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Gene Review

ECs0258  -  DNA polymerase IV

Escherichia coli O157:H7 str. Sakai

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Disease relevance of ECs0258

  • In Escherichia coli, the Y-family DNA polymerases Pol IV (DinB) and Pol V (UmuD2'C) enhance cell survival upon DNA damage by bypassing replication-blocking DNA lesions [1].
  • To better characterize the Pol IV-dependent untargeted mutagenesis, i.e., the DNA Pol IV mutator activity, we analyzed the genetic requirements of this activity and determined the forward mutation spectrum generated by this protein within the cII gene of lambda phage [2].

High impact information on ECs0258

  • All three SOS-inducible DNA polymerases (Pol II, Pol IV and Pol V) are involved in induced mutagenesis [3].
  • On SOS induction, it is believed that only about 15 molecules of Pol V are assembled per cell (S. Sommer, personal communication), whereas Pol IV levels reach approximately 2500 molecules [4].
  • This common binding site for delta, Pol IV and alpha subunit is shown to be formed by residues that are highly conserved among many bacterial beta homologs, thus defining an evolutionarily conserved hydrophobic crevice for sliding clamp ligands and a new target for antibiotic drug design [5].
  • Escherichia coli DNA polymerase IV incorporated 2-hydroxy-dATP opposite template guanine or thymine and 8-hydroxy-dGTP exclusively opposite adenine in vitro [6].
  • Point mutation requires induction of the RpoS-dependent general stress response, and the SOS DNA damage response leading to upregulation of the error-prone DNA polymerase DinB (Pol IV), and occurs during a transient limitation of post-replicative mismatch repair activity [7].

Chemical compound and disease context of ECs0258


Associations of ECs0258 with chemical compounds

  • Pol IV forms a covalent Schiff's base intermediate with substrate DNA that is trapped by sodium borohydride, as proscribed by a beta-elimination mechanism [9].
  • We show in vitro that LexA cleavage is induced during RecBC-mediated repair of ciprofloxacin-mediated DNA damage and that this results in the derepression of the SOS-regulated polymerases Pol II, Pol IV and Pol V, which collaborate to induce resistance-conferring mutations [10].


  1. Y-family DNA polymerases respond to DNA damage-independent inhibition of replication fork progression. Godoy, V.G., Jarosz, D.F., Walker, F.L., Simmons, L.A., Walker, G.C. EMBO J. (2006) [Pubmed]
  2. Escherichia coli DNA polymerase IV mutator activity: genetic requirements and mutational specificity. Wagner, J., Nohmi, T. J. Bacteriol. (2000) [Pubmed]
  3. All three SOS-inducible DNA polymerases (Pol II, Pol IV and Pol V) are involved in induced mutagenesis. Napolitano, R., Janel-Bintz, R., Wagner, J., Fuchs, R.P. EMBO J. (2000) [Pubmed]
  4. Properties and functions of Escherichia coli: Pol IV and Pol V. Fuchs, R.P., Fujii, S., Wagner, J. Adv. Protein Chem. (2004) [Pubmed]
  5. Structural and biochemical analysis of sliding clamp/ligand interactions suggest a competition between replicative and translesion DNA polymerases. Burnouf, D.Y., Olieric, V., Wagner, J., Fujii, S., Reinbolt, J., Fuchs, R.P., Dumas, P. J. Mol. Biol. (2004) [Pubmed]
  6. Involvement of Y-family DNA polymerases in mutagenesis caused by oxidized nucleotides in Escherichia coli. Yamada, M., Nunoshiba, T., Shimizu, M., Gruz, P., Kamiya, H., Harashima, H., Nohmi, T. J. Bacteriol. (2006) [Pubmed]
  7. Adaptive mutation and amplification in Escherichia coli: two pathways of genome adaptation under stress. Hersh, M.N., Ponder, R.G., Hastings, P.J., Rosenberg, S.M. Res. Microbiol. (2004) [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. Lyase activities intrinsic to Escherichia coli polymerases IV and V. Shen, X., Woodgate, R., Goodman, M.F. DNA Repair (Amst.) (2005) [Pubmed]
  10. Inhibition of mutation and combating the evolution of antibiotic resistance. Cirz, R.T., Chin, J.K., Andes, D.R., de Crécy-Lagard, V., Craig, W.A., Romesberg, F.E. PLoS Biol. (2005) [Pubmed]
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