Abstract
We have investigated the mechanism of division inhibition in E. coli following UV-irradiation or nalidixic acid treatment. After UV, two separate mechanisms, both dependent upon recA+, appear to block division. One mechanism is dependent upon sfiA and sfiB, is inhibited by low levels (4 micrograms/ml) of rifamycin and is expressed in tif mutants at 42 degrees C. The second mechanism is independent of sfiA, and sfiB, is resistant to rifamycin and does not occur in cells lacking DNA replication forks. We suggest that this second mechanism is the result of the failure to terminate DNA replication in inhibited cells. Nalidixic acid inhibition of cell division also appears to involve both mechanisms but as found previously replication forks are also necessary to induce the sfi pathway.
MeSH Terms
Bacterial Proteins/metabolism
Cell Division/drug effects,radiation effects
DNA Replication
DNA, Bacterial/radiation effects
Escherichia coli/drug effects,radiation effects
Genes, Bacterial
Nalidixic Acid/pharmacology
Rec A Recombinases
Rifampin/pharmacology
Ultraviolet Rays
Chemicals
Bacterial Proteins
DNA, Bacterial
Nalidixic Acid
Rec A Recombinases
Rifampin
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Burton P
Holland I B
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21 references, click to expand
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