期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1984
卷号：81
期号：14
页码：4490-4494
DOI：10.1073/pnas.81.14.4490
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Blocks in DNA replication cause a rapid arrest of cell division in Escherichia coli. We have previously established that the function SfiA (SulA), induced under these conditions as part of the SOS response, is involved in this inhibition of division. To separate the effects of SfiA from those of other SOS functions, we have constructed a plac-sfiA operon fusion, permitting specific induction of SfiA protein by addition of the lac operon inducer isopropyl beta-D-thiogalactopyranoside (IPTG). In lon mutants, in which the unstable SfiA protein has a longer half-life, IPTG caused a rapid arrest of cell division. Under these conditions, there is no concomitant induction of the SOS response. IPTG also caused a rapid arrest of cell division in lon+ strains. These results demonstrate that induction of the SfiA protein is sufficient to cause inhibition of division. Mutations in the sfiB gene can suppress IPTG-induced SfiA-mediated inhibition of division. At higher SfiA concentrations, however, even sfiB mutants cease division; an additional mutation genetically inseparable from sfiB restores normal division. These observations reinforce the hypothesis that the SfiB protein, probably required for cell septation, is the target of action of the SfiA division inhibitor.
