The viability

of cells increased levels of RNase HI is re

The viability

of cells increased levels of RNase HI is reduced. Wild type cells carrying a P araBAD rnhA expression plasmid (pECR15) show a growth defect that depends on Veliparib supplier the concentration of arabinose present in the growth medium. Even growth on glucose, which suppresses expression from the P araBAD promoter, leads to a mild growth defect, presumably due to a combination of the high plasmid copy number and the leakiness of the P araBAD promoter. Cells carrying a control plasmid (P araBAD eCFP, pAST110) show no growth restriction. (PDF 447 KB) References 1. Champoux JJ: DNA topoisomerases: structure, function, and mechanism. Annu Rev Biochem 2001, 70:369–413.PubMedCrossRef 2. Deweese JE, Osheroff MA, Osheroff N: DNA Topology and

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Overexpressionof Lonafarnib RNase H partially complements the growth defect of an Escherichia coli delta topA mutant: R-loop formation is a major problem in the absenceof DNA topoisomerase I. Proc Natl Acad Sci USA 1995, 92:3526–3530.PubMedCrossRef 8. Sternglanz R, DiNardo S, Voelkel KA, Nishimura Y, Hirota Y, Becherer K, Zumstein L, Wang JC: Mutations in the gene coding for Escherichia coli DNA topoisomerase I affect transcription and transposition. Proc Natl Acad Sci USA 1981, 78:2747–2751.PubMedCrossRef 9. DiNardo S, Voelkel KA, Sternglanz R, Reynolds AE, Wright A: Escherichia coli DNA topoisomerase I mutants have compensatory mutations in DNA gyrase genes. Cell 1982, 31:43–51.PubMedCrossRef 10. Richardson SM, Higgins CF, Lilley DM: The genetic control of DNA supercoiling in Salmonella typhimurium. EMBO J 1984, 3:1745–1752.PubMed 11. Stupina VA, Wang JC: Viability of Escherichia coli topA mutants lacking DNA topoisomerase I. J Biol Chem 2005, 280:355–360.PubMed 12. Bernhardt TG, de Boer PA: Screening for synthetic lethal mutants in Escherichia coli and identification of EnvC (YibP) as a periplasmic septal ring factor with murein hydrolase activity. Mol Microbiol 2004, 52:1255–1269.PubMedCrossRef 13. Mahdi AA, Buckman C, Harris L, Lloyd RG: Rep and PriA helicase activities prevent RecA from provoking unnecessary recombination during replication fork repair. Genes Dev 2006, 20:2135–2147.PubMedCrossRef 14.

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