Stability of DNA in Dark-repair Mutants of Escherichia coli B Treated with Nalidixic Acid

Abstract

SUMMARYBreakdown of DNA to acid-soluble fragments induced in strains of Escherichia coli B by nalidixic acid (10 ,ug./ml.) differed in linear rate according to the ability of the strain to repair DNA lesions. Strains which were exr (BS-2) and exr, uvr (BS-I) exhibited excessive DNA breakdown following nalidixic aeid treatment. The excision-defective uvr strains, BS-8, BS-12 and WWP-2 hcr, also degraded their DNA to acid-soluble fragments at a rate which initially was greater than that of the parental strain (E. coli B). This degradation was unaffected by the rad mutation. Removal of nalidixic acid from the system considerably lowered the rate of DNA breakdown. The responses to nalidixic acid and other agents potentiating DNA breakdown are compared.

Recombinational Repair of DNA Damage in Escherichia coli and Bacteriophage λ

“…Whatever the molecular mechanism of the replication fork damage with quinolones, treatment with oxolinic acid instantly inhibits DNA replication but does not cause a loss of super-coiling for at least 10 min, which indicates that the treatment itself does not induce breaks in the chromosome (403,609). However, nalidixic acid-treated cells of E. coli (124,222,254) and B. subtilis (123) slowly degrade their DNA. In B. subtilis, the degradation starts at the replication point and proceeds towards the replication origin, affecting the template and the newly synthesized DNA strands equally (511).…”

Biology of bacterial deoxyribonucleic acid topoisomerases.

“…Generating the signal for induction of recA by nalidixic acid requires the presence of wild-type alleles of recB and recC (49,79). Since the recB and recC gene products exhibit DNA exonuclease V activity in vitro (for review, see 154), the idea developed that exonuclease V degrades DNA (34,143) when DNA synthesis is rapidly blocked.…”

“…3; see reference 81 for review of lex and recA interactions). Since DNA degradation is potentially harmful and probably contributes to the cytotoxicity of nalidixic acid (15,16,34,49,66,130), the presence of wild-type recB and recC alleles might not always be favorable for survival. Such a case has been reported; wild-type cells are more sensitive than recB and recC mutants to inhibitors of gyrase if the cells Many different point and deletion mutations were used in these experiments; supercoiling was measured in only three (Pruss, unpublished data), and in all three, levels were higher than normal.…”