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. 1980 Oct;144(1):185–191. doi: 10.1128/jb.144.1.185-191.1980

Further characterization of sfiA and sfiB mutations in Escherichia coli.

O Huisman, R D'Ari, J George
PMCID: PMC294617  PMID: 6998947

Abstract

The sfiA and sfiB mutations, originally isolated in thermoresistant ultraviolet-resistant revertants of a tif lon strain, also suppressed filamentation in tsl strains (mutated at the lexA locus). When deoxyribonucleic acid synthesis was arrested, however, sfi-independent filamentation occurred. Other SOS functions were not affected by sfiA and sfiB mutations; in particular, ultraviolet-induced repair and mutagenesis of bacterial deoxyribonucleic acid were normal, as was tsl-tif-induced synthesis of recA protein. Genetic studies (i) established the identity of map location of the sfiA and sulA loci, (ii) showed that the two sfiB mutations are recessive, and (iii) showed that of six independent sfiA mutations, three are recessive and three are dominant. One sfiB strain was shown to have a 6% growth disadvantage relative to a sfi+ or sfiA strain. It is proposed that the sfiA locus may define the structural gene of a hypothetical inducible SOS-associated division inhibitor.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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