Current Microbiology

, Volume 56, Issue 5, pp 474–480

The shf Gene of a Shigella flexneri Homologue on the Virulent Plasmid pAA2 of Enteroaggregative Escherichia coli 042 Is Required for Firm Biofilm Formation

Authors

  • Rika Fujiyama
    • Department of PediatricsKagoshima University Graduate School of Medical and Dental Sciences
    • Department of PediatricsKagoshima University Graduate School of Medical and Dental Sciences
  • Naoko Imuta
    • Department of PediatricsKagoshima University Graduate School of Medical and Dental Sciences
  • Koichi Tokuda
    • Department of PediatricsKagoshima University Graduate School of Medical and Dental Sciences
  • Kunihiro Manago
    • Department of PediatricsKagoshima University Graduate School of Medical and Dental Sciences
  • Yoshifumi Kawano
    • Department of PediatricsKagoshima University Graduate School of Medical and Dental Sciences
Article

DOI: 10.1007/s00284-008-9115-y

Cite this article as:
Fujiyama, R., Nishi, J., Imuta, N. et al. Curr Microbiol (2008) 56: 474. doi:10.1007/s00284-008-9115-y

Abstract

Enteroaggregative Escherichia coli (EAEC) is an increasingly important cause of diarrhea in both developing and industrialized countries, and is characterized by strong biofilm formation on the intestinal mucosa. Sequencing of the virulent plasmid pAA2 of the prototype EAEC 042 revealed a cluster of three open reading frames (ORFs; shf, capU, and virK) ca. 93% identical to a similar cluster located in Shigella flexneri. The function of the first ORF Shf protein is not known, but the closest well-characterized homologue is the IcaB protein of Staphylococcus epidermidis, which plays a crucial role in exopolysaccharide modification in bacterial biofilm formation. To investigate the role of this cluster in the virulence of EAEC, we mutated three genes at this locus. All the mutants maintained the aggregative phenotype in the liquid phase. However, the insertional mutant of shf formed a less abundant biofilm in a microtiter plate assay than did the wild type, while the capU mutant and the virK mutant did not. The complementation of the shf mutant with this cluster restored the thick biofilm similar to that of the wild type. The shf transcriptional level decreased in the transcriptional regulator aggR mutant and was restored when the mutant was complemented with aggR. These results suggest that the shf gene is required for the firm biofilm formation of EAEC 042, and transcription of the shf gene is dependent on AggR.

Copyright information

© Springer Science+Business Media, LLC 2008