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Gene Review

sulA  -  SOS cell division inhibitor

Escherichia coli str. K-12 substr. MG1655

Synonyms: ECK0949, JW0941, sfiA
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Disease relevance of sulA

  • In E. coli PQ37, a test organism used for the assessment of genotoxicity, lacZ, the beta-galactosidase gene is placed under the control of sfiA, one of the SOS genes through an operon fusion [1].
  • To measure sfiA expression in the different strains, we first constructed a lambda transducing phage carrying an sfiA::lac operon fusion [2].
  • Hydroxyurea at concentrations higher than 10(-2) M induced the recA and sfiA genes of E. coli as well as the lambda prophage by a pathway independent of the recBC genes [3].

High impact information on sulA

  • The work reported here establishes the existence of the latter type of replication-division coupling in E. coli, and shows that the sfiA gene product is an inducible component of this division inhibition mechanism which is synthesized at high levels after perturbations of DNA replication [4].
  • The influence of the growth delay induced by near u.v. radiation on the SOS response was monitored by comparing the level of sfiA expression by means of a sfiA::lacZ fusion in both a nuvA+ cell and an isogenic nuvA mutant [5].
  • The kinetics of sfiA induction in near u.v.-illuminated nuvA+ cells, whether treated with 254 nm light or not, is unusual and follows the growth curve: only after 50 min is sfiA derepression observed [5].
  • The sfiA operon was turned on at a 10-fold lower concentration of methylmethane sulfonate or dimethyl sulfate in tagA strains, lacking specific 3-methyladenine-DNA glycosylase, than in wild-type strains [6].
  • 3-Methyladenine residues in DNA induce the SOS function sfiA in Escherichia coli [6].

Chemical compound and disease context of sulA


Biological context of sulA

  • Compared with the aidB gene, a component of the SOS system, the sulA (sfiA) gene, responded to changes in cytoplasmic pH and in the level of intracellular thiols in an opposite way [12].
  • The filamentation of ruv strains is abolished by mutations in sfiA or sfiB that prevent SOS induced inhibition of cell division, but this does not restore resistance to UV radiation [13].
  • Many recombination, DNA repair and DNA replication mutants have high basal levels of SOS expression as determined by a sulAp-lacZ reporter gene system on a population of cells [14].
  • To distinguish between these two models, a method to quantify SOS expression in individual bacterial cells was developed by fusing an SOS promoter (sulAp) to the green fluorescent protein (gfp) reporter gene and inserting it at attlambda on the Escherichia coli chromosome [14].
  • Mutations in these genes also cause decreases in cell viability and alterations in UV-inducible sulAp-lacZ (SOS) expression [15].

Associations of sulA with chemical compounds

  • Treatment with the known carcinogen N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) revealed that the promoter for the ColD plasmid-borne cda gene had responses 12, 5, and 3 times greater than the recA, sulA, and umuDC promoters, respectively, and also considerably higher sensitivity [16].
  • On the other hand, cyclic AMP does not affect the uv-mediated induction of the recA, sfiA, and umuDC genes [17].
  • Pretreatment with ferricyanide inhibited H2O2-induced expression of the sfiA gene which is the member of the gene family controlled by the recA and lexA genes [18].
  • The results obtained show that expression of the recA and sfiA genes was inhibited neither in the UV-irradiated nrdA mutant at 42 degrees C nor in the wild-type strain in the presence of hydroxyurea [19].
  • The induction of recA, umuC and sfiA genes by quercetin was studied in the presence and in the absence of S9 mix [20].

Regulatory relationships of sulA


Other interactions of sulA

  • In Escherichia coli, the cell division block observed during the SOS response requires the product of the sfiA gene, whose expression is regulated negatively by the LexA repressor and positively by the RecA protease [2].
  • The infA3 mutation, which suppresses tif-mediated filamentation, reduced induction of sfiA expression in a tif infA3 strain at 42 degrees C or after UV irradiation [2].
  • We found that the initial steady rate of sfiA expression was proportional to the UV dose and was identical in uvr+ and uvrA backgrounds [24].
  • The induction of sfiA gene is decreased by the presence of S9 mix, whereas an opposite effect was observed concerning umuC and recA [20].
  • After exposure to H2O2, mutagenesis and filamentation also occurred with the dose response characteristic of SOS induction and mode one killing, but these responses were not dependent on the lexA-regulated umuC mutagenesis or sfiA filamentation functions, respectively [25].

Analytical, diagnostic and therapeutic context of sulA

  • Construction of a ColD cda promoter-based SOS-green fluorescent protein whole-cell biosensor with higher sensitivity toward genotoxic compounds than constructs based on recA, umuDC, or sulA promoters [16].
  • The positioning of constrictions in Escherichia coli filaments pinching off anucleate cells was analyzed by fluorescence microscopy of dnaX(Ts), dnaX(Ts) sfiA, dnaA46(Ts), gyrA(Am) supF(Ts), and gyrB(Ts) mutants [26].


  1. The induction of SOS function in Escherichia coli K-12/PQ37 by 4-nitroquinoline oxide (4-NQO) and fecapentaenes-12 and -14 is bile salt sensitive: implications for colon carcinogenesis. Nair, P.P., Davis, K.E., Shami, S., Lagerholm, S. Mutat. Res. (2000) [Pubmed]
  2. Effect of suppressors of SOS-mediated filamentation on sfiA operon expression in Escherichia coli. Huisman, O., D'Ari, R. J. Bacteriol. (1983) [Pubmed]
  3. Induction of the SOS response by hydroxyurea in Escherichia coli K12. Barbé, J., Villaverde, A., Guerrero, R. Mutat. Res. (1987) [Pubmed]
  4. An inducible DNA replication-cell division coupling mechanism in E. coli. Huisman, O., D'Ari, R. Nature (1981) [Pubmed]
  5. Near ultraviolet DNA damage induces the SOS responses in Escherichia coli. Caldeira de Araujo, A., Favre, A. EMBO J. (1986) [Pubmed]
  6. 3-Methyladenine residues in DNA induce the SOS function sfiA in Escherichia coli. Boiteux, S., Huisman, O., Laval, J. EMBO J. (1984) [Pubmed]
  7. Gene expression caused by alkylating agents and cis-diamminedichloroplatinum(II) in Escherichia coli. Fram, R.J., Crockett, J., Volkert, M.R. Cancer Res. (1988) [Pubmed]
  8. Survival and SOS induction in cisplatin-treated Escherichia coli deficient in Pol II, RecBCD and RecFOR functions. Bhattacharya, R., Beck, D.J. DNA Repair (Amst.) (2002) [Pubmed]
  9. An inhibitor of SOS induction, specified by a plasmid locus in Escherichia coli. Bagdasarian, M., Bailone, A., Bagdasarian, M.M., Manning, P.A., Lurz, R., Timmis, K.N., Devoret, R. Proc. Natl. Acad. Sci. U.S.A. (1986) [Pubmed]
  10. The effect of probiotics on the genotoxicity of furazolidone. Raipulis, J., Toma, M.M., Semjonovs, P. Int. J. Food Microbiol. (2005) [Pubmed]
  11. Effect of alkylating agents on the expression of inducible genes of Escherichia coli. Vericat, J.A., Guerrero, R., Barbé, J. J. Gen. Microbiol. (1986) [Pubmed]
  12. Induction of the alkylation-inducible aidB gene of Escherichia coli by cytoplasmic acidification and N-ethylmaleimide. Smirnova, G.V., Oktyabrsky, O.N., Moshonkina, E.V., Zakirova, N.V. Mutat. Res. (1994) [Pubmed]
  13. Effect of ruv mutations on recombination and DNA repair in Escherichia coli K12. Lloyd, R.G., Benson, F.E., Shurvinton, C.E. Mol. Gen. Genet. (1984) [Pubmed]
  14. Measurement of SOS expression in individual Escherichia coli K-12 cells using fluorescence microscopy. McCool, J.D., Long, E., Petrosino, J.F., Sandler, H.A., Rosenberg, S.M., Sandler, S.J. Mol. Microbiol. (2004) [Pubmed]
  15. Overlapping functions for recF and priA in cell viability and UV-inducible SOS expression are distinguished by dnaC809 in Escherichia coli K-12. Sandler, S.J. Mol. Microbiol. (1996) [Pubmed]
  16. Construction of a ColD cda promoter-based SOS-green fluorescent protein whole-cell biosensor with higher sensitivity toward genotoxic compounds than constructs based on recA, umuDC, or sulA promoters. Norman, A., Hestbjerg Hansen, L., Sørensen, S.J. Appl. Environ. Microbiol. (2005) [Pubmed]
  17. Modulating action of cyclic AMP on the expression of two SOS genes in Escherichia coli K-12. Barbé, J., Gibert, I., Guerrero, R. Can. J. Microbiol. (1987) [Pubmed]
  18. Effects of penetrating and non-penetrating oxidants on Escherichia coli. Smirnova, G.V., Muzyka, N.G., Glukhovchenko, M.N., Oktyabrsky, O.N. Biochemistry Mosc. (1997) [Pubmed]
  19. SOS system induction in Escherichia coli cells with distinct levels of ribonucleotide reductase activity. Villaverde, A., Barbé, J. Mutat. Res. (1992) [Pubmed]
  20. Influence of S9 mix in the induction of SOS system by quercetin. Llagostera, M., Garrido, S., Barbé, J., Guerrero, R., Rueff, J. Mutat. Res. (1987) [Pubmed]
  21. How Escherichia coli sets different basal levels in SOS operons. Huisman, O., D'Ari, R., Casaregola, S. Biochimie (1982) [Pubmed]
  22. Induction of the SOS gene (umuC) by 4-quinolone antibacterial drugs. Power, E.G., Phillips, I. J. Med. Microbiol. (1992) [Pubmed]
  23. Evidence for a specific regulation of recA gene transcription in Escherichia coli. Villaverde, A., Gibert, I., Barbé, J. Mutat. Res. (1988) [Pubmed]
  24. Induction by UV light of the SOS function sfiA in Escherichia coli strains deficient or proficient in excision repair. Quillardet, P., Hofnung, M. J. Bacteriol. (1984) [Pubmed]
  25. Mutagenesis and stress responses induced in Escherichia coli by hydrogen peroxide. Imlay, J.A., Linn, S. J. Bacteriol. (1987) [Pubmed]
  26. Actively replicating nucleoids influence positioning of division sites in Escherichia coli filaments forming cells lacking DNA. Mulder, E., Woldringh, C.L. J. Bacteriol. (1989) [Pubmed]
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