SdiA, an Escherichia coli homologue of quorum‐sensing regulators, controls the expression of virulence factors in enterohaemorrhagic Escherichia coli O157:H7

The quorum‐sensing system in bacteria is a well‐known regulatory system that controls gene expression in a cell density‐dependent manner. A transcriptional regulator (LuxR homologue), signal synthase (LuxI homologue) and autoinducer (acyl homoserine lactone) are indispensable for this system in most Gram‐negative bacteria. In this study, we found that SdiA, an Escherichia coli LuxR homologue, is a negative regulator of the expression of virulence factors EspD and intimin in enterohaemorrhagic E. coli (EHEC) O157:H7. The expression of EspD and intimin was inhibited at the RNA level upon SdiA overexpression. SdiA has a DNA‐binding motif in its C‐terminal part and can bind to the promoter regions of the esp and eae genes in vitro. Extracellular factors, which accumulate in culture supernatants of O157:H7 at the stationary phase of growth and inhibit EspD and intimin synthesis, bind to the N‐terminal part of SdiA in vivo and in vitro. O157:H7 overproducing the N‐terminal part of SdiA exhibited hypertranscription of EspD and intimin, suggesting that the overproduced N‐terminal part had inhibited the activity of intact SdiA through titration of the extracellular factors. These results indicate that a quorum‐sensing system including the SdiA protein controls colonization by O157:H7.