The RpoS Sigma factor relieves H‐NS‐mediated transcriptional repression of csgA, the subunit gene of fibronectin‐binding curli in Escherichia coli

Abstract

Summary: Curli encoded by the c urlin s ubunit gene, csgA, are fibronectin‐ and laminin‐binding fibres expressed by many natural Escherichia coli and E. coli K‐12 strains in response to low temperature, low osmolarity and stationary‐phase growth conditions. Curli expression is dependent on RpoS, a sigma factor that controls many stationary phase‐inducible genes. Many commonly used K‐12 strains carry an amber mutation in rpoS. Strains able to form Curli carry an amber suppressor whereas curli‐negative E. coli K‐12 strains, in general, are sup°. Introduction of supD, supE, or supF suppressors into sup0 strains resulted in expression of temperature‐regulated curli. In curli‐deficient, RpoS−E. coli K‐12 strains, csgA is transcriptionally activated by mutations in hns, which encodes the histone‐like protein H‐NS. Curli expression, fibronectin binding, and csgA transcription remain temperature‐ and osmoregulated in such double mutants. Our data suggest that RpoS+ strains, and hence curli‐proficient strains of E. coli K‐12, are relieved for the transcriptional repression mediated by the H‐NS protein upon accumulating RpoS as cells reach stationary phase.