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Phleomycin-induced lethality and DNA degradation in Escherichia coli K12

Journal Article:

Abstract

The cell lethality and DNA fragmentation caused by phleomycin (PM) were studied in E. coli K12 strains with special reference to the effects of repair or recombination deficiencies and metabolic inhibitors. Unlike excision-defective derivatives of E. coli B, uvrA, uvrB, and uvrC mutants of strain K12 showed no peculiarities compared with wild type in regard to cell survival. Likewise, mutant alleles at uvrD and polA loci had no effect. In contrast, rec mutants were more sensitive to PM-killing than were rec/sup +/ strains. PM-induced strand breakage in DNA was observed in all strains tested including the above-mentioned mutants. There was no significant distinction between the uvr mutants and the wild type strain, indicating that the uvr-endonuclease was not responsible for the strand breaks. Involvement of endonuclease I was also ruled out. At least some of the PM-induced strand breaks were repairable. PM-induced lethality and strand breakage were totally dependent on energy supply. Inhibition of protein synthesis resulted in a partial and parallel suppression of the two effects. Our results suggest that the lethality is due to DNA strand breakage and the repair of such damage is postulated to be controlled by rec genes.
Authors:
Publication Date:
Jan 01, 1975
Product Type:
Journal Article
Reference Number:
ERA-03-007480; EDB-78-005823
Resource Relation:
Journal Name: Mutat. Res.; (Netherlands); Journal Volume: 29
Subject:
59 BASIC BIOLOGICAL SCIENCES; DNA; BIOLOGICAL REPAIR; STRAND BREAKS; ESCHERICHIA COLI; MORTALITY; ANTIBIOTICS; CELL KILLING; DECOMPOSITION; BACTERIA; BIOLOGICAL RECOVERY; CHEMICAL REACTIONS; DRUGS; MICROORGANISMS; NUCLEIC ACIDS; ORGANIC COMPOUNDS; REPAIR; 550200* - Biochemistry; 550700 - Microbiology
OSTI ID:
7211838
Research Organizations:
Stanford Univ., CA
Country of Origin:
Netherlands
Language:
English
Other Identifying Numbers:
Journal ID: CODEN: MUREA
Submitting Site:
TIC
Size:
Pages: 21-33
Announcement Date:

Journal Article:

Citation Formats

Nakayama, H. Phleomycin-induced lethality and DNA degradation in Escherichia coli K12. Netherlands: N. p., 1975. Web.
Nakayama, H. Phleomycin-induced lethality and DNA degradation in Escherichia coli K12. Netherlands.
Nakayama, H. 1975. "Phleomycin-induced lethality and DNA degradation in Escherichia coli K12." Netherlands.
@misc{etde_7211838,
title = {Phleomycin-induced lethality and DNA degradation in Escherichia coli K12}
author = {Nakayama, H}
abstractNote = {The cell lethality and DNA fragmentation caused by phleomycin (PM) were studied in E. coli K12 strains with special reference to the effects of repair or recombination deficiencies and metabolic inhibitors. Unlike excision-defective derivatives of E. coli B, uvrA, uvrB, and uvrC mutants of strain K12 showed no peculiarities compared with wild type in regard to cell survival. Likewise, mutant alleles at uvrD and polA loci had no effect. In contrast, rec mutants were more sensitive to PM-killing than were rec/sup +/ strains. PM-induced strand breakage in DNA was observed in all strains tested including the above-mentioned mutants. There was no significant distinction between the uvr mutants and the wild type strain, indicating that the uvr-endonuclease was not responsible for the strand breaks. Involvement of endonuclease I was also ruled out. At least some of the PM-induced strand breaks were repairable. PM-induced lethality and strand breakage were totally dependent on energy supply. Inhibition of protein synthesis resulted in a partial and parallel suppression of the two effects. Our results suggest that the lethality is due to DNA strand breakage and the repair of such damage is postulated to be controlled by rec genes.}
journal = {Mutat. Res.; (Netherlands)}
volume = {29}
journal type = {AC}
place = {Netherlands}
year = {1975}
month = {Jan}
}