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Gene Review

virF  -  transcriptional activator of virulence loci

Shigella flexneri 5a str. M90T

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Disease relevance of virF


High impact information on virF

  • H-NS bound cooperatively to these two sites below 32 degrees C, but not at 37 degrees C. DNA supercoiling within the virF promoter region did not influence H-NS binding but was necessary for the H-NS-mediated transcriptional repression [1].
  • The role of promoter curvature as thermosensor is also compatible with the present observation that, with increasing temperature, the virF bending centre moves downstream at a rate having its maximum around the transition temperature, abruptly unmasking a binding site for the transcriptional activator FIS [3].
  • Here we report on the relevance of DNA geometry to the thermoregulation of virF and demonstrate that the virF promoter hosts a major DNA bend halfway between two H-NS sites [3].
  • As the undermodification of tRNA is not affected by the quality of the growth medium, we conclude that such an environmental change in growth conditions partly restores virulence gene expression by counteracting poor translation of the virF mRNA mediated by an oQ-deficient tRNA [4].
  • Plasmid DNA restriction endonuclease patterns of 2457T and 2457O, along with hybridization analysis, showed that a SalI fragment carrying the virF gene in 2457O had increased in size relative to its counterpart in 2457T [5].

Chemical compound and disease context of virF


Biological context of virF

  • The expression of these four antigens is positively regulated by the 30 kD protein encoded by virF, whose nucleotide sequence had been determined and which was previously found to be essential for virulence [7].
  • Plasmid pWR600, carrying a 1,260-bp HpaII fragment encoding a wild-type virF gene, was able to restore the virulent phenotype and translucent colonial morphology to nine independently isolated 2457O hosts [5].
  • Subcloning and nucleotide sequencing indicated that this positive regulator gene was virF [2].
  • The virF and virB loci encode regulatory proteins required for transcriptional activation of the virulence regulon [8].
  • DNA sequence analysis mapped the insertion element, designated IS1SFO, within an A.T-rich region of the virF open reading frame and identified a 9-bp virF target sequence that was duplicated at the insertion site of IS1SFO [5].

Associations of virF with chemical compounds

  • The direction of transcription of virF was determined by using a chloramphenicol resistance cartridge [6].
  • Polyacrylamide gel electrophoresis of three DNA fragments containing the virF, the virB and the VirG promoters demonstrates, in agreement with computer predictions, that they have an intrinsically curved structure, confirming the preference of H-NS for bent DNA [9].

Regulatory relationships of virF

  • Expression of four virulence antigens of Shigella flexneri is positively regulated at the transcriptional level by the 30 kiloDalton virF protein [7].

Other interactions of virF

  • The previously reported regulatory activity of the virF gene some 30 kb distance away was shown to act exclusively through virB [10].
  • Results obtained from molecular genetic studies, mainly of the genes, virG, virF and kcpA are discussed [11].
  • The virF gene appears to have a central role in activation of the 230 kb plasmid-encoded virulence genes [10].

Analytical, diagnostic and therapeutic context of virF

  • Multiplex PCR analysis of DNA obtained from spontaneous avirulent derivatives indicated that virF and virB were deleted or otherwise inactivated in over 97% of the isolates [8].
  • Random and site-directed mutagenesis of the virF gene encoding VirF yielded a number of mutations along the length of the protein which severely affected the ability of VirF to activate gene expression [12].


  1. Thermoregulation of Shigella and Escherichia coli EIEC pathogenicity. A temperature-dependent structural transition of DNA modulates accessibility of virF promoter to transcriptional repressor H-NS. Falconi, M., Colonna, B., Prosseda, G., Micheli, G., Gualerzi, C.O. EMBO J. (1998) [Pubmed]
  2. Cloning of regions required for contact hemolysis and entry into LLC-MK2 cells from Shigella sonnei form I plasmid: virF is a positive regulator gene for these phenotypes. Kato, J., Ito, K., Nakamura, A., Watanabe, H. Infect. Immun. (1989) [Pubmed]
  3. The virF promoter in Shigella: more than just a curved DNA stretch. Prosseda, G., Falconi, M., Giangrossi, M., Gualerzi, C.O., Micheli, G., Colonna, B. Mol. Microbiol. (2004) [Pubmed]
  4. Putrescine or a combination of methionine and arginine restores virulence gene expression in a tRNA modification-deficient mutant of Shigella flexneri: a possible role in adaptation of virulence. Durand, J.M., Björk, G.R. Mol. Microbiol. (2003) [Pubmed]
  5. Spontaneous insertion of an IS1-like element into the virF gene is responsible for avirulence in opaque colonial variants of Shigella flexneri 2a. Mills, J.A., Venkatesan, M.M., Baron, L.S., Buysse, J.M. Infect. Immun. (1992) [Pubmed]
  6. DNA sequence and product analysis of the virF locus responsible for congo red binding and cell invasion in Shigella flexneri 2a. Sakai, T., Sasakawa, C., Makino, S., Yoshikawa, M. Infect. Immun. (1986) [Pubmed]
  7. Expression of four virulence antigens of Shigella flexneri is positively regulated at the transcriptional level by the 30 kiloDalton virF protein. Sakai, T., Sasakawa, C., Yoshikawa, M. Mol. Microbiol. (1988) [Pubmed]
  8. Virulence plasmid instability in Shigella flexneri 2a is induced by virulence gene expression. Schuch, R., Maurelli, A.T. Infect. Immun. (1997) [Pubmed]
  9. A role for H-NS in the regulation of the virF gene of Shigella and enteroinvasive Escherichia coli. Prosseda, G., Fradiani, P.A., Di Lorenzo, M., Falconi, M., Micheli, G., Casalino, M., Nicoletti, M., Colonna, B. Res. Microbiol. (1998) [Pubmed]
  10. A dual transcriptional activation system for the 230 kb plasmid genes coding for virulence-associated antigens of Shigella flexneri. Adler, B., Sasakawa, C., Tobe, T., Makino, S., Komatsu, K., Yoshikawa, M. Mol. Microbiol. (1989) [Pubmed]
  11. Molecular genetic approaches to the pathogenesis of bacillary dysentery. Yoshikawa, M., Sasakawa, C., Makino, S., Okada, N., Lett, M.C., Sakai, T., Yamada, M., Komatsu, K., Kamata, K., Kurata, T. Microbiol. Sci. (1988) [Pubmed]
  12. In vivo DNA-binding and oligomerization properties of the Shigella flexneri AraC-like transcriptional regulator VirF as identified by random and site-specific mutagenesis. Porter, M.E., Dorman, C.J. J. Bacteriol. (2002) [Pubmed]
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