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Gene Review

seqA  -  replication initiation regulator SeqA

Escherichia coli O157:H7 str. EDL933

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Disease relevance of seqA

  • Dam-dependent phase variation of Ag43 in Escherichia coli is altered in a seqA mutant [1].
  • In addition to transcripts about 300 nucleotides long, P4 prophage produces a family of shorter transcripts, about 80 nucleotides long, containing seqA or seqB [2].
  • Genetic analysis demonstrated that CII-mediated activation of the phage pI and paQ promoters, which are required for efficient lysogenization, is less efficient in the absence of seqA function [3].
  • Interestingly, seqA is only present in a few DamMT-specifying proteobacteria [4].
  • Null mutation of the dam or seqA gene suppresses temperature-sensitive lethality but not hypersensitivity to novobiocin of muk null mutants [5].

High impact information on seqA

  • In contrast to wild-type and dnaA(Ts) cells, seqA mutant cells frequently go through two initiation events per cell division cycle, and all the origins present in each cell are not initiated in synchrony [6].
  • In part, this can be attributed to the observed decrease in the level of DNA methylation in the seqA mutant [1].
  • The amounts of the intercalative agent required to relax the supercoiled chromosome in mukB and seqA mutants were lower and higher, respectively, than for the wild-type parent, confirming that these cell cycle genes modulate the topology of the E. coli chromosome [7].
  • We have used ethidium bromide titration for direct measurement of the changes in the negative supercoiling of Escherichia coli chromosome caused by mutations inactivating the cell cycle functions mukB and seqA [7].
  • Increasing DnaA activity in a strain capable of suppression, by introducing a copy of the wild-type allele, increasing the suppressor gene dosage or introducing a seqA mutation, reversed the suppression [8].

Biological context of seqA

  • Both seqA and seqC single mutants were still sensitive to P4 prophage immunity, whereas P4 seqA seqC double mutants showed a virulent phenotype [9].
  • Mutations in either seqA or seqC that alter its complementarity to seqB abolished or reduced P4 lysogenization proficiency and delayed the shutoff of the long transcripts originating from PLE that cover the entire operon [9].
  • However, the asynchronous initiation of chromosome replication in the seqA strain was not reversed in the mukBseqA double mutant [10].
  • Introduction of the wild-type seqA gene on a low-copy plasmid suppresses the cold sensitivity of a dnaAcos mutant known to overinitiate at temperatures below 39 degrees C. In addition, the seqA2 mutation is a suppressor of several dnaA (Ts) alleles [11].

Anatomical context of seqA


Associations of seqA with chemical compounds

  • The dam mutant showed an accumulation of the acidic phospholipids cardiolipin, whereas, the seqA mutant showed a higher proportion of phosphatidylglycerol compared with the wild-type strain [13].

Other interactions of seqA

  • Site specific binding to hemimethylated oriC, of the heavy density membrane obtained from seqA mutant, could be restored by addition of a low amount of His-tagged SeqA protein [14].

Analytical, diagnostic and therapeutic context of seqA

  • Flow cytometry demonstrated that the fusion restored synchronous replication of chromosomal DNA from multiple origins in seqA null mutant cells, indicating that SeqA-Gfp is biologically active [15].
  • A possible reason for this failure might be a profound modification of the outer membrane of the seqA mutant (as revealed by the fact that membrane from the mutant sediments more slowly than that from the wild type during ultracentrifugation) [16].


  1. Dam-dependent phase variation of Ag43 in Escherichia coli is altered in a seqA mutant. Correnti, J., Munster, V., Chan, T., Woude, M. Mol. Microbiol. (2002) [Pubmed]
  2. Bacteriophage P4 immunity controlled by small RNAs via transcription termination. Dehó, G., Zangrossi, S., Sabbattini, P., Sironi, G., Ghisotti, D. Mol. Microbiol. (1992) [Pubmed]
  3. SeqA-mediated stimulation of a promoter activity by facilitating functions of a transcription activator. Słomińska, M., Konopa, G., Ostrowska, J., Kedzierska, B., Wegrzyn, G., Wegrzyn, A. Mol. Microbiol. (2003) [Pubmed]
  4. DomainSieve: a protein domain-based screen that led to the identification of dam-associated genes with potential link to DNA maintenance. Brézellec, P., Hoebeke, M., Hiet, M.S., Pasek, S., Ferat, J.L. Bioinformatics (2006) [Pubmed]
  5. Null mutation of the dam or seqA gene suppresses temperature-sensitive lethality but not hypersensitivity to novobiocin of muk null mutants. Onogi, T., Yamazoe, M., Ichinose, C., Niki, H., Hiraga, S. J. Bacteriol. (2000) [Pubmed]
  6. Coordinating DNA replication initiation with cell growth: differential roles for DnaA and SeqA proteins. Boye, E., Stokke, T., Kleckner, N., Skarstad, K. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  7. Escherichia coli cell cycle control genes affect chromosome superhelicity. Weitao, T., Nordström, K., Dasgupta, S. EMBO Rep. (2000) [Pubmed]
  8. Suppression of a DnaX temperature-sensitive polymerization defect by mutation in the initiation gene, dnaA, requires functional oriC. Blinkova, A., Ginés-Candelaria, E., Ross, J.D., Walker, J.R. Mol. Microbiol. (2000) [Pubmed]
  9. Control of transcription termination by an RNA factor in bacteriophage P4 immunity: identification of the target sites. Sabbattini, P., Forti, F., Ghisotti, D., Dehò, G. J. Bacteriol. (1995) [Pubmed]
  10. Mutual suppression of mukB and seqA phenotypes might arise from their opposing influences on the Escherichia coli nucleoid structure. Weitao, T., Nordström, K., Dasgupta, S. Mol. Microbiol. (1999) [Pubmed]
  11. SeqA limits DnaA activity in replication from oriC in Escherichia coli. von Freiesleben, U., Rasmussen, K.V., Schaechter, M. Mol. Microbiol. (1994) [Pubmed]
  12. Altered biological properties of cell membranes in Escherichia coli dnaA and seqA mutants. Wegrzyn, A., Wróbel, B., Wegrzyn, G. Mol. Gen. Genet. (1999) [Pubmed]
  13. Phospholipid changes in seqA and dam mutants of Escherichia coli. Daghfous, D., Chatti, A., Marzouk, B., Landoulsi, A. C. R. Biol. (2006) [Pubmed]
  14. Replication cycle dependent association of SeqA to the outer membrane fraction of E. coli. d'Alençon, E., Taghbalout, A., Kern, R., Kohiyama, M. Biochimie (1999) [Pubmed]
  15. The assembly and migration of SeqA-Gfp fusion in living cells of Escherichia coli. Onogi, T., Niki, H., Yamazoe, M., Hiraga, S. Mol. Microbiol. (1999) [Pubmed]
  16. Co-ordination between membrane oriC sequestration factors and a chromosome partitioning protein, TolC (MukA). Bahloul, A., Meury, J., Kern, R., Garwood, J., Guha, S., Kohiyama, M. Mol. Microbiol. (1996) [Pubmed]
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