftsK conferred increased resistance to DNA damage.  
  Call Number Serial 414  
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