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Author (up) Bhattacharya, R.; Beck, D.J. file  url
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  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) Huisman, O.; D'Ari, R. file  url
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  Title An inducible DNA replication-cell division coupling mechanism in E. coli Type Journal Article
  Year 1981 Publication Nature Abbreviated Journal Nature  
  Volume 290 Issue 5809 Pages 797-799  
  Keywords Bacterial Proteins/physiology; *Cell Division; *DNA Replication; Escherichia coli/genetics/*physiology; Gene Expression Regulation/radiation effects; Genes, Regulator; Hot Temperature; Thymine/metabolism; Ultraviolet Rays  
  Abstract Cell division is a tightly regulated periodic process. In steady-state cultures of Enterobacteriaceae, division takes place at a well defined cell mass and is strictly coordinated with DNA replication. In wild-type Escherichia coli the formation of cells lacking DNA is very rare, and interruptions of DNA replication arrest cell division. The molecular bases of this replication-division coupling have been elusive but several models have been proposed. It has been suggested, for example, that the termination of a round of DNA replication may trigger a key event required for cell division. A quite different model postulates the existence of a division inhibitor which prevents untimely division and whose synthesis is induced to high levels when DNA replication is perturbed. The work reported here establishes the existence of the latter type of replication-division coupling in E. coli, and shows that the sfiA gene product is an inducible component of this division inhibition mechanism which is synthesized at high levels after perturbations of DNA replication.  
  Call Number Serial 410  
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